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Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response
Author(s) -
Boyer Jean D.,
Kumar Sanjeev,
Robinson Tara,
Parkinson Rose,
Wu Ling,
Lewis Mark,
Watkins David I.,
Weiner David B.
Publication year - 2006
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1111/j.1600-0684.2006.00179.x
Subject(s) - viral load , immune system , immunology , simian immunodeficiency virus , major histocompatibility complex , viral replication , virology , biology , rhesus macaque , viremia , lentivirus , mhc class i , disease , macaque , virus , viral disease , medicine , paleontology , pathology
In the present era of increasing resistance of human immunodeficiency virus (HIV) to antiviral drugs, exploration of adjunct therapies directed at immune responses in combination with antiretroviral drugs may be of value for the treatment of acquired immunodeficiency syndrome. In this study, we designed a model for immune therapy using SIVmac251 infection in rhesus macaques. We explored the outcomes of primary infection on viral loads and the resulting T‐cell immune responses in primates. The SIV‐infected rhesus macaque model exhibited features similar to those observed in HIV‐1 infection of humans. Major histocompatibility complex (MHC) segregation with viral loads were found to associate with viral containment and hence the duration of the disease‐free latency period. Thus a better understanding of the relative roles of MHC class I allele in control of viral replication may provide important information for prophylactic or therapeutic vaccine designs. Mamu‐A01 is significantly associated with higher immune response and control of viral replication. This allele is frequent in rhesus macaques of Indian origin (22%). Interestingly, Mamu‐B01 (26% animals) was associated with lower immune responses and higher viral loads. Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. The results are important for understanding SIV disease progression in different MHC Mamu alleles and also for improving the interpretation and quality of pre‐clinical studies in rhesus monkeys.