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Naturally SIV‐infected sooty mangabeys: are we closer to understanding why they do not develop AIDS?
Author(s) -
Silvestri Guido
Publication year - 2005
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.1600-0684.2005.00122.x
Subject(s) - simian immunodeficiency virus , biology , virology , immunology , disease , adaptation (eye) , immunodeficiency , virus , host (biology) , immune system , human immunodeficiency virus (hiv) , genetics , medicine , neuroscience , pathology
Simian immunodeficiency viruses (SIV) infection of sooty mangabey (SM) monkeys ( Cercocebus atys ), a natural host species, does not induce CD4+ T cell depletion and acquired immunodeficiency syndrome (AIDS) despite chronic high levels of virus replication. In contrast, SIV infection of non‐natural host species, such as rhesus macaques (RM), induces a disease that closely resembles AIDS in humans. The mechanisms underlying the lack of disease progression in SIV‐infected SMs are incompletely understood, but certainly reflect a complex evolutionary adaptation whereby the host immune system is not significantly damaged by the highly replicating virus. It is now widely recognized that a better understanding of these mechanisms may provide clues to the pathogenesis of immunodeficiency in HIV‐infected humans. In this article I discuss five different hypotheses that may account for the non‐pathogenic course of infection in SIV‐infected SMs and briefly review the available data supporting each of these hypotheses.