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CORRELATIONS BETWEEN AIDS AND CFS






CORRELATIONS BETWEEN CFS AND AIDS

FOREWORD

Chronic Fatigue Syndrome is not the only illness that is frustratng
contemporary medical science. Gloom pervaded the Ninth International AIDS
Meeting (held in Berlin in June 1993), as clinicians and researchers
acknowledged that little progress was being made in fighting the illness.
The drug that has been touted for years by the U.S. government as stopping
the progression of AIDS and extending patients' lives, AZT, does neither.
In fact, researchers revealed, AZT is so toxic that it may actually hurt
AIDS patients more than it helps. And the immune system marker used to
evaluate AIDS patients' health (and AZT's action), T4 cell counts, it was
admitted in Berlin, has essentially no correlation with patients' health.

Although uneasiness and distress permeated news reports during and
following the Berlin meeting, no reporter asked the obvious question: Is it
possible that so little progress has been made in combatting AIDS because a
mistake has been made in the definition of the epidemic?

This book will attempt to answer not only that question, but also other,
potentially even more alarming, ones: Is CFS actually part of the AIDS
epidemic? Are CFS and AIDS, in fact, the same illness?

Since the Berlin conference, for anyone interested in observing it,
evidence linking these two refractory epidemics, AIDS and Chronic Fatigue
Syndrome, has continued to accumulate.

Anxiety about the direction of AIDS research had really begun at the
previous international AIDS conference, held in Amsterdam in 1992.

The bombshell of 1992's AIDS conference was the announcement that some
researchers had identified cases of AIDS without evidence of infection with
the "AIDS virus," HIV.

These "non-HIV AIDS cases" had severely depleted T4 (or CD4) cells, like
AIDS patients; they also developed life-threatening opportunistic
infections.

What wasn't known to most observers was that one of the researchers who had
first publicly identified some of the non-HIV AIDS cases, Dr. Sidhur Gupta
of the University of California, Irvine, is a Chronic Fatigue Syndrome
researcher.

And some of the non-HIV AIDS cases, it was soon revealed, were actually CFS
patients.

Shortly after the June 1992 AIDS conference in Amsterdam, Chronic Fatigue
Syndrome researcher Dr. Paul Cheney announced that he had 20 CFS patients
in his practice who had the same immune system deficiencies as the non-HIV
AIDS cases.

The hallmark of the HIVnegative AIDS cases, as defined by the Centers for
Disease Control and Prevention, is a depletion of the T4 (or CD4) cells.

Therefore, the CDC decided to call the HIV-negative, AIDS-like disease
"ICL" (an abbreviation of the tongue twisting "idiopathic CD4-positive
T-lymphocytopenia," which means, simply, an unexplained loss of T4 cells).

Most healthy people have a T4 cell count of approximately 1,000; a T4 cell
count below 800 is considered abnormal. In order to be diagnosed with ICL,
a person must have a T4 cell count of less than 300.

One of the most puzzling things about the ICL cases to AIDS researchers --
other than the fact that they don't have HIV -- is that most of the
patients do not fit into recognized AIDS "risk behavior" categories; that
is, they are not gay men, IV drug users, or the sexual partners of people
in those risk groups.

How can AIDS exist in the absence of the virus that causes it? None of the
AIDS researchers gathered in Amsterdam in June 1992 seemed able to answer
that question.

The mystery of what role HIV plays in causing the immune system
deterioration and symptoms seen in AIDS deepened in early October 1992 when
a British medical journal carried a report about a strain of HIV that does
not appear to cause any kind of illness.

An Australian research team wrote to The Lancet to report on five people
who had received blood from a man later found to be infected with HIV.
However, ten years following the transfusions, the five blood recipients,
as well as the original, HIV-positive donor, remained free of AIDS symptoms
and were apparently healthy. The Australian researchers concluded that all
six people were infected with a non-disease-causing strain, or type, of
HIV.

Studies have shown that HIV is spread only through blood products (i.e., in
transfusions), or through exchange of bodily fluids, such as during sex.
AIDS is considered to be primarily a sexually-transmitted disease, but one
that requires many exposures -- some estimates run as high as 500 exposures
-- to catch.

CFS appears to be transmitted much more easily; some researchers have
guessed that it might be spread by saliva, as when people share eating
utensils. Dr. Cheney, in fact, has reported that as many as 40 percent of
his CFS patients also have a close associate -- not a sexual partner -- who
has an illness similar to CFS.

Dr. Cheney's statistic -along with the mystery of why AIDS could develop
without HIV infection and why HIV infection does not always lead to AIDS --
raises the possibility that a virus or bacteria that spreads more easily
than HIV could be attacking people's immune systems.

Dr. Cheney described the immune system damage seen in CFS patients for the
Food and Drug Administration in May 1993. Dr. Cheney told the FDA that five
of his CFS patients had died during the preceding six months. Two of these
patients committed suicide, which is all too common among CFS patients. But
three of Dr. Cheney's patients who died, like AIDS patients, succumbed to
overwhelming infections that their damaged immune systems just couldn't
fight off.

But Dr. Cheney's CFS patients, like the ICL patients, appeared not to be
infected with HIV, even though they developed AIDS-like immunodeficiencies
and, in some cases, life-threatening opportunistic infections.

One of the AIDS-like immunodeficiencies seen in CFS involves cells in the
immune system that are important in fighting infections: natural killer
cells. Natural killer cells are the scavengers of the immune system; they
attack and kill anything that appears to be foreign, including the body's
own cells that are infected with viruses or other disease-causing agents.
Because of that activity, natural killer cells are considered to be part of
the immune system's front line of defense against both viruses and cancer.

Natural killer cells are also essential in protecting against tuberculosis,
but at the same time, they are disabled by the TB germ. If a person's
natural killer cells are not working properly, they are at much increased
risk for developing active tuberculosis.

In both AIDS and Chronic Fatigue Syndrome patients, natural killer cells
are almost completely disabled. One study of CFS patients found that their
natural killer cells' functioning was decreased by 86 percent.

In other words, if a healthy person's natural killer cells worked at 100
percent capacity, a CFS patient's natural killer cells are working at only
14 percent.

Of all the conditions in which natural killer cell activity has been
studied, only AIDS patients have been found to have natural killer cells as
disabled as those of CFS patients.

However, most AIDS researchers have concentrated on studying the immune
system cells implicated in the non-HIV AIDS cases, the T4 (or CD4) cells.
T4 cells have been thought to be a good indicator of failing or improving
health in AIDS patients; when their numbers decreased, patients were
thought to be at higher risk of developing serious infections. Conversely,
rising numbers of T4 cells were seen as proof that therapies, such as AZT,
were improving patients' health.

As a result of this belief that T4 cell numbers correlated well with health
status, very few scientists have studied the natural killer cells and how
they fit into the puzzle of AIDS.

In early 1993, however, a study was published in the prestigious British
medical journal Nature which not only forged several more links between the
AIDS and Chronic Fatigue Syndrome epidemics, but also went a long way
toward explaining why natural killer cells stop working in both syndromes.

National Cancer Institute researcher Dr. Robert C. Gallo and his colleagues
made an astonishing assertion in the Nature study: They reported that a
virus found to be actively growing in both AIDS and Chronic Fatigue
Syndrome patients, Human Herpes Virus 6 (HHV-6), infects and kills natural
killer cells. Moreover, according to the report from the Gallo laboratory,
HHV-6 is the only virus known to be able to do that.

This landmark study answered two previously unanswered questions: It
explains at least part of what the actively growing (or "replicating")
HHV-6 is doing in AIDS and Chronic Fatigue Syndrome patients, and it partly
explains why natural killer cells don't work in those patients.

In fact, Dr. Gallo and his coworkers suggested that HHV-6 "may contribute
to the immune dysfunctions associated with CFS and AIDS."

Even studies of T4 cells published in early 1993 inadvertently linked the
AIDS and Chronic Fatigue Syndrome epidemics.

The government scientist responsible for Chronic Fatigue Syndrome research
at the National Institutes of Health, Dr. Stephen Straus, finally admitted
in early 1993 -- after 13 years of trying to prove that Chronic Fatigue
Syndrome is a type of depression -- that immune system deficiencies are
part of the illness. Dr. Straus and his colleagues published data showing
that CFS patients, like AIDS patients, experience a drop in the number of
T4 cells in their blood.

Dr. Straus proposed a novel mechanism to explain the loss of T4 cells in
CFS patients: The T4 cells of CFS patients are not destroyed, as they are
in AIDS patients, according to Dr. Straus; the T4 cells are just hiding in
the lymph nodes where they cannot be detected by blood tests.

Therefore, according to Dr. Straus, the T4 cell depletion observed in CFS
patients is completely different from the T4 cell depletion seen in AIDS
patients.

Unfortunately, Dr. Straus was unable to produce any evidence to support
this theory (and still has not). Dr. Straus did not suggest, in
contradiction to what Dr. Cheney has found, that any of his CFS patients
had T4 cell counts so low they could be identified as ICL patients.

Almost simultaneously, Dr. Yvonne Rosenberg, a scientist working at the
Henry M. Jackson Foundation Research Laboratory in Rockville, Maryland,
announced that her studies had indicated that T4 cells in AIDS patients are
not as decimated as they might appear to be. Instead, Rosenberg suggested,
at the prestigious Keystone Conference held the last week of March, 1993,
that AIDS patients' T4 cells are sequestered in the lymph nodes where they
remain unmeasured by blood tests.

Although Dr. Anthony Fauci, the man in charge of AIDS research in the
United States, attended the conference and presented the work his research
group had performed on the lymph nodes of AIDS patients, neither he nor any
other government scientist chose to comment about the parallel finding
about T4 cells in the lymph nodes of AIDS and CFS patients.

And, as the Centers for Disease Control and Prevention (CDC) lurches toward
finishing its several-year-long surveillance study to estimate how many
people in the U.S. have Chronic Fatigue Syndrome, new information on that
subject has come from a surprising source. A group of researchers at the
New England Medical Center (in Boston) studying Lyme disease discovered
that up to 50 percent of people diagnosed with Lyme disease actually have
Chronic Fatigue Syndrome.

The Lyme disease researchers set out to answer another question altogether.
They were trying to figure out why Lyme disease treatment is unsuccessful
in so many cases.

Lyme disease is caused by a bacterium similar to the one that causes
syphilis; it is treated with antibiotics. But a large percentage of people
diagnosed as having Lyme disease didn't improve when treated with
antibiotics, and the Boston researchers were trying to find out why.

They discovered that the patients whose Lyme disease didn't respond to
antibiotics didn't have Lyme disease.

Even more surprisingly, they found that almost 50 percent of those wrongly
diagnosed with Lyme disease had, instead, a putatively viral illness:
Chronic Fatigue Syndrome.

In addition to its importance to people with Lyme disease and their
physicians, this study potentially has enormous importance for the CDC
surveillance study. The CDC study is examining people diagnosed with CFS,
to see how many of them fit the very strict CDC definition. From those
numbers, CDC investigators will extrapolate to the rest of the population
and attempt to estimate how many Americans have CFS.

But they are not examining people who have been diagnosed with other, more
accepted illnesses, like Lyme disease.

As the New England Medical Center study showed, there could be thousands --
or hundreds of thousands -- of people who have Chronic Fatigue Syndrome who
have been diagnosed as having some other disease. Those people are quite
unlikely to be counted by the CDC.

The CDC's estimate of how many Americans have CFS could, therefore, be
terribly wrong unless this type of misdiagnosis is taken into
consideration.

And this kind of misdiagnosis is likely to continue until there is a
diagnostic test available for CFS.

Many researchers are attempting to create such a test for CFS. One line of
research that originally appeared to be promising involved finding a
retrovirus, like the virus that supposedly causes AIDS, in CFS patients.
Some researchers had believed that finding such a retrovirus, and proving
that it causes CFS, would result in a definitive way to diagnose the
syndrome, as the HIV antibody test has done for AIDS.

But the "CFS retrovirus" research apparently ran into some roadblocks, and
little progress has been made since the single report describing the
retrovirus was published in early 1991.

Meanwhile, HIV has come under intensified scrutiny as a diseasecausing
organism.

Although the controversy over whether HIV causes AIDS -- with or without
the help of "co-factors" -has continued, few attacks on the retrovirus have
appeared in the medical literature. In June 1993, however, an Australian
research team published a devastating attack on the HIV antibody test,
often called the "AIDS test."

The Australian research team, in fact, raised serious questions not only
about whether HIV causes AIDS, but even about its existence as a distinct,
infectious retrovirus.

Writing in the June 11, 1993, issue of the journal Bio/Technology, Eleni
PapadopoulosEleopulos and her colleagues examined the HIV antibody test and
found that it had many problems.

Eleopulos and her co-workers found that the HIV antibody test is not
consistent; that is, the same blood sample tested in several laboratories
does not give the same results in every test performed. They suggest that
some of the biological molecules that the HIV antibody test is measuring
may be just background junk, cell proteins that are contaminating the test.

Even more disturbing, through an extensive study of the HIV literature,
Eleopulos and her colleagues raised the question of whether HIV has ever
really been isolated as a discrete entity. The answer they reached is that
it has not.

This research caused Eleopulos and her co-workers to conclude that, not
only is the HIV antibody test extremely unreliable and perhaps not at all
useful, but that it may be a test for something that does not cause AIDS.

This takes us back to the original questions: Is it possible that a mistake
has been made in formulating the definition of AIDS? Is Chronic Fatigue
Syndrome actually part of the AIDS epidemic?

If this is even a remote possibility, why haven't other books been written
about it? Why isn't every health reporter in the country writing about it,
every investigative reporter investigating?

The answer, I believe, is pretty simple, and it is a problem that has
dogged the AIDS epidemic from the beginning: denial.

From the very beginning of the AIDS epidemic, the syndrome has been
characterized as affecting "the other": Haitians (i.e., blacks), gay men,
IV drug users, and these groups' sexual partners. These individuals have
been contrasted -- and still are -- with the "innocent victims" of the AIDS
epidemic: the unknowing wives, and their babies.

AIDS patients, and people who test HIV-positive (whatever that actually
turns out to mean), have been so badly treated, so discriminated against,
so scapegoated and demonized that it is not surprising that there is an
almost reflexive recoiling from the possibility that AIDS is not the
narrowly-defined illness that it has been portrayed as being.

People have been murdered for testing HIV-positive; they have been accused
of murder; they have been driven to suicide; they have been jailed; they
have been denied jobs and health insurance and places to live.

Given all this, denial that AIDS could be even more widespread than
government officials admit is not too surprising. What rational person
would want to be diagnosed with an illness that could produce such terrible
repercussions in every area of life?

Oddly enough, this denial appears to be most fiercely concentrated among
medical researchers, and not among the patients themselves.

Chronic Fatigue Syndrome patients, in fact, know they suffer from a
profoundly debilitating, life-altering illness that is destroying their
immune systems.

Until the denial among medical professionals about the relationship between
the AIDS and Chronic Fatigue Syndrome epidemics is overcome, however, it is
difficult to imagine how either epidemic can be ended.

CHAPTER ONE

SOME CFS PATIENTS MAY BE "NON-HIV AIDS" CASES

A disturbing announcement was made at the July 1992 international AIDS
conference held in Amsterdam: Several people with symptoms of AIDS, but who
had no evidence of infection with either HIV-1 or HIV2 (the viruses
generally believed, at the time, to cause AIDS), had been identified by the
U.S. Centers for Disease Control. A few weeks later, in early September,
Newsweek made an even more shocking announcement: that Chronic Fatigue
Syndrome researcher Dr. Paul Cheney had in his practice 20 CFS patients who
had the same immune system deficiencies as the non-HIV AIDS cases revealed
at the Amsterdam conference.

What wasn't known to most observers was that one of the researchers who had
first said publicly that he was aware of such cases, Dr. Sidhur Gupta of
the University of California, Irvine, is himself a Chronic Fatigue Syndrome
researcher.

The fact that some CFS patients were developing exactly the same immune
system problems as AIDS patients, however, raised the questions not only of
what was causing that immune system destruction but also of the
relationship that exists between the two syndromes.

