Effects of 28 day treatment with azidothymidine (AZT) initiated 1 to 72 hours after infection with simian immunodeficiency virus (SIV). NLM AIDSLINE Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.

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Effects of 28 day treatment with azidothymidine (AZT) initiated 1 to 72 hours after infection with simian immunodeficiency virus (SIV).

Symp Nonhum Primate Models AIDS. 1990 Nov 28-30;8:56 (abstract no. 40). Unique Identifier : AIDSLINE PRIM8/900040
Martin LN; Murphey-Corb M; Soike KF; Davison-Fairburn B; Delta Regional Primate Research Center, Tulane University,; Covington, LA, U.S.A.


Abstract: We have studied the effects of AZT treatment initiated 1, 8, 24 or 72 hr. postinfection (PI) with 10 ID-50 SIV/Delta B670 using 5 monkeys per group. After initiation, the animals were treated every 6 hr. with 25 mg/kg (100 mg/kg/day) for 28 days. AZT treatment resulted in decreased hematocrit compared to untreated infected monkeys (controls) with recovery by 15 days after treatment ceased. Treatment begun as early as 1 hr. PI did not prevent infection. Treatment initiated 1 or 8 hr. PI reduced several indicators of disease progress compared to controls or to monkeys in which treatment was delayed for 24 or 72 hr. including reduced mean antigenemia levels, reduced peak levels of antigenemia attained, reduced duration of antigenemia, reduced titers of infectious SIV in serum, and delayed SIV-induced selective decreases in CD4+CD29+ helper-inducer cells. One animal in each of the 1 and 8 hr. treatment initiation groups had no detectable antigenemia in contrast to the other groups. Clinical signs were much less frequently observed when treatment was initiated 1 to 8 hr. PI. Delaying treatment for 24 to 72 hr. decreased the effectiveness. The 24 and 72 hr. groups did not display the decreases in antigenemia, the delay in depletion of CD4+CD29+ cells, nor the decreased clinical signs observed in the 1 or 8 hr. treatment initiation groups. However, treatment initiated at 24 or 72 hr. did prevent the development of persistent antigenemia observed in 2 of the 5 controls. After the 28 days of treatment ended, the time of recurrence of antigenemia depended on the time treatment had been initiated. Antigenemia recurred earliest in the untreated controls, followed in sequence by the 72, 24, 8 and 1 hr. treatment initiation groups. These results indicate that antiviral intervention with viral replication and dissemination in the first hours after infection is important for delaying disease progress.
Keywords: Animal Antigens, Viral/IMMUNOLOGY CD4-Positive T-Lymphocytes/IMMUNOLOGY/MICROBIOLOGY Haplorhini Leukocyte Count Recurrence Simian Acquired Immunodeficiency Syndrome/EPIDEMIOLOGY SIV/*DRUG EFFECTS/GROWTH & DEVELOPMENT/IMMUNOLOGY T-Lymphocytes, Suppressor-Effector/IMMUNOLOGY/MICROBIOLOGY Virus Replication Zidovudine/*THERAPEUTIC USE ABSTRACTKWDanimalantigens,viral/immunologycd4-positivet-lymphocytes/immunology/microbiologyhaplorhinileukocytecountrecurrencesimianacquiredimmunodeficiencysyndrome/epidemiologysiv/KWDdrugeffects/growth&development/immunologyt-lymphocytes,suppressor-effector/immunology/microbiologyvirusreplicationzidovudine/KWDtherapeuticuseabstract
910730
M9170954

Copyright © 1991 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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