Enhanced cellular immune response and reduced CD8(+) lymphocyte apoptosis in acutely SIV-infected rhesus macaques after short-term antiretroviral treatment

Losing the decisive virus-specific functions of both CD4(+) and CD8(+) T ly mphocytes in the first weeks after immunodeficiency virus infection ultimat ely leads to AIDS. The SIV/rhesus monkey model for AIDS was used to demonst rate that a 4-week chemotherapeutic reduction of viral load during acute SI V infection of macaques allowed the development of a competent immune respo nse able to control virus replication after discontinuation of treatment in two of five monkeys. Increasing SIV-specific CD4(+) T-helper-cell prolifer ation was found in all macaques several weeks after treatment, independent of their viral toad. However, only macaques with low Viral loads showed per sistent T-cell reactivity of lymph node cells. In contrast to animals with higher viral loads, T-helper-cell counts and memory T-helper cells did not decline in the two macaques controlling viral replication. Lymphocyte apopt osis was consistently low in all treated macaques. In contrast, high CD8(+) lymphocyte death but only slightly increased CD4(+) lymphocyte apoptosis w ere observed during the first weeks after infection in untreated control an imals, indicating that early apoptotic death of virus-specific CTL could be an important factor for disease development. Antiretroviral treatment earl y after infection obviously retained virus-specific and competent T lymphoc ytes, whereby a virus-specific immune response could develop in two animals able to control the Viral replication after cessation of treatment, (C) 20 01 Academic Press.