The hallmark of the HIVnegative AIDS cases, as established by the Centers
for Disease Control, is a depletion of a type of immune system cell called
T4 (or CD4) cells. The T4 cells of AIDS patients can fall to very low
levels and, although recent studies have suggested that there is no real
correlation with health status, a decreasing T4 cell count is generally
viewed as a sign of worsening disease.

The CDC decided to call the HIV-negative, AIDS-like disease "ICL" (an
abbreviation for "idiopathic CD4-positive Tlymphocytopenia," which simply
means an unexplained depletion of T4 cells).

Most healthy people have a T4 cell count of approximately 1,000; a T4 cell
count below 800 is considered abnormal. In order to be diagnosed with ICL,
a person must have a T4 cell count of less than 300.

One of the most puzzling things about the ICL cases to AIDS researchers --
other than the fact that they didn't have HIV -- is that most of the
patients do not fit into recognized AIDS "risk behavior" categories; that
is, they were not gay men, IV drug users, or the sexual partners of people
in those risk groups. These cases may, in fact, be dramatic evidence that
federal officials have not told the public the whole truth about the nature
and the full scope of the AIDS epidemic.

The mystery of what role HIV actually plays in causing the immune system
deterioration and symptoms seen in AIDS deepened in early October 1992. The
British medical journal The Lancet reported that five people had received
blood from a man later found to be infected with HIV; however, ten years
later, the five transfusion recipients as well as the original,
HIV-positive blood donor remained free of AIDS symptoms and were apparently
healthy. The Australian researchers who reported those cases concluded that
these six people were infected with a nondisease-causing strain, or type,
of HIV.

The link between the immune system dysfunction seen in AIDS and in CFS was
made explicit in early 1993 when government scientists admitted that CFS
patients, like AIDS patients, suffer a decline in T4 cells. The
government's leading CFS researcher, Dr. Stephen Straus at the National
Institute of Allergy and Infectious Diseases, published a research paper in
The Journal of Clinical Immunology in which a decrease in the number of T4
cells in CFS patients was documented.

Dr. Straus proposed a novel mechanism to explain the loss of T4 cells in
CFS patients: The T4 cells of CFS patients were not depleted, as they were
in AIDS patients, according to Dr. Straus; they were just hiding in organ
tissues. Unfortunately, Dr. Straus was unable to produce any evidence to
support this theory (and still has not done so). Dr. Straus did not suggest
that any of his CFS patients had T4 cell counts so low that they could be
identified as ICL patients.

Meanwhile, Dr. Cheney, in addition to announcing that some of his CFS
patients had low enough T4 cell counts to be considered nonHIV AIDS cases,
reported that as many as 40 percent of his CFS patients also had a close
associate with an illness similar to CFS. This information -- along with
the mystery of why AIDS could develop without HIV infection and why HIV
infection does not always lead to AIDS -- raised the possibility that a
virus or bacteria that spreads more easily than HIV could be attacking
people's immune systems.

CHAPTER TWO

A VIRUS FOUND IN AIDS PATIENTS IS ALSO FOUND IN CFS PATIENTS WITH BRAIN
LESIONS AND MAY BE THE PRIMARY ATTACKER OF THE IMMUNE SYSTEM

A virus that has been considered for several years a possible cause of
Chronic Fatigue Syndrome is Human Herpes Virus 6 (HHV-6). This virus was
first discovered in AIDS and cancer patients in the mid-1980s at the
National Cancer Institute. It was subsequently found that people with
Chronic Fatigue Syndrome, like people with AIDS, can have extremely high
levels of antibodies to HHV-6.

As more is learned about HHV6, its ability to attack the immune system --
and perhaps other parts of the body, like the nervous system -- has been
documented in more and more frightening ways. Even more alarmingly, the
most recent research on HHV-6 suggests that it, and not HIV, is the primary
infection that destroys an important part of the immune system in AIDS.

That part of the immune system is the natural killer (NK) cells. NK cells
are crucial to the immune system's front-line defense against both viruses
and cancer, because they attack and kill any cells they perceive to be
foreign. If the NK cells aren't working properly -which they aren't, in
both AIDS and CFS -- this very important protection is knocked out.

The research team that discovered the existence of HHV-6, working with Dr.
Robert C. Gallo at the National Cancer Institute, announced in early April
1993 that HHV-6 is the only virus known to be able to infect and kill NK
cells.

Furthermore, Dr. Gallo and his colleagues asserted, HHV-6 infection allows
the AIDS virus, HIV, to invade NK cells and kill them.

The question of how many other kinds of cells require HHV-6 to be present
before HIV can invade them remains, at this time, unanswered.

HHV-6 is capable of wreaking all kinds of havoc, not all of which is
confined to the immune system. In January 1992, a study was published
showing that a large percentage of CFS patients who had HHV-6 actively
growing in their blood streams also showed evidence of organic brain
disease.

When CFS patients from the first detected outbreak of CFS in the U.S. --
which occurred in Incline Village, Nevada, in the mid-1980s -- were
studied, brain scans showed that 80 percent of those infected with actively
growing HHV-6 had (several years after the initial outbreak) developed
brain lesions.

No one knows what the lesions mean or are doing to the patients, or whether
HHV-6 is actively growing at the site of the brain damage.

But the Incline Village CFS patients were also found to have NK cells that
weren't functioning properly. Now, we know that HHV-6 is, most likely,
directly responsible for the dysfunction in the CFS patients' NK cells, but
the virus' involvement in causing the brain lesions has yet to be proven
conclusively.

The scientists studying the Incline Village patients concluded that there
was an infectious agent, capable of being spread from person to person, in
the CFS patients: HHV-6.

This very important study of CFS patients not only indicates that CFS is a
contagious illness, but also suggests that HHV-6 is its cause.

CHAPTER THREE

HHV-6 KILLS AN IMPORTANT IMMUNE SYSTEM CELL IN AIDS AND CFS PATIENTS

Human Herpes Virus 6 (HHV-6) was first discovered in people with damaged
immune systems who had cancer or AIDS. However, when studies showed that it
seemed to infect about 90 percent of the world's population by age three,
HHV-6 was generally portrayed by scientists as a fairly harmless virus.

More recent research, however, has thrown the supposition about HHV-6 being
harmless into doubt. For one thing, there are two different types of HHV-6;
one is isolated from infants, and seems to cause only a mild childhood
illness, with fever and rash, called roseola.

The other type of HHV-6, however, is found in very sick adults who have
AIDS, cancer, Chronic Fatigue Syndrome, or other immune system
abnormalities. And the newest research on this type of HHV-6 suggests that
it may be the cause of the immune system deficiencies seen in both AIDS and
CFS.

National Cancer Institute researcher Robert Gallo and his coworkers are
generally credited with the discovery of HHV-6, and Dr. Gallo and his lab
workers have continued to study the virus intensively. (Dr. Gallo's claims
to virus discovery have to be taken with a grain of salt, however. He also
claimed, for a number of years, to have discovered HIV, the "AIDS virus."
After a lengthy investigation and charges of viruslifting by other
scientists, however, Dr. Gallo admitted that he had simply "discovered" a
virus that had been sent to him by Pasteur Institute scientist Luc
Montagnier and his research group. For having made false claims about
discovering the "AIDS virus," Dr. Gallo was judged guilty of scientific
misconduct by the National Institutes of Health in December 1992.)

The HHV-6 that Dr. Gallo and his colleagues are studying at the National
Cancer Institute is the type that infects adults who have AIDS, cancer, or
Chronic Fatigue Syndrome.

In April 1993, Dr. Gallo and his colleagues published an astonishing report
in the prestigious British medical journal Nature. They reported that HHV-6
was able to infect and kill the natural killer cells, which are an
important part of the immune system, and that it was the only virus ever
found to do so.

Natural killer cells are the body's front-line defense against viruses and
some kinds of cancer. When natural killer cells encounter a cell that is
"foreign" -- either because it is infected with a virus or because it has
become cancerous -- they engulf and destroy it. Unlike other types of
immune system cells, natural killer cells do not require any type of
priming or activating by another part of the immune system; that is why
they are considered to be the first line of defense in protecting the body
against certain invaders.

In both AIDS and Chronic Fatigue Syndrome patients, the natural killer
cells just don't work the way they do in healthy people. One researcher
found a natural killer cell activity deficit of 86 percent in the Chronic
Fatigue Syndrome patients she studied. AIDS patients have similar deficits
in natural killer cell activity. Before Dr. Gallo's study linking HHV-6 and
natural killer cell destruction, no one had been able to explain why
natural killer cells stopped working in AIDS and CFS patients.

Dr. Gallo and his colleagues, however, not only showed that HHV-6 can
infect and kill natural killer cells, but actually suggested that the virus
"may play a role in the acquired immunodeficiency syndrome (AIDS) and in
the chronic fatigue syndrome, two disorders associated with a defective NK
cell activity."

They are also the first researchers to confirm that the immune system
abnormalities seen in AIDS and CFS are actually the same.

In fact, in the conclusion of their research report, Dr. Gallo and
co-workers stated that their results "elucidate a novel mechanism whereby
HHV-6 may contribute to the immune dysfunction associated with CFS and
AIDS."

Further studies of HHV-6 in AIDS and CFS patients may provide even more
examples of how this virus causes the immune system abnormalities the two
syndromes share and may even suggest even more strongly that CFS and AIDS
are simply different manifestations of the same illness.

CHAPTER FOUR

HHV-6 SEEMS TO BE CAUSING LUNG DISEASE IN IMMUNOSUPPRESSED INDIVIDUALS

People who receive organ transplants are given drugs that suppress their
immune systems so that they do not reject the transplanted organs, thus
placing them in a state that is similar to AIDS or CFS. While they are in
that immunosuppressed state, they are especially vulnerable to infections,
just like CFS and AIDS patients are. Now it appears that an often-fatal
lung illness that can occur following bone marrow transplantation may be
caused by a virus that infects AIDS and CFS patients, Human Herpesvirus 6
(HHV6).

If HHV-6 is causing lung disease in bone marrow transplant recipients, that
raises the question: Is HHV-6 also causing lung disease in CFS and AIDS
patients?

Another extremely serious immunological complication that occurs after bone
marrow transplantation, Graft-Versus-Host Disease (GVHD), may also be
caused by HHV-6. Both of these findings were published in the New England
Journal of Medicine in July 1993.

The lung illness caused by HHV-6 is pneumonitis, which is inflammation of
the lung (basically, a type of pneumonia). When lung tissues from patients
who'd had bone marrow transplants and subsequently developed pneumonitis of
unknown cause were examined by a research group in Seattle, the tissues
were found to contain considerable amounts of HHV-6.

That led the researchers to conclude that HHV-6 was probably causing some
cases of the oftenfatal pneumonitis in bone marrow transplant patients.

This is the first time that HHV-6 has been implicated in causing a lung
illness.

Graft-Versus-Host Disease (GVHD) is another potentially lifethreatening
illness that strikes bone marrow transplant recipients. In GVHD, the
donor's healthy Tcells (which are impaired in AIDS and CFS) attack the
recipient's tissues; GVHD is a form of organ rejection. The symptoms of
GVHD include fever, rash, hepatitis, diarrhea or abdominal pain, vomiting,
and weight loss.

Some of the bone marrow transplant patients studied by the Seattle
researchers who developed pneumonitis caused by HHV-6 also developed severe
GVHD.

Those patients were also found to have very high levels of HHV-6,
particularly in their lungs.

That is to say, three conditions occurred together in the patients: high
levels of HHV-6, pneumonitis, and severe GVHD.

This led the Seattle researchers to suggest that HHV-6 is the likely cause
of both the pneumonitis and the GVHD seen in some bone marrow transplant
recipients.

Another report about HHV-6 also appeared in the same issue of the New
England Journal of Medicine. This report was from Japan, where researchers
had observed a ""mononucleosis-like illness'' they believed to be caused by
HHV-6.

The 43-year-old man described by the Japanese research team was admitted to
the hospital with a high fever, rash, swollen lymph nodes, a swollen
spleen, and inflamed tonsils; he was also suffering from liver dysfunction.

This man, too, had high levels of HHV-6 during his illness, leading the
Japanese researchers to conclude that the man's ""mononucleosis-like
illness'' had been caused by HHV-6.

Although some researchers have suggested that HHV-6 is a basically harmless
virus that infects approximately 90 percent of the world's population by
the age of three, new information being published about the virus indicates
that some varieties, or strains, are capable of causing profound immune
dysfunction and serious illness. These three problems may be just the tip
of the iceberg in terms of the damage that HHV-6 is able to inflict on the
immune system.

CHAPTER FIVE

A VIRUS FOUND GROWING IN CFS PATIENTS HAS BEEN LINKED TO MISCARRIAGE

One of the viruses that has been found to be active in both CFS and AIDS
patients, Human Herpes Virus 6 (HHV-6), has been linked by Japanese
scientists to miscarriage.

HHV-6 is a virus that primarily invades the T-cells of the immune system
(though it can also live in other immune system cells). T-cells are
critical in regulating immune responses -- both in getting an immune
response started, and in shutting it down. When the T-cells don't work
because a virus is attacking them, the immune response can be severely
affected, as is seen in both CFS and AIDS.

Very recently, HHV-6 has been found to be the only virus that is capable of
invading and killing natural killer (NK) cells. NK cells don't work
properly in both CFS and AIDS; a deficiency of NK cell activity, in fact,
has been cited by numerous researchers to be the most consistent immune
system abnormality found in CFS patients. If the NK cell activity of AIDS
patients is examined, it, too, is found to be consistently abnormal. HHV-6,
which is known to be actively growing in both AIDS and CFS patients, has
been identified as the only virus known to be able to infect and kill NK
cells. It is reasonable to assume that it is causing the abnormal NK cell
activity seen in both sets of patients.

HHV-6 has also been linked, in CFS patients, to the development of brain
lesions (areas of dead or damaged brain tissue). A recent study found that
CFS patients with a lot of active HHV-6 also had developed brain lesions
that are visible on specialized brain scans; patients without active HHV-6
did not have brain lesions.

A Japanese research team from the Nara Medical University studied 30
patients who'd had miscarriages early in pregnancy (at 6-12 weeks). When
tissue from the miscarriages was examined, they were found to contain HHV-6
antibodies that were four times higher than those found in pregnant women
who did not miscarry. In a report published in the British medical journal
The Lancet in November 1992, the Japanese research team suggested that
active HHV-6 "may predispose" to miscarriage in pregnant women.

CHAPTER SIX

HHV-6 INFECTIONS CAN BE FATAL

Human Herpes Virus 6, HHV-6, has been presented to the world as rather a
Dr. Jekyll-Mr. Hyde kind of a virus: On the one hand, researchers like Dr.
Jay Levy at the University of California-San Francisco point out that HHV-6
infects so large a percentage of people world-wide that it must be
essentially harmless. On the other hand, some pediatricians have reported
that HHV-6 infections have been fatal.

It is possible, given that more than 10 different strains, or types, of
HHV-6 have been identified, that different strains of the virus cause
different levels of illness, ranging from almost unnoticeable (a "silent"
infection) to deadly.

High levels of antibodies to HHV-6 have been found in several groups of
very sick patients, including AIDS and CFS patients.

No one knows for sure what damage HHV-6 is doing in those patients. In the
laboratory, however, it has been demonstrated that at least some strains of
HHV-6 are very efficient killers of immune system cells -- especially T4
(or CD4) and natural killer cells, the two types of cells most affected in
both CFS and AIDS.

And HHV-6 has recently been found in more than one-third of a group of
Kaposi's sarcoma tumor biopsies, suggesting that it may play a role in
causing this unusual cancer seen in AIDS patients.

Recently, the HHV-6 strains have been divided by researchers into two
groups, or variants: Variant A, viruses which have been isolated from sick
adults (those with CFS, AIDS, or cancer); and Variant B, which has been
found in relatively healthy babies.

Most of the fatal HHV-6 infections identified in the medical literature,
however, have occurred in very young children. Cases of fatal hepatitis, or
liver disease, caused by HHV-6 in children were reported in the medical
literature in 1990 and 1991. HHV-6 infection was localized, not
surprisingly, primarily in the children's livers.

In summer 1992, however, a group of New York University re searchers
reported a fatal, systemic -- that is, spread throughout many different
organs and tissues -- HHV-6 infection in a 13-month-old girl.

