title: Enhanced cellular immune response and reduced CD8(+) lymphocyte apoptosis in acutely SIV-infected Rhesus macaques after short-term antiretroviral treatment.
abstract: Losing the decisive virus-specific functions of both CD4(+) and CD8(+) T lymphocytes in the first weeks after immunodeficiency virus infection ultimately leads to AIDS. The SIV/rhesus monkey model for AIDS was used to demonstrate that a 4-week chemotherapeutic reduction of viral load during acute SIV infection of macaques allowed the development of a competent immune response able to control virus replication after discontinuation of treatment in two of five monkeys. Increasing SIV-specific CD4(+) T-helper-cell proliferation was found in all macaques several weeks after treatment, independent of their viral load. However, only macaques with low viral loads showed persistent 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 apoptosis was consistently low in all treated macaques. In contrast, high CD8(+) lymphocyte death but only slightly increased CD4(+) lymphocyte apoptosis were observed during the first weeks after infection in untreated control animals, indicating that early apoptotic death of virus-specific CTL could be an important factor for disease development. Antiretroviral treatment early after infection obviously retained virus-specific and competent T lymphocytes, whereby a virus-specific immune response could develop in two animals able to control the viral replication after cessation of treatment.
authors.affiliation: Department of Virology and Immunology, German Primate Center, Göttingen, Germany. mispri@www.dpz/gwdg.de  
authors.forename: M
authors.initials: M
authors.lastname: Spring
authors.forename: C
authors.initials: C
authors.lastname: Stahl-Hennig
authors.forename: N
authors.initials: N
authors.lastname: Stolte
authors.forename: N
authors.initials: N
authors.lastname: Bischofberger
authors.forename: J
authors.initials: J
authors.lastname: Heeney
authors.lastname: ten Haaft P
authors.forename: K
authors.initials: K
authors.lastname: Tenner-Ràcz
authors.forename: P
authors.initials: P
authors.lastname: Ràcz
authors.forename: D
authors.initials: D
authors.lastname: Lorenzen
authors.forename: G
authors.initials: G
authors.lastname: Hunsmann
authors.forename: U
authors.initials: U
authors.lastname: Dittmer
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D000818:Animals; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D017209:Apoptosis; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology*; D004195:Disease Models, Animal; D006801:Humans; D007156:Immunologic Memory; D008253:Macaca mulatta; D063065:Organophosphonates; D009943:Organophosphorus Compounds / Q000627:therapeutic use*; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D016097:Simian Acquired Immunodeficiency Syndrome / Q000188:drug therapy* / Q000276:immunology*; D015302:Simian Immunodeficiency Virus / Q000502:physiology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D000068698:Tenofovir; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents; D063065:Organophosphonates; D009943:Organophosphorus Compounds; D018894:Reverse Transcriptase Inhibitors; D000068698:Tenofovir; D000225:Adenine