IMR Press / FBL / Volume 9 / Issue 1 / DOI: 10.2741/1123

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

The paradox of simian immunodeficiency virus infection in sooty mangabeys: active viral replication without disease progression
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1 Viral Immunology Unit, Pasteur Institute, 28 rue du Dr. Roux, 75724 Paris Cédex 15, France
Front. Biosci. (Landmark Ed) 2004, 9(1), 521–539;
Published: 1 January 2004

Simian immunodeficiency virus SIVsm causes an asymptomatic infection in its natural host, the sooty mangabey, but induces an immunodeficiency syndrome very similar to human AIDS when transferred to a new host species such as the rhesus macaque. Unexpectedly, SIVsm replication dynamics is comparable in the two species, with rapid accumulation of viral mutations and a high viral load detected in both mangabeys and macaques. In contrast, clear differences are observed in immune parameters. Pathogenic SIV infection in macaques is associated with decreased CD4+ T cell numbers and signs of generalized immune activation, such as increased numbers of cycling and apoptotic T cells, hyperplasic lymphoid tissues, and exacerbated immune responses. Mangabeys with asymptomatic SIV infection show normal T cell regeneration parameters and signs of a moderate immune response, appropriate in the setting of chronic viral infection. The comparative analysis of simian models thus suggests that viral load alone cannot account for progression to disease, and that the capacity of primate lentiviruses to induce abnormal immune activation underlies AIDS pathogenesis.

AIDS pathogenesis
simian immunodeficiency virus
sooty mangabey
Cercocebus torquatus atys
natural host
T lymphocyte regeneration
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