The child's illness began with a fever and lack of appetite; soon, however,
she began to show evidence of hemorrhaging -- uncontrolled bleeding or
leaking of blood vessels -- on her face, trunk, arms, legs, and around her
lips. This child also developed liver disease. She died from congestive
heart failure on the fifth day after being hospitalized.

When an autopsy was performed on the child, HHV-6 infected white blood
cells were found in numerous internal organs: heart, lungs, liver, spleen,
thymus, kidney, and bladder, as well as in the gastrointestinal tract,
salivary glands, bone marrow, lymph nodes, middle ear, peripheral nerves,
and skeletal muscle.

Not too surprisingly, the physicians concluded that this disseminated, or
very widespread, HHV-6 infection had killed the little girl.

If certain strains of HHV-6 are capable of causing fatal illnesses --
assuming that this is a strain-dependent phenomenon, which it may not be --
it seems that a reasonable next step in HHV6 research would be to identify
the most deadly strains.

CHAPTER SEVEN

A NEW VIRUS, HHV-7, HAS ALSO BEEN FOUND IN CFS PATIENTS

A new virus, called Human Herpes Virus 7 (HHV-7), was isolated from a CFS
patient in 1992. This virus was found in the National Cancer Institute; it
has been studied most intensively in the laboratory of Dr. Robert C. Gallo.

Whenever Dr. Gallo and his colleagues claim to be studying a new virus it
should again be noted that he, and certain colleagues, have been under
investigation for several years because of allegedly fraudulent claims that
the Gallo lab isolated the AIDS virus (HIV) in 1983. In fact, on December
31, 1992, Dr. Gallo and one of his colleagues involved in the isolation of
HIV were found by the National Institutes of Health (only one of the
regulatory bodies investigating Dr. Gallo and his colleagues) to be guilty
of scientific misconduct.

The other virus found actively growing in both AIDS and CFS patients, Human
Herpes Virus 6 (HHV-6), was also isolated in the Gallo laboratory in the
mid-1980s; Dr. Gallo's account of the discovery of that virus, like his
account of the discovery of the AIDS virus, has been challenged by other
scientists.

It is not known whether HHV-6 -- which is closely related to HHV7 --
contributes to causing CFS, or AIDS. It is known that HHV-6 infects and
kills not only T4 cells, one of the major cells that is affected in AIDS,
but also infects and kills natural killer cells, which are dysfunctional in
both AIDS and CFS.

Like HHV-6, HHV-7 is believed to infect T-cells.

And also like HHV-6, HHV-7 is quite similar to cytomegalovirus (CMV), which
can cause blindness and other serious illnesses in AIDS patients. However,
HHV-7 is different enough from both HHV-6 and CMV to be declared by Dr.
Gallo's research team to be an entirely new human virus.

An important question not posed by these investigators is: Where are these
"new" viruses, found to be infecting both AIDS and CFS patients, coming
from?

CHAPTER EIGHT

A NATURAL IMMUNE SYSTEM ANTI-VIRAL PATHWAY DOESN'T WORK IN CFS

The immune system has evolved many different mechanisms to fight invaders:
viruses, bacteria, parasites, and anything perceived as "non-self," such as
defective or cancerous cells. Some of those mechanisms are incredibly
specific, like antibodies; others are pretty general, like natural killer
cells. One of the continuing mysteries of the immune system is how all of
these mechanisms interact, overlap, and appear to compensate for each other
to protect against infectious agents.

One way the immune system protects against viruses is through a biochemical
pathway with the name "2'-5'A synthetase/RNase L pathway." This pathway's
anti-viral effects are turned on by interferon, one of the chemicals
(called cytokines) produced by T-cells and other cells of the immune
system.

Although this sounds rather technical -- and it is -- the most important
fact about the pathway is very simple: It malfunctions in both CFS and AIDS
patients.

Basically, the pathway works like this: When a virus is detected by the
immune system, interferon is produced. Interferon stimulates the inactive
chemical 2'5'A synthetase; it interacts with other chemicals and produces a
biologically active substance called 2'-5'A. "Biologically active" means
that the 2'5'A is capable of acting on other molecules and making them
active, too.

And that is what 2'-5'A does; it activates another immune system substance,
RNase L. Activated RNase L is then able to stop the invading virus from
reproducing itself and spreading the infection.

When this pathway works correctly, interferon production results, through
the steps outlined, in stopping viruses from spreading throughout the body.
But in CFS patients -- and AIDS patients -- the pathway doesn't work
properly.

Dr. Robert Suhadolnik, working at Temple University in Philadelphia, has
discovered that CFS patients have too much of both active substances in the
pathway, 2'-5'A and RNase L.

As a result, not only viral reproduction, but also much of the cell's own
internal activity, is halted. That means that the cells of the immune
system are unable to react properly to invaders.

The failure of this pathway is another example of how an overreaction by a
portion of the immune system in a person with CFS can actually result in
decreased immunity.

The defect in the anti-viral pathway also suggests that CFS patients, like
AIDS patients, are vulnerable to opportunistic infections that can make
them very sick.

Interestingly, one of the experimental treatments for CFS (and one which
has also shown promise in treating AIDS) is Ampligen, a chemical that is
structurally similar to interferon. It appears to correct the defect seen
in the 2'-5'A Synthetase/RNase L pathway. Studies using Ampligen to treat
CFS are currently being reviewed by the Food and Drug Administration.

Another interesting observation made by Dr. Suhadolnik demonstrates how a
malfunction in the immune system in CFS can result in either up- or
down-regulation. While most CFS patients studied by Dr. Suhadolnik have
increased amounts of RNase L, he has also reported that he has seen some
CFS patients in whom there is virtually no detectable RNase L -- which is
exactly what is found in AIDS patients.

That finding has led some researchers to speculate that a retrovirus --
like HIV, the "AIDS virus" -- may be involved in causing CFS.

This natural anti-viral pathway may provide not only an understanding of
what goes wrong in CFS, but also a way to diagnose the syndrome. In July
1992, a research firm in Houston, Texas, announced that the firm had
developed a diagnostic test for CFS. The company is Oncore Analytics, Inc.,
and the test measures the anti-viral pathway. The Oncore test is performed
on a blood sample.

The virus that causes CFS has not yet been identified and, in fact, there
are still researchers and clinicians who do not believe that a virus -- or
any infectious agent -- causes CFS. If the Oncore test, which measures a
defect in an anti-viral pathway, is capable of reliably separating CFS
patients from healthy people, that would be another piece of evidence
suggesting that CFS is caused by a virus.

CHAPTER NINE

A MYSTERIOUS ORGANISM CALLED A MYCOPLASMA MAY BE PERIPHERALLY INVOLVED IN
CFS

Mycoplasmas are extremely small bacteria, and are perhaps the smallest
self-sufficient organisms that exist. Mycoplasmas can cause human disease
-- particularly pneumonia and a type of urinary tract infection -- but have
not been considered to be major human pathogens. Since 1986, however, there
has been speculation that a newly-discovered type of mycoplasma may be
involved as a co-factor in causing AIDS and, perhaps, even CFS.

The new mycoplasma was discovered in AIDS patients by Dr. Shyh-Ching Lo at
the Armed Forces Institute of Pathology. The mycoplasma appears to invade
many internal organs -- kidneys, spleen, brain, liver -- and causes the
organ tissue to die.

While Dr. Lo's suggestion that the mycoplasma might play some role in
causing AIDS is controversial, Dr. Luc Montagnier, the Pasteur Institute
researcher who discovered HIV, the "AIDS virus," has found the same kind of
mycoplasma infecting French AIDS patients. Dr. Montagnier, like Dr. Lo,
believes that this mycoplasma may play an important role in causing AIDS.

And Dr. Lo has been able to accomplish with the mycoplasma what no
scientist has been able to do using HIV: Dr. Lo has taken mycoplasma from
AIDS patients' tissues, injected them into animals, watched the animals die
of a wasting illness that resembles AIDS, and then re-isolated the
mycoplasma from the animals' tissues.

In other words, Dr. Lo has created a classical animal model for the
mycoplasma-caused illness. Such an animal model does not exist for HIV and
AIDS; no animal has ever been made to develop an AIDSlike illness after
being infected with HIV.

Dr. Lo also found the new mycoplasma in a number of non-AIDS patients --
previously healthy people who died very suddenly following a flu-like
illness. These cases prove that this particular mycoplasma can infect
people who do not have AIDS.

Fortunately, mycoplasma can be controlled by readily-available antibiotics
such as doxycycline or tetracycline. The fact that many CFS patients report
that their symptoms improve when they take doxycycline causes Dr. Lo to
suspect that the mycoplasma may be involved in causing some cases or
symptoms of CFS.

Unfortunately, Dr. Lo's work is still very much in the research stage, and
a diagnostic test for the mycoplasma is not readily available. But if a
physician suspects a CFS patient may be infected with the mycoplasma, it is
safe to treat the patient with an anti-mycoplasma antibiotic, just in case,
according to Dr. Lo.

Some CFS patients report considerable improvement in their symptoms when
they take antibiotics. "The burning feeling in my spine and head
disappear," CFS patient "Ruth" told me, when she takes ciprofloxacin, an
antibiotic. She added, "The joint pain -- especially the neck pain -goes
away, and I am able to think clearly when I take ciprofloxacin."

CHAPTER TEN

JUST AS IN AIDS, IMMUNE SYSTEM CELLS CALLED MONOCYTES DO NOT WORK PROPERLY
IN CFS PATIENTS

Cells called monocytes are an essential part of the immune system.
Monocytes are found in the circulating blood, and they perform a variety of
functions: They ingest and kill invaders, they communicate with other
immune system cells to indicate when an immune response should be mounted,
and they make a number of enzymes that are essential to properly
functioning immunity.

Monocytes are the precursor cells to another very important type of immune
system cell called macrophages. Macrophages are essentially the mature
forms of monocytes; they are found situated in organ tissues (rather than
in the blood, like monocytes). Macrophages perform basically the same
functions as monocytes.

Like just about every other cell in the immune system, monocytes do not
work properly in CFS patients. Some research teams have found that about
half of CFS patients have monocytosis, in which too many monocytes are
produced. When there is an excess of monocytes, there can be an excess of
the lymphokines that the monocytes produce; these lymphokines can make
patients feel very sick.

Additionally, a Spanish research team from the University of Navarra, in
Pamplona, studied monocyte function in CFS patients and found it to be
disturbed in a large percentage of patients. The Spanish researchers
examined the delicate fibers on the surfaces of monocytes and macrophages,
called "vimentin filaments," that are thought to help the cells move about
in the body and to play a role in immune responses.

When the monocytes and macrophages of CFS patients were compared to those
of healthy people, the Spanish scientists found a "marked reduction" in the
vimentin filaments. Consequently, they found, the monocytes and macrophages
of CFS patients are quite dysfunctional.

In fact, 30 of 35 people who fit the U.S. CDC criteria for CFS (six men and
29 women who ranged in age from 19 to 51) had, according to the Spanish
research team, "monocyte dysfunction."

CHAPTER ELEVEN

AS IN AIDS, THE IMMUNE SYSTEM IS BOTH OVER-STIMULATED AND DEPRESSED IN CFS

The balance maintained between the interacting parts of the immune system
appears to be extraordinarily delicate, we are learning as scientists
unravel more and more of its mystery. What is becoming clear is that it's
possible for one part of the immune system to be over-stimulated at the
same time as other parts are depressed.

In CFS, the immune system cells called T-cells are often over-stimulated;
this state is called "T-cell activation." Research has shown that, when
Tcells are activated, they make immune system chemicals called cytokines;
interleukin and interferon are examples of cytokines. When the T-cells make
excessive amounts of cytokines, they can actually cause symptoms similar to
those seen in CFS.

Fever, swollen glands, sore throat, aching muscles and joints, sleep
disturbance, and even psychological symptoms can be caused by excessive
amounts of cytokines.

Dr. Paul Cheney, who was one of the first physicians to recognize CFS in
the U.S. -- and who has a number of CFS patients who can be designated
"non-HIV AIDS cases" because they have very low T4 cell counts -- explains
it this way: The sicker his patients feel, the more T4 cells (which are
also called CD4 cells) they have. The less sick the patients feel, the
lower their CD4 cell counts are.

Dr. Cheney says that the notion of "sick" is used differently with respect
to AIDS and CFS patients.

"Sick is a semantic term in the sense that it implies different meaning in
CFS than it does in AIDS," Dr. Cheney says. "We have sort of defined AIDS
patients as what happens to them, and when bad things happen to them, they
have low CD4 counts. CFS patients feel bad all the time, and their CD4
counts are actually high."

Dr. Cheney blames his sickest patients' symptoms on having activated
T-cells. "It will make you royally sick" to have activated T-cells, he
points out. "And, I'll tell you, the sickest people I have, the people who
come in here who are really, really, sick, they'll have CD4 counts of
2,000," which is about twice as high as normal. "And the cytokines that are
being expressed, of course, typically cause CD4 cell proliferation" -- so
the T-cells, which are already too high, increase even more. This is the
type of T-cell malfunction that can occur when the immune system is
over-stimulated.

But Dr. Cheney also has CFS patients with very low CD4 cells counts; so
low, in fact, that they can be diagnosed as being "non-HIV AIDS," or ICL,
cases. Dr. Cheney believes that both sets of patients -- those with high
CD4 cell counts and those with low CD4 cell counts -- have CFS. He thinks
that the patients with the low T4 cell counts, however, are in "a different
state" from other CFS patients.

Dr. Cheney says that his CFS patients who have fewer than 200 CD4 cells --
a level that is considered very dangerous for AIDS patients -- are "not
feeling so good." He also points out, however, that those patients who have
CD4 counts between 300 and 500 typically don't feel too bad, even though
1000 T4 cells is considered "normal."

"Looking at this group as a whole, the patients with low CD4 counts are
relatively less sick -less symptomatic, I should say," Dr. Cheney says.
"Their symptoms aren't as severe. They seem to be more stable. If I had to
guess what is happening, I think what is happening is that you are looking
at the same disease in two different states."

One of those states is "upregulated," in which the T-cells are activated
and producing large amounts of cytokines; the other is a state of
down-regulation, in which even the numbers of immune system cells drop.

Sometimes increased amounts of certain cytokines can cause the depression
of some types of immune system cells. One of the cytokines that is elevated
in CFS, for instance, is interleukin 1 (abbreviated IL-1). IL-1 has been
shown to cause other parts of the immune system -- like natural killer cell
activity -- to be suppressed. This is only one example of how an elevation
in one part of the immune system can cause the depression of another part.

CHAPTER TWELVE

ONE RESEARCHER THINKS THAT CFS SHOULD BE CALLED "LYMPHOKINE OVERDOSE
DISEASE"

Dr. William A. Carter is a Professor of Oncology and Hematology at
Hahnemann University in Philadelphia. He is also the codeveloper of an
experimental drug called Ampligen, which has shown promise in treating both
Chronic Fatigue Syndrome and AIDS, and is currently under review by the
Food and Drug Administration. At a conference held in late 1991, Dr. Carter
discussed a clinical trial of Ampligen and explained that he thinks CFS
could be called "lymphokine overdose disease."

Lymphokines are substances produced by white blood cells (also called
lymphocytes) when the immune system encounters an invader. They include the
interferons (alpha-, beta-, and gamma-interferon), the interleukins (there
are at least 12 interleukins), tumor necrosis factor, and others. Most
lymphokines stimulate cells to do something: either to reproduce themselves
(interleukin-2 used to be called "T-cell growth factor," for instance), or
to interact with other components of the immune system (gamma-interferon
works in this way).

When Dr. Carter made his 1991 presentation at the 31st Interscience
Conference on Antimicrobial Agents and Chemotherapy, he was also
interviewed by the on-site Conference Journal. The lymphokine that Dr.
Carter spoke about in his interview was interleukin-1 (IL-1), the primary
action of which is to stimulate cells to produce interleukin-2 (IL-2).

Dr. Carter told the Conference Journal that his research group had
determined that more than twothirds of CFS patients have abnormally high
levels of lymphokines; because of that, he suggested that CFS might more
appropriately be named "lymphokine overdose disease."

According to Dr. Carter, many of the symptoms of CFS -- such as fatigue,
memory loss, and other problems with thinking -- are probably caused by the
high levels of lymphokines that patients are making in their own bodies.

