Greene WK, Meers J, Chadwick B, Carnegie PR, Robinson WF (1993) Nucleotide sequences of Australian isolates of the feline immunodeficiency virus: comparison with other feline lentiviruses. N Engl J Med 324: 1062įazely F, Haseltine WA, Rodger RF, Ruprecht RM (1991) Postexposure chemoprophylaxis with ZDV or ZDV combined with interferon-alpha: failure after inoculating rhesus monkeys with a high dose of SIV. J Acquir Immune Defic Syndr 4: 766–769ĭurand E, Le Jeunne C, Hugues F-C (1991) Failure of prophylactic zidovudine after suicidal self-inoculation of HIV-infected blood. N Engl J Med 324: 961–964ĭonovan RM, Dickover RE, Goldstein E, Huth RG, Carlson JR (1991) HIV-1 proviral copy number in blood mononuclear cells from AIDS patients on zidovudine therapy. N Engl J Med 324: 954–960ĭaar ES, Moudgil T, Meyer RD, Ho DD (1991) Transient high levels of viremia in patients with primary human immunodeficiency virus type 1 infection. MMWR RR-1 39: 1–14Ĭlark SJ, Saag MS, Decker WD, Campbell-Hill S, Roberson JL, Veldkamp PJ, Kappes JC, Hahn BH, Shaw GM (1991) High titers of cytopathic virus in plasma of patients with symptomatic primary HIV-1 infection. J Infect Dis 165: 105–110Ĭenters for Disease Control (1990) Public health service statement on management of occupational exposure to human immunodeficiency virus, including considerations regarding zidovudine post-exposure use. N Engl J Med 326: 1385–1391īoucher CAB, O'Sullivan E, Mulder JW, Ramautarsing C, Kellam P, Darby G, Lange JMA, Goudsmit J, Larder BA (1992) Ordered appearance of zidovudine resistance mutations during treatment of 18 human immunodeficiency virus-positive subjects. We also suggest that the limitation of viral titers in PBMC may be of critical importance in the control of lentiviral infection.īagasra O, Hauptman SP, Lischner HW, Sachs M, Pomerantz RJ (1992) Detection of human immunodeficiency virus type 1 provirus in mononuclear cells by in situ polymerase chain reaction. This shows that for complete assessment of antiviral agents, both cell-free and cell-associated virus titers must be examined. In contrast, it appears that the immune response has little impact on PBMC virus titers. The decline in plasma virus titers in immunocompetent cats combined with the effect of cyclosporine on plasma titers strongly suggests that the immune system plays a major role in clearing FIV from plasma. In all groups (untreated, zidovudine and cyclosporine) the titers in PBMC were high for the duration of the experiment. Neither zidovudine or cyclosporine treatment significantly influenced the titer of FIV in PBMCs. In the untreated group, plasma virus titers declined rapidly to an undetectable level by 14 weeks p.i. the plasma virus titers in cyclosporine-treated cats were significantly higher than in the untreated group. Similarly, cyclosporine treatment initially lowered plasma virus titers at 2 weeks p.i., but at 4 weeks p.i. This reduction of plasma virus titer by zidovudine was not maintained at subsequent sampling times. Zidovudine treatment did not prevent establishment of infection with FIV, but plasma virus titers were significantly lower than controls at 2 weeks p.i. Treatments were begun 24 h post infection (p.i.) and continued for 4 weeks. The plasma and peripheral blood mononuclear cell (PBMC) titer of feline immunodeficiency virus (FIV) in experimentally infected cats was assessed following administration of either zidovudine or cyclosporine.
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