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M94A0721.TXT
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1994-10-21
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Document 0721
DOCN M94A0721
TI Antiretroviral therapy of HIV: a virologists perspective.
DT 9412
AU Corey L; University of Washington, Seattle.
SO Annu Conf Australas Soc HIV Med. 1993 Oct 28-30;5:19 (abstract no.
TPI-4). Unique Identifier : AIDSLINE ASHM5/94348934
AB While the availability of nucleoside reverse transcriptase (RT)
inhibitors have revolutionised care of HIV infected persons, controversy
exists about the overall utility of these medications. When should
therapy be initiated? With what agent? When should alternative therapy
be utilised, what alternative should be given and when should
antiretrovirals be stopped? Much of this controversy exists (in this
persons opinion) because the expectations and questions asked in often
quoted studies have differed. RT inhibitors differ from most other
antimicrobials in that they inhibit the frequency of newly infected
cells, and do not inhibit production from persistently infected cells.
Moreover, they are all prodrugs with the active triphosphate derivative
requiring intracellular metabolism. For AZT and D4T this is dependent
upon cell cycle activation. As such, in vivo inhibition of HIV is only
partial. All clinical trials of RT inhibitors have stratified patients
by CD4 cell count. However, a variety of virologic assays indicate that
viral load whether measured in plasma or PBMCs may differ by as much as
4 logs among persons with similar CD4 cell counts. In addition, RT
inhibitors alone inhibit replication by about 1/2 log and in combination
by 1-1.5 log. As such, the varied effects of these compounds in large
scale trials is not unexpected. It appears that whether one uses
monotherapy, combination therapy or sequential therapy, the duration of
effectiveness is greatest the earlier one initiates therapy. In
addition, adding or switching to alternative therapy after AZT appears
to be most effective when CD4 counts are > 150 cells/mm3. In AZT treated
patients, the effectiveness of any of these current nucleosides (ddl or
ddC) in those with < 100 CD4 cells is unclear. In these patients
prophylaxis of opportunistic infections should be optimised. The data
leading to the above observations will be discussed.
DE Antiviral Agents/*THERAPEUTIC USE Drug Therapy, Combination Human HIV
Infections/*DRUG THERAPY Leukocyte Count/DRUG EFFECTS
Prodrugs/THERAPEUTIC USE Reverse Transcriptase/*ANTAGONISTS & INHIB T4
Lymphocytes/DRUG EFFECTS Virus Replication/DRUG EFFECTS
Zidovudine/THERAPEUTIC USE MEETING ABSTRACT
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).