CFS patients who have very high levels of IL-1 responded well to Ampligen
treatment, Dr. Carter told the Conference Journal. Just as importantly, the
patients in Dr. Carter's study who had high levels of IL-1 and who received
a placebo (inert, or phony) substance instead of Ampligen got progressively
worse.

One of the most disturbing findings made by Dr. Carter and his research
team was that CFS patients with abnormally high levels of IL-1 had
"anatomic holes" in their brains that were detected by using brain scans.
It was not clear to the research team whether the holes were reversible or
permanent.

From this information, Dr. Carter and his colleagues concluded that IL-1 is
important in causing the symptoms of CFS, particularly the mental symptoms.
Dr. Carter said that increased IL-1 could be used as a "footprint" to help
diagnose severe CFS.

CHAPTER THIRTEEN

CFS, LIKE AIDS, MAY BE PRIMARILY A TUMOR NECROSIS FACTOR DISEASE

Tumor Necrosis Factor, TNF, was one of the first lymphokines to be
discovered. Lymphokines -- also called cytokines -- are chemicals that are
produced by immune system cells; they help different kinds of cells to
communicate with each other in mounting immune responses.

TNF is produced by the immune system cells called macrophages, and was
named "Tumor Necrosis Factor" because it was observed to make cancer cells
die. TNF is also primarily responsible for causing the extreme weight loss
observed in people with cancer and AIDS.

TNF has been found by some researchers to be increased in CFS patients.
Other lymphokines -gamma-interferon, interleukin-2, and interleukin-6, for
example -have also found to be increased in CFS. But some researchers have
found these same lymphokines to be decreased in CFS, pointing out once
again that a malfunctioning of the immune system can result in
contradictory information being gathered.

Whether these cytokines are produced at increased or decreased levels in
CFS, it is clear that their normal production is disturbed in these
patients. Also, because different lymphokines and various types of immune
system cells interact with each other in not-yet-understood ways, it's not
clear exactly why CFS patients have abnormal amounts of TNF and other
cytokines.

TNF has also been observed to cause HIV to reproduce at higher levels than
it normally does. For that reason, Dr. Jay A. Levy, a prominent AIDS
researcher in California, has suggested that AIDS is primarily a TNF
disease. Dr. Levy has also suggested that, if TNF levels were decreased, a
lot of the symptoms and illnesses seen in AIDS patients would disappear.

Interestingly, an experimental drug that has shown promise in treating both
AIDS and CFS, Ampligen, has been shown to lower TNF levels, as well as
improving symptoms.

CHAPTER FOURTEEN

ZINC DEFICIENCY CAN CONTRIBUTE TO CFS

Zinc is a trace mineral that is very important in maintaining a healthy
immune system. But as many as 85 percent of CFS patients may have a serious
zinc deficiency, which is extremely common among AIDS patients as well.

Zinc is perhaps the most important "growth factor" in the human body; any
cells that are rapidly reproducing -- such as those involved in healing
wounds, immune system cells that are actively fighting infections, and
growing fetuses -- require a steady supply of zinc. Zinc deficiency in a
pregnant woman can cause very serious birth defects in her child. The most
dramatic birth defect caused by zinc is an encephaly, in which a child is
born with only part of a brain, or actually no brain at all.

Zinc deficiency can also cause stunted growth (in children), skin lesions,
hair loss, and increased susceptibility to infections because of impaired
immunity.

A physical sign of zinc deficiency -- which is, according to some
researchers, found in a large number of CFS patients -- is white spots on
the finger nails, a condition called "leukonychia." Some CFS researchers
have reported that a large majority of their CFS patients exhibit the white
spots on their fingernails that are indicative of zinc deficiency.

Zinc deficiency may be responsible for another symptom of CFS -- alcohol
intolerance. Many CFS patients are unable to tolerate alcohol. Zinc is
responsible for helping to form the enzyme that breaks down alcohol, called
alcohol dehydrogenase. Too little zinc may lead to insufficient production
of alcohol dehydrogenase and, therefore, to alcohol intolerance.

Zinc deficiency, then, may not only contribute to lowered immunity and
birth defects among CFS patients and their children, but also to the
alcohol intolerance that is often a symptom of the disease.

CHAPTER FIFTEEN

MAGNESIUM CAN BE A MISSING ELEMENT IN CFS

Magnesium is a trace element that is necessary for the activities of many
enzymes; serious deficiency can cause vascular problems, convulsions,
tremors, depression, and psychotic behavior. In 1990, a British research
team discovered that not only did CFS patients have a deficiency of
magnesium in their red blood cells, but that magnesium injections actually
helped some symptoms to improve.

In the British study, 35 CFS patients were divided into two groups. One
group received a magnesium injection once a week for six weeks; the other
group received a placebo injection (in this case, sterile water) once a
week for six weeks.

At the end of the study, the patients who were treated with magnesium had
much greater improvement in energy, pain, and emotional reactions than the
placebo group did.

The British investigators concluded that, while magnesium may not be a cure
for CFS, it could prove to be helpful in treating some symptoms of the
syndrome.

CHAPTER SIXTEEN

THERE IS A HORMONAL IMBALANCE IN CFS SIMILAR TO THE ONE IN AIDS

The U.S. government's leading Chronic Fatigue Syndrome researcher, Dr.
Stephen Straus at the National Institute of Allergy and Infectious
Diseases, has for several years wasted a great deal of the government's
resources by attempting to prove that CFS is a psychiatric illness, similar
to depression. In one recent study in which he compared certain hormonal
levels in CFS patients to those in people with depression, however, Dr.
Straus uncovered a hormonal abnormality that contradicted his own theory.

Dr. Straus, working with researchers at the National Institute of Mental
Health and the National Institute of Child Health and Human Development,
found that CFS patients have decreased amounts of a hormone called
cortisol, which is part of the natural "fight or flight" response.

CFS patients also have decreased amounts of the hormone that instructs the
brain to produce cortisol, which is called CRH (which is short for
"corticotropin releasing hormone").

Interestingly, cortisol deficiency is also one of the most common hormonal
abnormalities seen in AIDS.

Both cortisol and CRH deficiencies can cause lethargy and fatigue.
Therefore, Dr. Straus and his colleagues suggested that the CRH and
cortisol deficiencies together, or either deficiency alone, could
contribute to causing some of the symptoms of CFS.

In the course of this study, however, Dr. Straus inadvertently disproved
his hypothesis that CFS is a form of depression. The cortisol and CRH
levels found in patients with depression are actually opposite to those
found in CFS patients: People with depression have increased amounts of
both CRH and cortisol.

Although Dr. Straus's hormone study contributes to our understanding of one
system that doesn't work in CFS, it unfortunately doesn't help in finding a
treatment or cure. Because of the complex way in which hormonal systems
interact, giving CFS patients extra cortisol would signal the body that it
isn't necessary to make more cortisol. This could actually worsen the
deficiency.

In spite of government documents acknowledging that cortisol treatment of
CFS patients could be dangerous, Dr. Straus has proposed a clinical trial
to treat CFS patients with compounds like cortisol.

Dr. Straus's possibly dangerous plan to treat CFS patients with steroids
like cortisol fails, also, to take into account the fact that the growth of
Human Herpes Virus 6 (as well as other viruses) is stimulated by such
drugs.

If HHV-6 is causing CFS by growing out of control, cortisol treatment might
actually worsen the illness in ways that we don't even understand yet.

A medical bulletin broadcast on the Cable News Network (CNN) in early 1993
reinforced the point that treatment with steroids such as cortisol can have
unexpected negative side effects. CNN broadcast a report about a young boy
whose asthma was being treated with steroids (like cortisone) when he
contracted a mild case of chicken pox.

Chicken pox is caused by a herpes virus called Herpes zoster. Although it
is a childhood illness from which most people recover with no deleterious
after-effects, this particular young boy actually died from his chicken
pox.

The reason he died, according to the CNN report, was because the steroid
being used to treat his asthma caused the Herpes zoster virus to grow out
of control and kill him.

CHAPTER SEVENTEEN

CFS PATIENTS' "CRIMSON CRESCENTS" MAY BE DIAGNOSTIC OF THE SYNDROME

A Long Island physician who studies CFS, Dr. Burke A. Cunha, has discovered
what he calls "crimson crescents" in the throats of CFS patients. The
crescents are so distinctive that Dr. Cunha believes that their presence
indicates that CFS is present, even if the physician (or the patient)
observes no other indication of the syndrome. Even more intriguing, Dr.
Cunha has found that the crescents are associated with high levels of Human
Herpes Virus 6 (HHV-6), a virus that is found to be actively growing in
AIDS and CFS patients.

Dr. Cunha described his finding in a medical journal, and in November 1992,
it was the cover story of the Infectious Disease News, a newsletter for
primary care physicians. The crescents are described as being "crimson
purple," and looking like half of a crescent moon.

Dr. Cunha says the crescents occur in 80 percent of CFS patients.

After he reported his finding in the Annals of Internal Medicine, Dr. Cunha
says he received calls from physicians all over the country. They told Dr.
Cunha that, once they knew to look for the crescents, they were also
finding them in their CFS patients.

Dr. Cunha thinks that many physicians may not have seen the crescents
because they occur on both sides of the back of the throat, behind the back
molars. Most physicians, Dr. Cunha remarked to Infectious Disease News,
don't really look at the sides of the throat.

Dr. Cunha is convinced that the crimson crescents are highly correlated
with CFS. "If your patient has crimson crescents, you can now say it is
probably chronic fatigue syndrome," Dr. Cunha told Infectious Disease News.

Dr. Cunha also said, however, that he has found the crimson crescents in
three to five percent of all patients who complain of sore throat -- which
may mean that the number of people who have CFS has been grossly
underestimated. The crescents have not been seen in patients with other
illnesses that produce sore throats, such as mononucleosois, strep throat,
cytomegalovirus infection of the throat, or common viral sore throat.

Dr. Cunha thinks that the crescents may occur in CFS patients because they
are caused by the active HHV-6 found in the patients.

"I believe that the virus that causes chronic fatigue comes from young
adults or children who give it to adults," Dr. Cunha told Infectious
Disease News. "...I don't know why there is a difference, but the children
do not have chronic fatigue. HHV-6 is a virus of children, and it may
manifest as chronic fatigue in adults."

Dr. Cunha is trying to culture HHV-6 out of the crescents, but he has found
that laboratories that perform throat cultures usually do not have the
facilities to detect HHV-6, which is a fairly new human virus. To try to
find HHV-6, he plans to perform biopsies on the crescents, Dr. Cunha told
Infectious Disease News.

Dr. Cunha also pointed out that increased HHV-6 and decreased natural
killer cell activity are the two most consistent laboratory findings in
CFS. He thinks that the presence of the crimson crescents by themselves,
however, are evidence enough that CFS is present.

"If you are a physician out in the middle of nowhere and you can't get
HHV-6 titers and you can't get the natural killer cell percentage, then the
crimson crescents may be the only way besides history that can suggest the
diagnosis" of CFS, Dr. Cunha told Infectious Disease News.

CHAPTER EIGHTEEN

CFS PATIENTS MAY DEVELOP A CANCER SIMILAR TO ONE FOUND IN AIDS PATIENTS

The "crimson crescents" identified in the throats of CFS patients by Long
Island physician Burke A. Cunha are, he has pointed out, closely associated
with increased antibodies to Human Herpes Virus 6 (HHV-6). Dr. Cunha's
description of these crimson-topurple crescents suggests that they may be
manifestations of Kaposi's sarcoma (KS), a type of lesion or tumor seen in
AIDS. A finding that strengthens this possibility is that HHV-6 has
recently been found in Kaposi's sarcoma tissue. That fact raises several
questions: Is HHV-6 the cause of KS? And, given that increased antibodies
to HHV-6 are closely associated with the crimson crescents of CFS, are
those lesions caused by the virus? And, most importantly, are the "crimson
crescents" of CFS actually a form of KS lesion?

Although the conventional wisdom about AIDS says that KS develops only in
certain "risk groups," such as gay men, autopsies have shown that greater
than 94 percent of all AIDS patients have some form of the tumor-like
growths in their internal organs. Experts have agreed that, since KS can
occur in many different physical forms internally and externally (on the
skin), the possibility exists that the crescents are a type of KS, which
also varies in color from red or crimson to deep purple. That possibility
should be easy to prove or disprove, once biopsies have been performed on a
number of the crimson crescents; however, the research has not yet been
performed.

The identity of the crimson crescents may also become mired in a dispute in
the scientific community over the nature of KS itself. Some researchers
believe KS to be a true cancer, manifest only in typical tumors (such as
those observed on the skin). Others believe it is actually an overwhelming
inflammatory response, occurring in numerous types of abnormal tissue
responses, both in internal organs and on the skin. It does not appear that
this dispute among scientists will be resolved any time soon.

Called a "neoplasm" -- which simply means a clump of growing cells -- most
researchers agree that KS is not a typical cancer. It can produce lesions
and tumors, both internally and on the skin, across a spectrum of different
forms; other cancers usually manifest themselves in one particular form,
such as breast cancer, for instance, which almost always forms a solid
tumor.

In addition, the type of KS seen in AIDS is different from the generally
harmless type of KS which was first described around a century ago in
older, Mediterranean men.

And although KS in AIDS patients was initially believed to be caused by
HIV, the "AIDS virus," numerous cases of AIDS-type KS have now been
identified in HIV-negative people.

Speculation has abounded for several years that KS may be caused by a
separate, as-yet-unidentified virus, but none has been discovered to date.

In May 1993, however, a research group from the University of Ferrara in
Italy reported in the British medical journal The Lancet that they'd found
HHV-6 in 35 percent of 20 biopsies of KS tissue. While more work needs to
be done to verify this finding, the Italian scientists suggested that
HHV-6's "possible contributions" to the development of KS should be
investigated; in other words, they suspect that HHV-6 may be the
longsought-after cause of KS.

If the crimson crescents found in CFS patients, which are also associated
with HHV-6, are found to be a form of KS, that would make it very difficult
for anyone to argue that CFS and AIDS are unrelated diseases.

CHAPTER NINETEEN

LIKE AIDS PATIENTS, CFS PATIENTS MAY BE ESPECIALLY SUSCEPTIBLE TO
TUBERCULOSIS

Tuberculosis is a sometimesfatal illness that was all but eradicated before
the AIDS epidemic began. It is possible for healthy people to become
infected with the tuberculosis germ (a bacterium) without becoming sick;
this is called a latent infection. But because people with AIDS do not have
intact immune systems, they do become sick -- and, at the same time, are
contagious to other people -- when they encounter the TB germ.

TB is of particular concern to public health officials because of the way
it is spread, which is in saliva droplets that contain bacteria. While
prolonged, close contact between people breathing the same air -- like
people in jail -- is usually required for TB to spread, it is more casually
contagious than almost any other equally serious illness.

And people whose immune systems aren't functioning properly -- like AIDS
and CFS patients, as well as cancer patients -- become infected, and sick,
with tuberculosis much easier than healthy people.

The natural killer (NK) cells are a front-line defense against other cells
infected with TB germs but, in both AIDS and CFS, the NK cells don't work
properly.

Ironically, new studies have shown that NK cells do not function properly
in people who have TB. Therefore, the very cells that should be protecting
the body against the TB infection are made less effective by that
infection.

Therefore, a person whose NK cells were not working well in the first place
can become very sick, very fast, from TB.

Most people are aware by now that AIDS patients are particularly vulnerable
to TB. What isn't commonly known is that CFS patients are also more
susceptible to TB than are healthy people, according to the Associate
Director of the Centers for Disease Control and Prevention Tuberculosis
Division, Dr. Donald E. Kopanoff.

Dr. Kopanoff told Spin magazine in December 1991 that CFS patients, because
they are in generally poor health, are at much greater risk for contracting
active TB than the rest of the public.

Another part of the immune system that doesn't work properly in CFS
patients is the cellmediated immunity; this is the type of immunity that is
controlled primarily by T4 cells. Both CFS and AIDS patients sometimes have
severely decreased numbers of T4 cells, which is partially why their
cell-mediated immunity doesn't work.

The cell-mediated immunity produces the type of immune response that causes
a bump to rise at the site of a skin test for TB (and other diseases, as
well). If the cell-mediated immunity is not working properly, no bump is
formed at the site of the test, even if the person is infected with TB.

