Immunological and virological studies of natural SIV infection of disease-resistant nonhuman primates

摘要: Nonhuman primates naturally infected with simian immunodeficiency virus (SIV), while maintaining chronic viremia, do not develop any disease associated lentiviral infection. Thus they provide a unique model to define the mechanism(s) by which remain but disease-resistant. The purpose of this article is summarize our current knowledge virological and immunological studies that have been performed in sooty mangabeys SIVsmm disease-susceptible rhesus macaques experimentally SIVsmm. Data on demonstrate are predominantly SIV nef sequences distinct from those shown cause inappropriate host, factor may contribute resistance. Hyperimmunization variety antigens or infection contributes accelerated death if hyperimmunizations initiated at time infection, whereas similar hyperimmunization lead seropositive mangabeys. However, both species SIV, leads increased load, suggesting load per se cannot account for disease, least nonhuman primates. Immunological concerning changes subsets T cells, based cytokine profile (TH0/TH1/TH2), showed early post show dominant TH1 profile, rapidly TH0. On other hand, continuously TH2-like profile. Studies also high frequency vivo-activated cells peripheral blood SIV-infected Of interest, however, finding level ELISA seronegative Although fail levels apoptotic following incubation immobilized anti-CD3, PBMC varying intervals an increase seen CD8+ unrelated viremia. Sooty maintain regulate replication throughout their lifetime, develops prior ELISA-based seroconversion, only enough shortly regulatory function gradually lost cell loss death. HIV profound effects expression number costimulatory adhesion molecules. There appear be differences nature intracellular phosphorylated proteins activated We believe careful detailed mechanisms issues described above understanding constellation responsible disease-resistant state These findings can employed evaluating nonvirus sterilizing form SIV/HIV vaccines.