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1996-02-27
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Document 0622
DOCN M9630622
TI Lymphocyte-tropic simian immunodeficiency virus causes persistent
infection in the brains of rhesus monkeys.
DT 9603
AU Stephens EB; Liu ZQ; Zhu GW; Adany I; Joag SV; Foresman L; Berman NE;
Narayan O; Department of Microbiology, Molecular Genetics and
Immunology,; Marion Merrell Dow Laboratory for Viral Pathogenesis,
University; of Kansas Medical Center, Kansas City 66160-7240, USA.
SO Virology. 1995 Nov 10;213(2):600-14. Unique Identifier : AIDSLINE
MED/96074535
AB Molecularly cloned SIVmac239 is the prototypical SIVmac
lymphocyte-tropic virus that replicates productively in lymphocytes but
poorly in macrophages. In macaques, the virus causes activation and
productive infection of T lymphocytes which invade the central nervous
system (CNS) early after infection in the animal. However, infected
animals develop immunosuppression and AIDS but rarely overt neurological
disease. In this study, we examined multiple regions of the brain and
spinal cord for the presence of SIV env sequences and histological
lesions in five macaques that had been infected with SIVmac239 for 1.7
to 2.25 years. Histopathological examination of the brain revealed no
lesions consistent with encephalitis; however, viral DNA was found in
all five brains. In one animal the virus caused infection in a widely
disseminated pattern from the frontal cortex to the distal end of the
spinal cord, whereas in the other four animals infection in the CNS
occurred in a nonspecific, focal pattern. Sequence analyses were
performed on gp120 sequences isolated from selected regions of the CNS
and compared to gp120 sequences isolated from corresponding lymph nodes,
a tissue known to support productive replication of SIVmac239.
Examination of the viral sequences from the CNS tissue from two animals
(macaques 10F and 14F) revealed a low mutation rate when compared to the
sequences isolated from the lymph node tissues. The percentage change in
the amino acid sequence was approximately 1% for CNS clones versus > or
= 3% for clones isolated from the lymph node. The majority of the CNS
viral sequences of macaques 10F and 14F had none of the genetic markers
shown in a previous study to be associated with macrophage-tropic
variants and indeed retained a nucleotide sequence of similar to the
original lymphocyte-tropic virus used for inoculation despite almost 2
years of persistent infection in the animals. Construction of chimeric
viruses with V1-V5 regions of selected macaque 10F and macaque 14F
CNS-gp120 clones confirmed the predicted lymphocyte-tropic nature of
these env genes. In contrast, the gp120 sequences isolated from the CNS
tissue of one of the other three animals (macaque 13F) had a mutation
rate comparable to that observed for the lymph node clones. The CNS
clones from this animal had amino acid substitutions that were
previously shown to be associated with macrophage tropism. Compared to
the chimeric viruses constructed with V1-V5 sequences from macaques 10F
and 14F, viruses constructed with the V1-V5 sequences of several macaque
13F brain clones did not yield infectious virus.(ABSTRACT TRUNCATED AT
400 WORDS)
DE Amino Acid Sequence Amino Acids/ANALYSIS Animal Base Sequence
Brain/*VIROLOGY Cell Line Cloning, Molecular CD4-Positive
T-Lymphocytes/VIROLOGY DNA Primers Gene Products, gag/ANALYSIS
Genome, Viral Human HIV Envelope Protein gp120/ANALYSIS/CHEMISTRY
Lymph Nodes/PATHOLOGY/VIROLOGY Lymphocytes/*VIROLOGY Macaca mulatta
Macrophages/VIROLOGY Molecular Sequence Data Simian Acquired
Immunodeficiency Syndrome/PATHOLOGY/*VIROLOGY Spinal Cord/VIROLOGY
Support, U.S. Gov't, P.H.S. SIV/GENETICS/*PHYSIOLOGY Virus Latency
Virus Replication JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).