Therefore, when the immune system is not functioning properly, there is no
easy and reliable way to distinguish infected from uninfected individuals.
The millions of people suffering with CFS all over the world could turn TB
into a disaster of enormous proportions, which is another reason patients
should demand that the truth be told about this epidemic.

CHAPTER TWENTY

CFS PATIENTS HAVE A BRAIN DEFECT SIMILAR TO THAT FOUND IN AIDS DEMENTIA

It has been known for some time that CFS patients have abnormal blood flow
in their brains; that is, some areas of the brain are not getting as much
blood as they should. Very recently, however, studies of patients with AIDS
dementia have shown that they, too, have abnormal brain blood flow, raising
the question of whether a similar disease process is taking place in both
sets of patients.

It has only been possible to measure blood flow in the brain with the
development, over the last few years, of very specialized types of brain
scan technologies. One type of brain scan that can detect blood flow
abnormalities is called SPECT (which stands for "single photon emission
computer tomography").

Dr. Ismael Mena has studied CFS patients' brains using SPECT scans at the
University of California-Los Angeles, where he is a professor of radiology.
Over several years' investigation, Dr. Mena has consistently reported that
71 percent of CFS patients have a diminished flow of blood in their brains.

Dr. Mena has also commented, at scientific conferences, that CFS patients
do not have equal blood flow on the two halves of their brains. That is,
when the blood flow on the right and left sides (or hemispheres) of the
brain were compared in individual CFS patients, the flow in the two halves
of the brain can differ by twice as much as they do in healthy people.

This information suggests that some type of organic brain disease may be a
component of CFS. While it has long been recognized that AIDS patients can
develop very serious mental problems, sometimes labeled "AIDS dementia,"
only recently have such patients been studied using SPECT scans. The
similarity between "AIDS dementia" patients' SPECT scans and those of CFS
patients are striking.

SPECT scans in AIDS patients were discussed at the 1992 international AIDS
meeting (in Amsterdam) by a research team from the Houston Immunological
Institute. Rather shockingly, they found that exactly the same percentage
of AIDS patients -- 71 percent -- as CFS patients had abnormalities in
brain blood flow. The Houston research team also found that more severe
cases of AIDS dementia showed greater abnormalities in brain blood flow,
and they suggested that SPECT scans could provide a very important
diagnostic tool for physicians treating patients with AIDS.

Abnormal SPECT scan results have not yet been firmly associated with any of
the mental abnormalities -- short-term memory loss, for instance, or
difficulty concentrating -- observed in CFS patients. But as this still-new
technique becomes more refined, it may well help unlock some of the
mysteries of the mind associated with not only CFS, but also AIDS.

CHAPTER TWENTY-ONE

THERE CAN BE A SIGNIFICANT WEIGHT FLUCTUATION IN CFS

People who have CFS sometimes experience a dramatic weight loss or gain.
Many women CFS patients I've spoken to have gained a significant amount of
weight since becoming ill. This may be due to lack of exercise, or possibly
even to the as-yet-not-understood hormonal problems associated with CFS.

Another possible explanation for CFS patients' weight gain is that organic
changes occur in the brain. The central nervous system, directed by the
brain, governs metabolism -- how fast calories, and stored fat, are burned.
Changes in the brain waves, sugar metabolism, oxygen flow, and even in the
physical appearance of the brain have been documented in CFS patients. It
is possible that virus-induced changes in the brains of CFS patients also
affect their metabolism, and thereby result in weight gain.

Significant weight loss, however, can also be a component of CFS. One
patient I interviewed, a young man named Al, lost 55 pounds in just one
year. His weight loss was so precipitous and unexpected, Al told me, that
his doctor concluded that he must have either cancer or AIDS.

In AIDS, weight loss is often caused by an overproduction of tumor necrosis
factor (TNF). If CFS, like AIDS, turns out to include a major disruption in
the production of TNF, that may explain why patients lose weight at certain
stages of the illness.

The fluctuation in weight experienced by CFS patients, however, is yet
another example of how major systems are dysfunctional -- sometimes
overactive, sometimes underactive -- in the syndrome.

CHAPTER TWENTY-TWO

DIZZINESS CAN BE A SEVERE PROBLEM IN CFS

Nearly all CFS patients have problems with balance and equilibrium, either
occasionally or constantly. It is not known what causes these or other
nervous system problems in CFS, or how to cure them.

One patient I interviewed, Al, told me that his dizziness was so
pronounced, at times, that the sidewalk he was walking on appeared to be
tilting up to meet him.

When this happened he would fall down, and be unable to get up or walk
until the dizziness passed.

Balance can be tested very simply by any physician, and CFS re searcher Dr.
Paul Cheney performs this test on his patients: The patient stands, feet
together, arms at the sides, and closes his or her eyes.

"Then," Dr. Cheney told me, "they fall over." This type of imbalance is
very common among his CFS patients, Dr. Cheney says.

AIDS patients can suffer very similar balance disturbances and dizziness,
and even have seizures (which CFS patients can also experience). Headache,
memory loss, confusion, and weakness of the limbs are other neurological
problems that can develop in both CFS and AIDS.

Whatever the exact cause of the balance problems in CFS, it is clear that
the central nervous system is very seriously affected by this syndrome.

CHAPTER TWENTY-THREE

AS IN AIDS, SINUSITIS CAN BECOME CHRONIC IN CFS

Infected or inflamed sinus passages, or sinusitis, can become a chronic
ailment in CFS patients, as it can in AIDS patients. Like many other
aspects of CFS, no formal studies have determined what percentage of CFS
patients develop chronic sinusitis. California researcher Dr. Carol Jessop
has noted, however, that 40 percent of her CFS patients develop recurrent
sinusitis, with bronchitis -- an inflammation of the air passage in the
lungs -- developing in 30 percent.

Since as many as 90 percent of CFS patients report having some type of
allergy problems, it is perhaps not too surprising that many would also
develop chronic sinus problems.

Sinusitis can, in fact, be one of the first signs that CFS is developing.

Sinusitis is also often a major problem for AIDS patients. As the immune
system becomes increasingly more depressed, it is less able to destroy the
bacteria and other organisms that are inhaled with every breath of air.
Pneumocystis carinii infection, which usually occurs in the lungs and
causes pneumonia (commonly called PCP), can also occur in the sinuses.
There is also the possibility that the sinus pain experienced by AIDS
patients can be due to Kaposi's sarcoma, or lymphoma, or another kind of
tumor.

CHAPTER TWENTY-FOUR

A RECENT RISE IN CHILDHOOD ASTHMA MAY BE AN EFFECT OF THE CFS EPIDEMIC

After a steady decline over several years in deaths caused by childhood
asthma, the number rose again sharply in the early 1990s. In March 1991, in
fact, the National Institute of Allergy and Infectious Diseases funded a
National Cooperative Inner-City Asthma Study to attempt to prevent the
soaring number of asthma deaths.

In early 1992, a study published in the New England Journal of Medicine
noted that Americans spent about $6.2 billion on asthma-related health care
in 1990.

Is the CFS epidemic responsible for at least part of the rise in asthma,
particularly childhood asthma, in the U.S.?

Asthma is caused by a temporary blockage of the airways in the lungs; the
airways typically are blocked by an inflammatory response of some type
(such as an allergic response) that can cause swelling in the airway, or by
accumulation of excess mucous.

Dr. David Bell studied an outbreak of CFS in Lyndonville, New York, in
which a number of children developed the syndrome. He found that more than
half of the 74 children involved in the outbreak had allergies and/or
asthma before developing CFS.

CFS, however, made these children's allergies/asthma worse, according to
Dr. Bell. Half of those who had allergies/asthma before they developed CFS
told Dr. Bell that their symptoms clearly worsened after they contracted
CFS.

Five percent of the children involved in the outbreak who had never had
allergies or asthma developed symptoms after being stricken with CFS.

No one knows why asthma and asthma-related deaths among children are
rising. But, given that allergies and other inflammatory responses are so
common among CFS patients (in both children and adults), the possibility
that the CFS epidemic may be contributing to the rise should be
investigated.

CHAPTER TWENTY-FIVE

ENDOMETRIOSIS SEEMS TO BE COMMON IN WOMEN WITH CFS

Endometriosis, a painful condition in which the tissue lining the inside of
the uterus (the endometrium) migrates outside the uterus, appears to occur
in much higher rates in women with CFS than it does in otherwise healthy
women.

The endometrial tissue can migrate to any location in the body once
endometriosis begins, but it is often found on the surfaces of organs and
structures nearest the cervix, or entrance to the uterus: the bowel,
bladder, fallopian tubes, ovaries, the uterine surface, and on the surfaces
of the supporting tissues.

The most common symptoms of endometriosis are pain during menstruation
(often a dull, persistent pain that seems to be located in the lower back),
irregular or heavy menstrual bleeding, pain during sexual intercourse, and
infertility.

The cause or causes of endometriosis are unknown.

A Long Island physician who has a large number of CFS patients in his
practice, Dr. Perry Orens, believes that there is definitely an increased
rate of endometriosis among women CFS patients. Dr. Orens believes that
there is an asyet-unidentified hormonal component in CFS that is causing
the increased incidence of endometriosis. This hormonal component of the
disease, Dr. Orens also believes, may explain why more women than men have
or appear to have -- or at least are diagnosed with -- CFS.

Other researchers have reported that as many as 30 percent of female CFS
patients have endometriosis.

CHAPTER TWENTY-SIX

PREGNANCY MAY BE A DISASTER FOR A CFS PATIENT

The effect of pregnancy on CFS patients varies widely, as do many other
aspects of the illness. Some physicians report that their pregnant patients
feel much better than they did before they became pregnant; others report
serious problems during or following pregnancy, for both mother and child.
Since CFS patients are not routinely staged -- that is, there are no
accepted guidelines to measure the length or severity of their illness --
these discrepancies may reflect what happens to women who become pregnant
in different stages of CFS.

Dr. Paul Cheney, for instance, reports that he has seen some pregnant
patients whose symptoms improve dramatically. Dr. Cheney suggests that this
might be because of the action of the placenta, the umbilical cord that
connects mother and fetus. Not only nutrients, but also blood, with all of
its immune system components (like cells, lymphokines, antibodies, etc.),
flow through the placenta. Dr. Cheney points out that one action of the
placenta is to down-regulate the mother's immunity, so that the mother's
immune system does not identify the fetus as something "foreign" that
should be destroyed.

On the other hand, some researchers have found that certain problems
associated with pregnancy -- like morning sickness -- and fertility can be
worsened in CFS patients. California researcher Dr. Carol Jessop has found,
too, that the incidence of miscarriage was somewhat higher than normal
among her CFS patients.

The most disturbing information about CFS and pregnancy, however, comes
from Canadian researcher Dr. Byron Hyde. At a research conference in 1991,
Dr. Hyde discussed some women patients who did not have CFS until after
they became pregnant. These patients gave birth to babies who died shortly
after they were born, because they had what Dr. Hyde described at a
research conference as "major, major birth defects" -such as being born
with serious heart defects, or without brains (which is called
"anencephaly").

Dr. Hyde has urged that these very serious effects on pregnancy should be
studied far more intensively than they have been to date.

CHAPTER TWENTY-SEVEN

MEN WITH CFS CAN DEVELOP CHRONIC PROSTATE INFECTIONS

Because the majority of patients first diagnosed with CFS were women,
little attention has been paid to the problems that are unique to men with
the disease. But one such problem is prostatitis, an infection and swelling
of the prostate gland, which is instrumental in the production of semen
(the fluid containing sperm). This symptom may parallel the recurrent
urinary infections and reproductive/endocrinological problems (like
premenstrual tension and endometriosis) that many women with CFS suffer.

Dr. Carol Jessop, who studies CFS in San Francisco, says that prostatitis,
along with sinusitis, is the most common recurring infection she has
observed in men with CFS.

It is not clear what is causing the prostatitis seen in men with CFS, but
there are indications that it may be in some way infectious, or caused by
an infectious agent. A CFS patient I interviewed, "Susan," told me that,
after she developed CFS, her boyfriend developed a prostate infection that
did not respond to standard treatment. Not only did Susan's boyfriend
develop a refractory prostatitis, but so did a number of his male friends
with whom he spent a lot of time, according to Susan.

Because CFS patients' natural killer cells -- which protect against both
viral infections and some kinds of cancers -- do not work properly, it is
possible that men with CFS are also more prone to developing prostate
cancer, as well as prostatitis. Like many aspects of CFS, however, this
possibility has not been the subject of a formal study.

CHAPTER TWENTY-EIGHT

CFS CAN CAUSE A PARTICULAR TYPE OF HEART MURMUR

A relatively high percentage of CFS patients develop of type of heart
murmur called "mitral valve prolapse." Like many other aspects of CFS, this
phenomenon has not undergone rigorous study; anecdotally, however, many
patients and physicians have noted the prevalence of mitral valve prolapse
among CFS patients.

This kind of heart murmur occurs when one of the valves in the heart (the
mitral valve, which is on the left side of the heart) collapses to a
certain degree (which varies from person to person). In minor cases, mitral
valve prolapse can cause little more than a distinctive clicking sound
heard when listening through a stethoscope. But in severe cases, mitral
valve prolapse can cause chest pain, fatigue, heart arrhythmias --
typically, causing the heart to beat too fast -- or even sudden death.

It is not known why heart problems develop in some CFS patients, and many
U.S. researchers doubt that they are connected to CFS. But Dr. Byron Hyde,
who studies CFS in Toronto, commented at a 1991 research conference that
the heart problems associated with CFS are "major." Dr. Hyde also pointed
out that no one in North America is studying this potentially
life-threatening aspect of the disease, a statement which is still true
today.

Heart failure, however, is a fairly common cause of death in AIDS, and the
heart can be affected by a number of problems encountered by AIDS patients.
For instance, Kaposi's sarcoma has been found in heart tissue, as well as
the tissue that covers the heart. KS has also been found in the aorta, and
on the arteries that feed the heart itself.

Additionally, for unknown reasons, heart tissue may simply die in AIDS, a
condition called "acute myocardial necrosis" that is fatal.

Viruses can attack the heart, especially the tissue around the outside of
the heart muscle, and cause a condition called "endocarditis." It would be
useful to determine if viruses that are active in both CFS and AIDS
patients -- especially HHV-6 -- are capable of causing some of the heart
problems found in both syndromes.

CHAPTER TWENTY-NINE

LIKE AIDS PATIENTS, CFS PATIENTS MAY BRUISE MORE EASILY THAN HEALTHY PEOPLE

Bruises are caused by the collection of blood under the skin, usually
resulting from some kind of trauma that causes superficial blood vessels to
break. There is variability in how easily people bruise, of course, just as
there is in how easily they sunburn. But when a person begins to bruise
much more easily than he or she ever has before, it can be the sign of a
serious immunological disease, like some forms of cancer (such as
leukemia), CFS, or AIDS.

CFS patients sometimes find that they bruise more easily after they become
sick. One reason for that can be the development of a condition called
"thrombocytopenia," which is a blood clotting disorder. One reason that
some CFS patients may develop thrombocytopenia and easy bruising is because
they have decreased numbers of the blood cells most directly responsible
for causing blood clots, called platelets.

Thrombocytopenia was recognized very early as an indication that AIDS might
be present. In a 1984 physicians' handbook, AIDS: A Basic Guide For
Clinicians (published by the W.B. Saunders Company), thrombocytopenia is
listed along with fever, weight loss, fatigue, and swollen lymph glands as
an indication to physicians that a patient might have AIDS.

A clue about why AIDS and CFS patients might develop thrombocytopenia
emerged in mid1993, when Japanese researchers reported in the Pediatric
Infectious Disease Journal that an infant with a severe HHV-6 infection had
also developed thrombocytopenia. The Japanese researchers noted that HHV-6
is known to interfere with the differentiation of bone marrow cells, like
those that develop into platelets. They suggested that the possibility that
HHV-6 is directly responsible for causing thrombocytopenia in some cases,
by infecting bone marrow cells and stopping them from developing into
mature platelets, should be further investigated.

In another twist to the CFS story, some researchers hypothesize that CFS
can be communicated between patients and their pets. It also appears that
CFS patients' sick pets can develop clotting disorders reminiscent of
thrombocytopenia.

In the Spring 1992 issue of the CFIDS Chronicle, which was entirely devoted
to patients' letters and stories, a woman patient wrote about the illness
and death of her dog, who suddenly became "strangely ill."

"Soon afterward, he began to suffer from nosebleeds, which in 1984 had been
the prelude to the onset of my CFIDS," the patient wrote. The dog's
condition continued to decline: He developed ulcers first in his mouth and
around his eyes, then over his whole body, and "he grew unsteady on his
feet, became dazed and disoriented," the patient wrote. The dog's
laboratory tests showed "immune dysfunction, possibly due to a viral
agent," according to this patient, who became convinced that her dog died
from a bleeding disorder associated with CFS.

The fact that HHV-6 was isolated from a sick dog (which eventually died)
belonging to a CFS patient suggests that this virus could be causing
bleeding disorders in more than one species.

CHAPTER THIRTY

CFS CAN LEAD TO SERIOUS DISEASES OF THE MOUTH AND GUMS

The soft tissues inside the mouth, particularly the gums, are quick to
reflect ill-health. One reason for this is that the gums contain many blood
vessels along which viruses and bacteria can travel. Gum disease, when it
occurs in the absence of an obvious explanation (such as inadequate oral
hygiene), can signal the presence of immunodeficiency, like that seen in
CFS and AIDS.

One of the signs of impaired immunity that appears in both AIDS and CFS is
oral thrush, which is an overgrowth of a common yeast, Candida albicans.
Thrush is an "indicator" illness in AIDS; that means, if a person
considered to be at "high risk" suddenly has thrush for no discernible
reason, physicians usually consider the diagnosis of AIDS.

Oral thrush can also occur in CFS patients; in fact, Dr. Paul Cheney has
said that oral thrush is "not uncommon" among CFS patients. To date, no
formal study has determined exactly what percentage of CFS patients develop
thrush.

Another condition that can signal immunodeficiency is a gum disease called
gingivitis, a bacterial infection that causes gums to swell, turn red, and
bleed (especially when the teeth are brushed). Some CFS patients can
actually gauge the severity of their illness by the condition of their
gums.

In 1991, the journal PAACNOTES, which is published by the Physicians
Association for AIDS Care (based in Chicago), warned that the type of
gingivitis developed by AIDS patients (called "ulcerative") is often
unresponsive to typical treatment.

Additionally, the periodontal disease seen in AIDS patients -which affects
the jaw bone and can cause teeth to fall out -- can result in loss of 90
percent of the affected bone in as little as 12 weeks, according to
PAACNOTES. The journal pointed out that, while some communities report that
these gum diseases occur in a very small percentage of AIDS patients (as
low as 10 percent), in other communities, they occur in more than 90
percent of AIDS patients.

In mid-1992, a research group at the University of California, San
Francisco, reported at the international AIDS meeting held in Amsterdam
that oral thrush is associated with AIDS progression and may be used to
determine how rapidly a person's health may be failing -- an observation
that may hold true for CFS patients, as well.

CHAPTER THIRTY-ONE

CFS CAN CAUSE PERCEPTION PROBLEMS FOR DRIVERS

The nervous system symptoms experienced by CFS patients can be the most
frightening: dizziness (also called vertigo) and visual problems such as
blurred or double vision, as well as inaccurate depth perception, are
extremely common. Transient, or temporary, blindness can occur in CFS. Like
AIDS patients, CFS patients can develop "floaters" that obscure the vision
and can be very distracting. These symptoms that impair vision may be the
most hazardous to the health of CFS patients -- especially if they drive.

Patients have told me that they've sometimes become so confused while
driving that they've had to pull over to the side of the road and rest
before continuing. While it's not known for sure, it's possible that
whatever is causing the visual and perceptual problems in CFS patients is
also causing the mental confusion they sometimes experience.

For instance, researchers have found that CFS patients have real problems
in processing information; they are unable to put pieces of information
together properly. That can result in memory loss, as well as difficulty in
judging both position and movement. For example, patients have told me that
sometimes they feel so dizzy, they seem to themselves to be walking at an
angle to the ground -- they really cannot tell whether they are standing
upright or leaning at a slant.

For unknown reasons, the color vision of CFS patients can become quite
disturbed. Also, they may lose their ability to see well at night, called
"night vision." This can be especially dangerous for CFS patients who go
out alone or who drive cars at night.

These perceptual problems may make even climbing stairs or taking an
escalator, as well as crossing streets or actually driving a car,
exceptionally dangerous for CFS patients while they are experiencing them.

And, of course, all these symptoms, as well as the general visual
disturbances reported by patients, worsen with increased fatigue.

CHAPTER THIRTY-TWO

PEOPLE WITH CFS OFTEN HAVE BIZARRE SLEEP PROBLEMS

Just about every physician who cares for CFS patients mentions sleep
disorder as one of the most important symptoms to control. Since fatigue
can be overwhelming to CFS patients, sleep is critical to restoring what
energy they possess. However, although they may sleep far more than they
did before becoming sick, CFS patients often report that they wake up
feeling just as tired as they did before sleeping.

Dr. Paul Cheney has characterized sleep as the single most important
symptom to treat in CFS. Not only is sleep disorder one of the easiest
problems to correct in CFS, according to Dr. Cheney, but he has found that
CFS patients will not respond well to other treatments if they are not
getting adequate sleep.

One possibile explanation for the unrefreshing sleep reported by CFS
patients is that they have less dreaming, or REM, sleep time than healthy
people.

REM sleep can be disrupted by many things. Nighttime twitching (seizures or
""fasiculations,'' abrupt movements of arms and legs) can interrupt REM
sleep. So can pain upon movement, which many CFS patients experience at
night.

CFS patients often have a body temperature that is slightly lower than that
of healthy people and as a result, have colder extremities. If fingers and
toes become too cold during sleep, they can become painful, and that pain
can wake the patient.

Other kinds of pain -- like night time headache pain -- can wake the
patient. So can frequent urination, which CFS patients -particularly those
prone to bladder infections -- tend to develop.

Breathing problems -- like sleep apnea, in which the person stops breathing
for a short period of time -- can contribute to CFS patients' sleep
dysfunction.

Nightmares can also disturb CFS patients' sleep. Although it is unknown
what causes nightmares, and their significance in CFS is also unknown, many
CFS patients report that their dreams have become more intense and more
violent and disturbing since they became ill. Children with CFS have
reported especially vivid nightmares.

Some researchers have suggested that the disturbed sleep patterns observed
in CFS patients may be due to some abnormality in brain chemistry.

Dr. Byron M. Hyde, a physician who studies CFS in Ottawa, Canada, has
suggested that major sleep disturbance may be one of the very first
symptoms of CFS to develop.

The sleep patterns of CFS patients have also been studied extensively by
another Canadian physician, Dr. Harvey Moldofsky, the director of the
University of Toronto Sleep Disorders Clinic.

There are bizarre occurrences that can disrupt CFS patients' sleep, such as
sudden, flashing lights in the eyes, which can also appear when the patient
is awake, or increasingly vivid and disturbing nightmares. No one knows
what these strange symptoms mean, what they are caused by, or if they
really have anything to do with CFS.

Another reason that the sleep of CFS patients is disturbed is that they can
suffer from night sweats, like AIDS patients. One study found that as many
as 40 percent of CFS patients experience night sweats.

It is suspected that a person's quality of sleep may correlate with immune
function, i.e. that poor quality of sleep may lead to impaired immune
functioning. How disturbed sleep and immune dysfunction may be interacting
in CFS is currently being studied by Canadian researchers. This research
could also have important implications for those studying AIDS and other
immune system disorders.

CHAPTER THIRTY-THREE

CFS IS OFTEN CHARACTERIZED BY NAUSEA

People with CFS have a variety of gastrointestinal problems: bloating,
pain, constipation, and diarrhea. Often these symptoms are treated with an
anti-ulcer drug named Tagamet, which has two primary actions: It blocks the
action of histamine (a naturallyproduced substance that governs the
production of stomach acid, as well as some allergic reactions), and it
stimulates natural killer cell activity. The fact that Tagamet can improve
some CFS patients' symptoms rather dramatically has suggested to some
observers that histamine may be very important in CFS.

But another gastrointestinal symptom suffered by CFS patients that has not
received much attention is nausea. It appears, however, to be pretty common
among CFS patients. Nausea can result from any number of causes, and no one
knows what is causing it in CFS patients. It may be a side-effect of some
kinds of neurological symptoms, such as dizziness but, to date, has not
been studied in any systematic fashion.

One study found that 50-60 percent of CFS patients report nausea as a
symptom. The same study commented that CFS can begin as something that
resembles a "stomach flu," with nausea, fever, diarrhea, muscle aches, and
fatigue.

Dr. Carol Jessop is a physician in San Francisco who has seen more than
1,000 CFS patients. At a CFS conference, Dr. Jessop commented that, among
the patients she has seen, nausea appears to increase as patients are sick
for longer periods of time. Dr. Jessop did not know how to explain this
finding, but suggested that nausea be included as one of the criteria used
to define and diagnose CFS.

Like AIDS patients, CFS patients can develop yeast infections in their
mouths and throats, called "thrush." That localized overgrowth of a type of
yeast that lives normally in people's gastrointestinal systems, called
Candida albicans, can spread from the mouth into the rest of the
gastrointestinal system in CFS patients, as it does in AIDS patients, if
the immune system is depressed severely enough to allow the overgrowth to
occur.

CHAPTER THIRTY-FOUR

CFS PATIENTS CAN DEVELOP SERIOUS BLADDER PROBLEMS

A serious bladder disease called "interstitial cystitis" appears to develop
fairly frequently in CFS. Cystitis is an acute, bacterial bladder
infection; the lining of the bladder becomes inflamed and scarred,
resulting in diminished bladder capacity. Its symptoms include blood in the
urine, as well as frequent urination with burning and pain.

Interstitial cystitis is extremely difficult to treat; the inner lining of
the bladder can become extremely inflamed, even raw and scarred. The
antibiotic treatments that cure most bladder infections generally do not
work on interstitial cystitis.

Part of the problem is that the cause or causes of interstitial cystitis
are not known. Auto-immune disease, allergies, stress, and chronic
bacterial or viral infections are among the suspected culprits.

A few patients can experience a lessening of the symptoms of cystitis when
treated with a bloodthinning chemical, heparin. It is not understood why
this drug, most often used to prevent blood clots, has this effect.

CFS patients can develop a whole range of urinary tract problems, from
inflammation to tender abdominal muscles to incontinence and, in male
patients, chronic prostatitis and even sexual dysfunction.

While most of these conditions are treatable, the reasons why they develop
remain mostly mysterious. They are probably due to CFS patients' immune
systems being unable to fight off infection by common bacteria.

Antibiotic treatment can sometimes worsen CFS patients' bladder problems,
resulting in yeast infections, similar to those that AIDS patients can
develop.

CHAPTER THIRTY-FIVE

FINGERS CAN BECOME SWOLLEN IN CFS

One of the reasons that some doctors have trouble taking CFS seriously is
because it appears to have a number of very strange symptoms; it is easy
for physicians to dismiss a wide range of symptoms as being manifestations
of psychiatric, rather than physical, illness.

One of those odd symptoms seen in CFS is finger swelling; finger swelling,
however, has gained the legitimacy of inclusion in the medical literature.
A study of the 1984 Incline Village, Nevada, CFS outbreak that was
published in a 1991 issue of Reviews of Infectious Diseases reported that
finger swelling was observed in 30-40 percent of the patients studied. No
explanation for this symptom was suggested by these investigators.

If inflammation and allergy are important aspects of the disease process of
CFS, as it appears they might be, the finger swelling might be found to
have a very simple explanation. Different kinds of allergies can cause
localized swelling -- from contact allergies like poison ivy to food or
drug allergies -- and the location of the allergic response doesn't always
seem to make sense.

Fingers can swell so much that, not only do fingertips become smooth and
sometimes shiny, the fingerprints can also disappear. This is a phenomenon
that has been documented most closely by Dr. Paul Cheney, who has all of
his patients go to the local police station to be fingerprinted.

There can be significant swelling of face, hands, and feet in CFS, much
like that which is seen in lupus. Unfortunately, unlike lupus patients, CFS
patients' swelling does not respond well if at all to steroid treatment.

CHAPTER THIRTY-SIX

CFS PATIENTS CAN DEVELOP SKIN RASHES AND OTHER DISORDERS, ESPECIALLY ACNE
AND SHINGLES

One of the still-unexplained manifestations of CFS is the appearance of
skin rashes. Rashes can have several causes; for example, they can be
caused by allergic reactions, either by something that comes in contact
with the skin (like poison ivy), or by something taken internally (like
medicine or a food to which a person is allergic).

Rashes can be caused by infectious agents. The measles virus causes a very
distinctive rash, as do Lyme disease and scarlet fever (both of which are
caused by bacteria).

Rashes can also have emotional or psychological causes, because of the
interaction between mind and body. Even anxiety can cause hives and other
kinds of rashes.

No one knows what causes CFS patients to develop rashes, but they occur in
about half of adult patients, commonly on the face and upper body.

For some unknown reason, rashes occur even more often in children with CFS
than they do in adults. Dr. David Bell, who studied a group of children
involved in a CFS outbreak in upstate New York, found that 80 percent of
the children developed rashes.

Patients have described many different kinds of rashes to me. One reason
that rashes might be so common in CFS is that allergies are worsened;
people who had allergies before they developed CFS often find that their
allergies are much more severe after they come down with CFS.

One reason for that might be the involvement of a naturallyproduced
chemical called histamine in CFS. Histamine, which is also increased in
AIDS, controls certain kinds of allergic reactions as well as the
production of stomach acid.

In addition to causing allergic reactions, histamine is also thought to
bind to immune system cells and produce a substance that results in the
suppression of the immune system.

So histamine production is another area which demonstrates how the immune
system can be both upregulated and down-regulated at the same time. While
too much histamine can produce an allergic reaction -which is an
over-reaction of the immune system -- it can also cause the suppression of
the immune system.

Another result of this general malfunctioning of the immune system is that
unexpected bacterial and viral infections can appear. Acne, which can
result from a bacterial infection, and the re-emergence of herpes virus
infections -- like cold sores or shingles -- are examples of the kinds of
infections that can occur when the immune system is depressed. AIDS
patients, of course, develop the same kinds of bacterial and viral
infections because of the down-regulation of their immune systems.

Numerous CFS researchers have reported that their adult patients can
develop acne -- even patients who've never had skin problems before they
became sick with CFS. Dr. Paul Cheney cautions that this type of acne, and
other skin infections, may require more aggressive treatment in CFS
patients than they would in healthy people for the treatment to be
successful.

Herpes viruses live in harmony with people, generally speaking; once we
become infected, the herpes viruses usually stay dormant, kept in check by
an intact immune system. But when the immune system is damaged, as it is in
CFS, herpes viruses can become reactivated and cause various kinds of skin
(and other) problems.

One herpes virus that most people are infected with is herpes simplex, the
virus that causes common cold sores. CFS patients sometimes have recurrent
cold sores, which signal that the herpes simplex virus is no longer being
controlled by their immune systems.

Another herpes virus, herpes zoster, causes chicken pox in children; later
in life, it can become reactivated to cause shingles, a very painful skin
condition in adults.

Both types of herpes virus reactivations -- cold sores (or other skin
lesions caused by herpes simplex) and shingles -- can occur in adult CFS
patients because of the "down-regulation" of their immune systems.

In children with CFS, chicken pox -- the childhood disease caused by the
herpes zoster virus -- can be particularly troubling. Dr. David Bell has
found that, among children with CFS whom he has studied, more than 80
percent had already had chicken pox before they contracted CFS. After
developing CFS, however, about 12 percent of those children who'd never had
chicken pox got the disease, and about 12 percent had it twice. Dr. Bell
even found that one of those 74 children had chicken pox three times after
developing CFS, and another had chicken pox five separate times after
coming down with CFS.

An experimental treatment for CFS, Kutapressin -- which is an extract of
pig liver -- has been found to be useful in treating herpes zoster-caused
shingles. If Kutapressin stops the reactivation of herpes viruses, that may
be why CFS patients' symptoms appear to improve when they are treated with
the drug.

CHAPTER THIRTY-SEVEN

THE HAIR CAN BE SEVERELY AFFECTED BY CFS

Hair loss can be caused by either severe or chronic illness, particularly
when a high fever is present. Since as many as 60 to 90 percent of CFS
patients have been reported to run fevers, perhaps it is not surprising
that some find that their hair is thinning_or even falling out altogether.

Dr. Paul Cheney has reported that his CFS patients "usually" have brittle,
thinning hair. CFS patients' hair sometimes also develops a reddish tint,
Dr. Cheney says.

California CFS researcher Dr. Jay Goldstein has found that diffuse, or
spotty, hair loss is one of the most common skin-related abnormalities in
his patients. He suggests that this hair loss may be caused by hormonal
imbalances, which can be treated with medications, usually steroids. In an
article Dr. Goldstein wrote in the September 1992 CFIDS Chronicle, however,
he pointed out that, "Some of my patients have had to buy wigs."

CFS patient "Nancy" told me that, when she was very sick with CFS, her hair
became so thin that her hairdresser suggested that Nancy have her thyroid
tested. Thinning hair can be indicative of severe thyroid deficiency, which
CFS patients can develop.

"My hair was falling out in clumps," Nancy told me. "At its worst point, I
looked like an AIDS or cancer patient who was undergoing chemotherapy. I
had barely enough hair to cover my scalp in parts."

CHAPTER THIRTY-EIGHT

CFS PATIENTS CAN HAVE FALSE POSITIVE TESTS FOR SYPHILIS

Like AIDS patients, CFS patients can test positive on an antibody test for
syphilis -- even if they do not have the illness.

Why is that? Some researchers have suggested that CFS patients are
experiencing what is called an "antibody storm," in which many different
kinds of antibodies are being created by a disturbed, overactive immune
system.

In a very detailed study of the immune systems of CFS patients, Miami
University researcher Dr. Nancy Klimas also found that CFS patients can
have false positive tests for syphilis.

Dr. Klimas and her colleagues suggested that the B-cells, the immune system
cells which make antibodies, are extremely dysfunctional in CFS. This
research team also suggested that the B-cell malfunction taking place in
CFS might result in the lowered natural killer cell activity that has also
been observed, since another function of B-cells is to stimulate natural
killer cells.

False positive syphilis tests are so common among AIDS patients that, for a
while, it was thought that syphilis might be intimately involved in causing
AIDS. Although AIDS patients can progress to the neurological form of
syphilis much more rapidly than otherwise healthy people do -- in a matter
of months, as opposed to 30 or 40 years -syphilis is no longer considered
to be a candidate for causing the symptoms of AIDS.

CHAPTER THIRTY-NINE

IN CFS PATIENTS, AS IN AIDS PATIENTS, THE T4 CELLS MAY BE SEQUESTERED IN
THE LYMPH NODES

One of the hallmarks of AIDS throughout the epidemic has been a decreasing
T4, or CD4, cell count. In early 1993, research published by government
scientists demonstrated that, like AIDS patients, CFS patients' T4 cell
counts are substantially decreased.

Most healthy people have T4 cell counts of about 1000. In AIDS, T4 cell
counts can fall precipitously; below 200, an AIDS patient is considered to
be in danger of developing a potentially life-threatening opportunistic
infection.

Dr. Stephen Straus, who is in charge of CFS research at the National
Institute of Allergy and Infectious Diseases (part of the National
Institutes of Health), directed the study of CFS patients' T4 cells.

Dr. Straus and his colleagues found that CFS patients had "significantly
decreased" numbers of a subtype of T4 cells.

In a government press release, however, Dr. Straus emphasized that the loss
of T4 cells in CFS patients was completely different from the loss of T4
cells in AIDS patients.

"This decrease does not indicate the CD4 T-cells [T4 cells] are being
destroyed, such as happens in AIDS," Straus commented in the press release,
"but that more CD4 T-cells appear to change location, shifting from the
blood into the tissues. These tissuebased cells escape detection by
research blood tests."

A careful reading of Dr. Straus and colleagues' actual research report,
however, reveals that this assertion -- that the T4 cells have changed
location from the blood into the tissues -- is based on absolutely no data
whatsoever. It is just a guess. All that Dr. Straus and his coworkers
actually showed was a significant decrease in T4 cells in CFS patients.

Not long after Dr. Straus's research report was published, a report in
Science magazine suggested that AIDS patients' T4 cell counts were not
really so low as they appeared to be because AIDS patients' T4 cells were
also hiding in the lymph nodes.

No one in the lay press appeared to notice these parallel explanations of
what was happening to the T4 cells of AIDS and CFS patients.

Dr. Straus's finding about the T4 cells of CFS patients is particularly
important because he has attempted, for several years, to prove that CFS is
a psychiatric disorder. Discovering this "abnormality of immune regulation"
in CFS patients, as he and his coworkers called it in their research report
published in the Journal of Clinical Immunology, did not discourage Dr.
Straus from pursuing his hypothesis about CFS being a psychological
disease. He and his colleagues suggested that, "The [immunologic]
abnormalities may be secondary to an underlying neuropsychiatric disorder
which affects immune function indirectly...."

Other studies documenting the immune system abnormalities found in CFS
patients_like non-functional natural killer cells, for instance_suggest
that CFS is primarily an immunological, not a psychological, illness.

CHAPTER FORTY

SUNBATHING MAY MAKE CFS SYMPTOMS WORSE

It is being increasingly recognized that exposure to sunlight isn't as good
for people as we once thought it was. As scientists document the damage
that pollution has done to the ozone layer that surrounds the earth and
protects all living things from the sun's harmful radiation, people are
being warned that unprotected sunbathing not only increases their chances
of developing wrinkles and skin cancer, but may also damage their immune
systems.

It is not known for sure how sunlight damages the immune system, but it may
be through a process similar to the way skin is hurt by the sun's rays. The
ultraviolet light that makes up part of the sun's radiation is known to be
able to damage skin cells' DNA, the genetic material that resides in every
type of cell. It's possible that immune system cells are damaged that way
by the sun, as well.

It's also possible that Vitamin D, a vitamin that people make in their
bodies after exposure to sunlight, contributes to the worsening of CFS
patients' symptoms. It's been suggested that vitamin D may not be processed
properly by CFS patients, and that the resulting chemical imbalance may
make their symptoms worse.

In any event, most doctors who treat CFS patients caution them to stay out
of the sun.

Dr. Charles W. Lapp, who works with Dr. Paul Cheney in Charlotte, North
Carolina, advises his patients to avoid sunbathing.

In a "Self-Care Manual" that Drs. Cheney and Lapp wrote for their patients
in 1991, they also advise patients to avoid the sun. They caution that
exposure to sunshine "may reactivate herpes group viruses or provoke skin
reactions."

Another reason for CFS patients to avoid the sun is that many find that
their eyes have become extremely sensitive to bright light, a condition
that is called "photophobia." Drs. Cheney and Lapp advise their CFS
patients to wear sunglasses to protect their eyes from the sun.

CHAPTER FORTY-ONE

AS IT PROGRESSES, CFS CAN BE MEASURED IN "STAGES"

One of the problems researchers encounter in studying CFS is that, like
AIDS, there is no good indication of when a patient actually becomes
infected with the disease-causing agent; therefore, it is difficult to
assess the progression, or "natural history," of the syndrome.

A Long Island physician, Dr. Perry Orens, has devised a set of criteria by
which to "stage" CFS, in terms of the progression of illness.

Dr. Orens's criteria range from what he has called Class I, in which the
patient meets the CDC criteria (50 percent reduction in activities lasting
at least six months), to Class IV, in which patients are completely
disabled and bedridden.

The system used to classify AIDS patients' disease in stages, called the
Walter Reed Classification System (developed at the Walter Reed Army
Hospital), is no more specific than Dr. Orens's CFS stages.

In Walter Reed Stages 0 through 2, the patient is essentially healthy;
antibodies for HIV and chronically swollen lymph nodes are the only
symptoms noted.

In Walter Reed Stage 3, T4 cell counts drop to below 400; in Stage 4, there
is a partial failure of the ability to respond to skin tests (i.e., cell
mediated immunity begins to fail, as it does in CFS patients). In Stage 5,
there is a complete failure of cell-mediated immunity (called "anergy,"
which is also seen in CFS patients) andor the development of thrush, a
yeast infection of the mouth. (CFS patients, of course, can also develop
thrush.)

In Stage 6 -- the stage at which patients are said to have AIDS --
opportunistic infections occur.

CFS patients can also develop "opportunistic infections." In his February
1993 testimony to a Food and Drug Administration Scientific Advisory
Committee, Dr. Paul Cheney pointed out that of his five CFS patients who'd
died during the preceding six months, three died as a result of
overwhelming opportunistic infections.

At the very least, it seems that many CFS patients could be classified as
being permanently or semi-permanently in Stage 4 of AIDS.

CHAPTER FORTY-TWO

SOME CFS PATIENTS BECOME SUICIDAL

Many CFS patients become severely depressed after they have been sick for a
period of time. This is not too surprising: Many patients lose their jobs
-- and therefore their livelihoods -their homes, and often, the
relationships most important to them, with family, friends, and spouses.

The inability -- or unwillingness -- of the medical establishment to deal
with CFS as a very serious, indeed overwhelming, illness contributes to the
depression experienced by CFS patients. Authors Barbara Brooks and Nancy
Smith address this problem in some depth in their book, CFIDS: An "Owner's
Manual" (BBNS Publishing, Silver Springs, MD).

"When a bad case of the CFIDS blues really has you down, suicide begins to
look good by comparison," Brooks and Smith write. "...Suicide, a negative
thought for normal people, becomes a positive picture for the
CFIDS-depressed person. When your future is so bleak and hopeless, it is no
wonder you lapse into such thoughts....Unfortunately, your sense of
self-blame may often be reinforced by society in general...."

Brooks and Smith also relate that, "As we spoke to support group leaders
around the country, the one thing that struck us was their report of an
increasing number of calls they were receiving from suicidal patients. The
numbers of patients who are losing everything -- their jobs, their homes,
their cars, and their health insurance -is on the rise. Employers seem to
be showing no compassion, and these patients are being dumped. They are
truly falling through the cracks of the social system...."

Dr. William A. Carter, a coinventor of the experimental AIDS and CFS
treatment Ampligen and a professor of oncology and hematology at Hahnemann
University (Philadelphia), was interviewed at the September 1991 31st
Interscience Conference on Antimicrobial Agents and Chemotherapy (held in
Chicago). In that interview, which was published in the Conference Journal,
Dr. Carter talked about how desperate CFS patients become.

"The effects of this disease are devastating," Dr. Carter said. "It has
enormous repercussions. It causes families to go into bankruptcy. We have
talked to very few families where the husband or wife still had a viable
marriage because it destroys marriages. And it puts a huge burden on the
medical system. The incidence of suicide is apparently quite high as the
patients become progressively debilitated."

Dr. Paul Cheney, one of the physicians who discovered the first outbreak of
CFS in Nevada in 1984, delivered testimony before the Food and Drug
Administration Scientific Advisory Committee in February 1993. Dr. Cheney
told the FDA, "We are frequently depositioned for disability and other
types of litigation. Many cases involve divorce as we witness the
disintegration of the family unit....The medical-legal aspects of our
practice steadily grow as this disease eats at the fabric of our
communities."

CHAPTER FORTY-THREE

HEALTH CARE WORKERS MAY BE AT INCREASED RISK FOR CFS

The Centers for Disease Control and Prevention (CDC) received so many calls
from doctors, nurses, and other health care workers stating that they had
developed CFS that a study of CFS in that ""risk group'' was planned for
1991-1992, as documents received under the Freedom of Information Act show.

That study of the incidence of CFS among health care workers, however, was
never carried out.

The explanation of the study, which was included in financial projections
for the CDC's Fiscal Year 1991 and 1992 New Collections (part of the
Department of Health and Human Services budget) states, in part:

"CDC has received a significant number of calls and letters from
physicians, nurses, and other health care providers reporting that they,
and in many cases, other members of their families, are suffering from
chronic fatigue syndrome. CDC plans to conduct a nationwide study of
chronic fatigue syndrome in health care providers to determine the
prevalence of the illness, its characteristics, and associated exposure
factors...."

The CFIDS Chronicle has documented -- probably by accident -- a large
number of cases of physicians, nurses, and other health professionals who
have developed CFS, many of whom have written articles for the patient
advocacy journal.

A Canadian medical researcher described, in the CFIDS Chronicle, how his
life had changed since he became ill with CFS. He wrote that it was hard to
remember that he used to race against the clock, writing grant applications
to fund his research, or to save the lives of the babies he cared for. This
doctor mourned the loss of weeks and months that had turned into more than
a year of idleness.

A former nurse also wrote to the CFIDS Chronicle, describing how unhappy it
made her that she, who used to care for other people, now could not even
take care of herself.

I have interviewed a surprising number of physicians who have CFS and, in
most instances, they have reported being just as badly treated by their own
profession as other CFS patients. Physicians who develop CFS are shocked, I
have found, that their colleagues do not take their illness seriously. Like
other CFS patients, physician-patients often find that they have to consult
numerous doctors before they find someone who is knowledgeable about CFS.

Like teachers and airline personnel, health care professionals may be at
greater risk for contracting CFS simply because they have close contact
with large numbers of people.

Until the infectious agent that causes CFS is positively identified,
however, no one can really explain why health care workers are more at risk
for contracting CFS.

CHAPTER FORTY-FOUR

CFS CAN RESULT IN FINANCIAL DISASTER

If a person becomes so ill that he or she cannot work, financial
difficulties usually follow. Unfortunately, even people who believed,
before they got sick, that they had built a financial safety net find that
it can be snatched from underneath them. And some financial safety nets --
like health insurance -- don't always catch CFS patients.

CFS patients, like AIDS and cancer patients, are also especially vulnerable
to medical fraud, which can quickly erode a person's, or a family's, life
savings. And, because insurance companies can choose pretty freely what
they will and won't pay for, it isn't even possible to use that yardstick
to determine whether a treatment or medication is new and promising or is
simply a scam.

Dr. Jay Goldstein has written extensively about the problems that his
patients have encountered in trying to get their insurance companies to pay
for CFS tests and treatments. One of the most common reasons for
non-payment, according to Dr. Goldstein, is that the insurance company
decides that a treatment is not medically necessary.

Insurance companies can also refuse to pay for treatments or tests that
they consider to be experimental. Any treatment that has not received Food
and Drug Administration (FDA) approval for treating a certain illness can
be ruled to be experimental by insurance companies. Currently, there is not
a single CFS treatment that has received FDA-approval.

Dr. Goldstein has also pointed out that it is often downright impossible
for a CFS patient to fight his or her insurance company; it is an
expensive, time- and energy-consuming process. Unfortunately, many CFS
patients just forego treatments and tests rather than try to fight their
insurance companies.

There is an especially tragic case of a CFS patient being abandoned by her
insurance company that was described in articles in both the New York Times
and New York Newsday in 1992. The patient, who had been a brain researcher
before becoming disabled by CFS, was simply told one day by her insurance
company that the benefits she had been receiving -- such as round-the-clock
nursing care -were no longer going to be provided. This patient's life had
been saved twice by her 24-hour-aday nurse, according to newspaper reports;
once when she developed a blood clot in one of her lungs, and a second time
when she unexpectedly began hemorrhaging.

Why did the insurance company cut off this patient's benefits? The company
denied that it was because of the amount of money her care was costing but,
since the patient had developed CFS, according to newspaper accounts, her
insurance company had paid more than one million dollars for her care.

In testimony presented to the Food and Drug Administration's Scientific
Advisory Committee on February 18, 1993, Dr. Paul Cheney said, "From an
economic standpoint, this disease is a disaster."

"Eighty percent of the cases evaluated at my clinic are unable to work or
attend school," Dr. Cheney told the FDA. "The average length of illness at
the time of presentation is 3.8 years. Ninety percent have become ill since
1980. The yearly case production, if plotted, is exponential. Most are
already on or will shortly be on some sort of disability plan, public or
private."

In addition to becoming disabled -- which has a huge societal cost, not
only in terms of direct payments to the disabled person, but also in terms
of person-years of work and taxable income lost -- Dr. Cheney told the FDA
that his patients had spent an average of $15,000 on medical care before
coming to his clinic.

CHAPTER FORTY-FIVE

A DRUG MADE FROM PIG LIVER APPEARS TO HELP SOME CFS PATIENTS

Kutapressin is a drug made from porcine (pig) liver that has been used,
apparently with no bad side effects, to treat herpes infections (such as
shingles) since the 1940s. When CFS was first identified in the early
1980s, it was thought to be caused by one of the herpes viruses, the
EpsteinBarr virus (EBV), and so a group of researchers in Texas decided to
test Kutapressin's effects on CFS patients.

It is not known how Kutapressin works, but researchers theorize that it may
affect the production of lymphokines like interleukin-2; an overproduction
of lymphokines can cause not only perturbations of the immune system, but
also symptoms similar to those seen in CFS.

In the informal Texas study, 270 CFS patients were treated with at least
ten injections of Kutapressin.

Patients' response to Kutapressin appeared to be at least partially
dose-related; 96 percent of the patients who received more than 40
injections had notable or marked improvement in their symptoms. Of the
patients who received 11-40 injections of Kutapressin, 71 percent reported
the same level of improvement.

There was only one bad reaction to Kutapressin injection out of more than
8000 injections of the drug, according to the Texas researchers; this
patient complained that some symptoms worsened, and the drug was stopped.

At the current time, there are tentative plans to test the efficacy of
Kutapressin in treating AIDS, as well as plans for formal tests of
Kutapressin in CFS patients.

CHAPTER FORTY-SIX

AN EXPERIMENTAL DRUG THAT APPEARS PROMISING FOR CFS AND AIDS IS BEING
EVALUATED BY THE FDA

In February 1993, the Food and Drug Administration's Anti-Viral Drug
Advisory Committee met to consider the merits of an experimental drug,
Ampligen, that appears to have promise for treating CFS (and, in earlier
trials, AIDS). So far, no drug has been approved for the treatment of CFS
by the FDA.

Ampligen appears to correct a defect in a very important natural anti-viral
pathway. When this pathway isn't working properly, viruses aren't attacked
by the body's natural defenses. In CFS patients, as in AIDS patients, this
anti-viral pathway is defective; furthermore, Ampligen appears to correct
the defect in both sets of patients.

At the February meeting at the FDA, Kim Kenney of the CFIDS Association of
America (in Charlotte, NC), told the FDA that approving a drug to treat CFS
is extremely important to patients, many of whom are desperate to get
better. She told the FDA that "the reactions of our constituents range from
impatience to desperation, depending on the severity of their condition.
Impatient to get back to work, to enjoy their families again. And for some,
desperation to reverse the severely debilitating effects of CFIDS,
including dementia, unrelenting muscle and joint pain, severe encephalitis,
not to mention the problems that accompany a severely impaired immune
system."

Dr. Daniel Peterson, one of the two physicians who identified the original
outbreak of CFS in Incline Village, Nevada, in 1984, told the FDA committee
that "a significant number" of his patients who fell ill in 1984 "never
recovered." Dr. Peterson also said that, over the last eight years, 20
percent of the patients he'd examined had become completely disabled. Dr.
Peterson also cautioned that the CDC's "crude incidence" of four per
100,000 "most certainly vastly underestimates the true incidence of the
disease."

Dr. Peterson told the FDA that, although Ampligen "appears to have great
potential in this disease process, it has been bogged down in a corporate
and bureaucratic quagmire, and yet the disability and anguish of the
patients and treating physicians remains unaddressed."

Jerry Crum, the CFIDS Association's co-chair of its Public Policy Advisory
Committee, also spoke at the February meeting with the FDA. Mr. Crum
described his illness, which began in 1985, for the committee:

"What I remember during three years of progressive deterioration were
seizures on an average of two to three per week and becoming severely
demented. My short-term memory was seriously impaired. When I went for
walks in my neighborhood, I couldn't find my way home. My IQ dropped from
130 to 85. I will never, ever forget what it feels like to have an IQ of
85. I was not "stupid." What I had was an indefinite sense of the world
around me....If I concentrated very hard, I could follow conversations....I
slept 14 or more hours per day and nothing alleviated the ever-present
muscle pain I suffered from. I was bleeding from my colon. A lumbar
puncture performed by Dr. Peterson confirmed severe encephalitis...."

Ampligen, however, allowed Mr. Crum to live a more normal life. His
seizures became infrequent, his IQ increased almost to its preillness
level, and he became capable of performing his job, which involved complex
mathematics, again. "The muscle aches diminished, and I required only ten
hours of sleep per night with a nap during the day," Mr. Crum told the FDA.
He credits Ampligen with allowing him to "regain a measure of quality to my
life, which I thought I would never experience again."

Perhaps most compellingly, however, Mr. Crum described for the FDA what
happened to him when he stopped taking Ampligen because, as he said,
"Receiving I.V. infusions three times per week is not pleasant." But,
within six weeks of discontinuing Ampligen therapy, he once again began
having seizures and his IQ again plummeted.

"In short, I regressed to the same seriously ill condition I was in prior
to receiving Ampligen," Mr. Crum told the FDA Committee.

Similar testimony from other patients, or their families if they were too
impaired to deliver or prepare testimony themselves, was also presented to
the FDA committee.

The FDA, however, has yet to grant approval to Ampligen or any other drug
to treat CFS.

CHAPTER FORTY-SEVEN

NOTHING IS BEING DONE TO PROTECT THE BLOOD SUPPLY FROM CFS-INFECTED BLOOD

Is it possible to become infected with CFS through a blood transfusion?
Numerous patients have told me that they first became ill after receiving a
blood transfusion; and although the Center for Disease Control and
Prevention (CDC) has cautioned CFS patients not to give blood, there is no
official mechanism in place to screen CFS patients out of the blood-giving
population.

A CFS patient who was concerned about the blood supply sent me a copy of a
letter written by the person then in charge of CFS research at the CDC, Dr.
William Reeves. In the letter, Dr. Reeves cautions the CFS patient not to
give blood.

The CDC has no official policy concerning blood donation by CFS patients,
Dr. Reeves wrote. "However, since ongoing research indicates an infectious
agent may be involved in some cases of CFS, it would seem prudent to
refrain from donating blood until this issue is resolved....You should
inform officials at the blood collection center that you have CFS; the
blood bank may have specific regulations concerning CFS or similar
diseases."

The Food and Drug Administration (FDA), the agency responsible for
regulating blood collection in the U.S., has no specific questions
regarding CFS in its guidelines.

Because the FDA does not specifically prohibit blood donation by CFS
patients, the American Red Cross has concluded that it is safe to accept
blood from CFS patients. I was told by a representative of the American Red
Cross in Washington, DC, that blood donations were accepted from CFS
patients as long as their illness was "inactive." There is no agreed-upon
definition for "inactive" CFS, however.

While physicians and researchers agree that it is entirely possible that
CFS can be contracted from blood transfusions, at the current time, there
are no mechanisms in place to protect the public from this occurrence.

That may change at least in part because of a blood banking scandal in
France. In the early 1980s, a decision was made by French government
officials to delay testing blood and blood products for HIV until a
Frenchmade test was available, even though a test developed in the U.S. was
available to French blood banks. As a result, a large percentage of French
hemophiliacs developed AIDS because they had been transfused with
contaminated blood products. In 1993, however, those responsible for making
the decision to delay testing -including more than one former, high
government official -- went on trial; some of those involved were sentenced
to spend time in jail.

CHAPTER FORTY-EIGHT

CFS HAS SPAWNED A POWERFUL PATIENT MOVEMENT THAT HAS BECOME MIRED IN DENIAL

Chronic Fatigue Syndrome patients have created a patient movement the size
of which probably has never been equaled in the United States. Patients
banded together initially out of selfprotection: The media, physicians,
their families -- it seemed like everyone -- were telling them that they
had psychiatric problems. As the theory that CFS is a psychoneurotic
disorder was disproved -- although there are still a few adherents to this
outdated theory -- CFS patients organized to achieve political power. A
great deal has been achieved by local, as well as national, CFS patient
groups in terms of getting CFS moved up on the national health agenda as a
problem to be taken seriously.

But while the CFS patient movement has argued that CFS is a neurological
and immunological illness, they have not acknowledged the syndrome's
connection to AIDS.

This denial on the part of CFS patient advocates is probably a response to
the discrimination suffered by AIDS patients. A diagnosis of AIDS can cause
a person to lose his or her apartment, job, and important relationships.
Routine health care can become very difficult to obtain for AIDS patients.
Discrimination against AIDS patients is, in fact, rampant.

Oddly, patients who are not involved with the CFS movement in any formal
way are much more likely to acknowledge the overwhelming similarities
between CFS and AIDS.

It may be that, for "official" patient groups, admitting that CFS is
closely related, if not identical, to AIDS is just too frightening.

While such denial is natural and understandable, it should not be allowed
to prevent an objective investigation of the possible link between CFS and
AIDS. That connection may help solve both puzzles at the same time.

CHAPTER FORTY-NINE

THE TWO "VARIANTS" OF HHV-6 APPEAR TO ACT VERY DIFFERENTLY

There are many strains of HHV6 -- that is, viruses that are enough alike to
be considered HHV6, but which differ from each other in small ways. Those
strains are further classified as being in a larger grouping, called a
"variant." The two variants of HHV6 appear to have very different
disease-causing properties. While this is rather technical information, it
may have important implications for understanding both Chronic Fatigue
Syndrome and AIDS.

The easiest way to visualize different virus strains is to imagine that a
virus is like a string of different-colored beads. If you have three
strings of beads that have exactly the same color sequence except for one
bead, those strings would be analogous to strains of a virus.

There are many different strains of HHV-6, and more appear to be discovered
all the time. Those strains, like the imaginary strings of beads, differ
from each other only very slightly.

But as more has been learned about HHV-6, it has become clear that the
virus strains differ from each other in ways that allow them to be divided
into two groups, called "Variant A" and "Variant B" HHV-6.

These two variants appear to be able to cause very different kinds of
illness, and may resolve the apparent paradox that HHV-6 infects about 90
percent of the world population as an apparently harmless, asymptomatic
infection, yet can also be associated with catastrophic immune system
diseases like AIDS, cancer, and Chronic Fatigue Syndrome.

Recent research has shown that Variant B HHV-6 is the type that infects
infants and children, usually by age three, and is associated with a mild
illness with fever and rash called roseola.

Variant A HHV-6, however, is the type that is found in very sick adults
with AIDS and CFS. Variant A HHV-6 appears to be able to attack the immune
system, and infect and kill very important cells. Cells that HHV-6 is known
to be able to infect include the cell considered to be the primary target
of HIV, the T4 cells, and other very important immune system cells, natural
killer cells.

Because HHV-6 can infect the same cells as HIV -- and both viruses have
been found cohabitating in the same cell -some researchers have suggested
that HHV-6 may be a "co-factor" in causing AIDS.

Now, however, it is known that HHV-6 is the only virus capable of infecting
and killing natural killer cells, the immune system's front-line defense
against viruses and some kinds of cancers.

So, along with HHV-6's ability to infect T4 cells, it is becoming clear
that HHV-6 is capable of inflicting a considerable amount of damage on the
immune system.

Although some scientists consider HHV-6 to be a "co-factor," along with
HIV, in causing AIDS, it might be more prudent to determine how much HHV-6
can damage the immune system all by itself.

Is HHV-6 the real AIDS virus?

CHAPTER FIFTY

A VIRUS THAT CAUSES AN "ACQUIRED IMMUNE DEFICIENCY SYNDROME" IN PIGS MAY BE
THE REAL CAUSE OF CFS AND AIDS

It may seem silly to look at a pig illness to identify the cause of CFS,
but it really isn't. Pigs and humans pass viruses back and forth all the
time; in fact, flu viruses change from year to year because they pass from
people to pigs and back again and in so doing, mutate, or change,
considerably.

There is an illness of pigs, African Swine Fever, that an expert in the
field has called "an acquired immune deficiency syndrome of pigs," because
it produces symptoms that are so similar to those of AIDS. African Swine
Fever is caused by a virus, African Swine Fever Virus (ASFV).

Like AIDS, there is no treatment for African Swine Fever, and no vaccine to
prevent ASFV infection. When African Swine Fever is suspected in a herd of
pigs, the entire herd is slaughtered to prevent the spread of the very
contagious, deadly virus. Because of the vast economic implications such
slaughters of pig herds would have on U.S. agriculture, it is against the
law to study ASFV on mainland U.S.A. The only place where the virus can be
studied, by law, is the Plum Island Animal Disease Center on Plum Island,
off the shore of Long Island, New York.

Similarities between the symptoms of ASF and AIDS -- as well as the fact
that Haiti, one of the areas in which AIDS appeared earliest, had recently
had an ASFV epidemic -- caught the attention of a young scientist in 1983.
Dr. Jane Teas, who was working as a researcher at Harvard, began
collaborating with Boston University scientist Dr. John Beldekas to try to
figure out if ASFV could be causing AIDS.

In 1986, Drs. Teas and Beldekas published a report in the British medical
journal The Lancet showing that they had found evidence of ASFV infection
in AIDS patients. But after that, the trail was stopped cold, when a group
of scientists gathered by the U.S. Department of Agriculture at Cold Spring
Harbor Laboratory (on Long Island) issued a memorandum that no further
research should be performed to test the ASFV hypothesis. Usually, when a
line of research proves not to be fruitful, scientists naturally stop
pursuing it; it was, however, unprecedented for a group of scientists
gathered by the government to declare that a line of research should no
longer be pursued. That is, however, exactly what the scientists gathered
by the USDA at the Cold Spring Harbor Laboratory did.

Shortly thereafter, however, two research groups to whom Dr. Teas and Dr.
Beldekas had provided information and scientific materials announced almost
simultaneous discoveries of a "new" human virus, found in AIDS patients:
HHV-6.

HHV-6 and ASFV are very similar viruses; they are the same size, and they
infect and kill the same kinds of cells. They both cause bleeding problems
(they are "hemorrhagic" viruses), and both attack the immune system,
allowing secondary (or "opportunistic") infections to become fatal. They
both cause neurological disease. Both viruses mutate (change) easily.

Furthermore, both HHV-6 and ASFV are characterized by having many strains,
or types, of virus. ASFV, it has been known for dec ades, can cause a whole
range of illness, from extremely acute (in which 100 percent of infected
animals die within days) to chronic (in which animals develop immune system
and neurological symptoms, but generally survive).

HHV-6, also, has many strains that can cause different levels of disease,
from an illness with mild fever and rash, to a fatal, hemorrhagic disease
in which the patient rapidly bleeds to death. HHV-6 can cause a collapse of
the immune system, and is associated with many kinds of neurological
phenomena, including the development of brain lesions. Like ASFV, HHV-6 is
found in people with acute illness -- that is, AIDS -and chronic illness,
CFS.

Where did this new human virus come from?

Is it a zoonosis, an animal virus that has mutated and become capable of
infecting humans?

When Dr. Teas and Dr. Beldekas were trying to determine if ASFV could be
involved in causing AIDS, a major objection to the theory was that pigs in
the U.S. were not sick. If a pig virus were causing AIDS, some experts
argued, then shouldn't the pigs be sick?

There is, in fact, a worldwide epidemic among domesticated pigs that bears
a great resemblance to African Swine Fever; it has been called "Mystery
Swine Disease." Although a "new" virus (called "Lelystadt virus" for the
city in which it was isolated) is thought to be causing "Mystery Swine
Disease," the new virus has not yet been compared to all the strains of the
old virus, ASFV.

Lelystad virus also has not been compared to the new human virus, HHV-6.

One reason that there has been very little progress in fighting both AIDS
and CFS may be because HHV-6 is actually the virus that is causing most, if
not all, of the damage to the immune system in both syndromes.

If HHV-6 is causing the immune system damage in AIDS and CFS and if HHV-6
is really a strain of ASFV, there is the very real possibility that some
scientists have deliberately misled the public.

If government scientists are afraid to admit what HHV-6 really is and how
widespread the immunological damage it causes is, then the problem of
ending the CFS epidemic may be as political as it is scientific.

References

Presentations made at a conference jointly sponsored by the National
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