Virus Subtype-Specific Features of Natural Simian Immunodeficiency Virus SIV smm Infection in Sooty Mangabeys

Author:

Apetrei Cristian12,Gautam Rajeev1,Sumpter Beth3,Carter Anders C.1,Gaufin Thaidra1,Staprans Silvija I.3,Else James3,Barnes Mary1,Cao Robert1,Garg Seema3,Milush Jeffrey M.4,Sodora Donald L.4,Pandrea Ivona56,Silvestri Guido37

Affiliation:

1. Divisions of Microbiology

2. Department of Tropical Medicine of the School of Public Health

3. Emory Vaccine Center and Yerkes National Research Primate Center, Emory University, Atlanta, Georgia

4. University of Texas Southwestern Medical Center, Dallas, Texas

5. Comparative Pathology, Tulane National Primate Research Center, Covington, Louisiana 70433

6. Department of Pathology, School of Medicine, Tulane University, New Orleans, Louisiana 70112

7. Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19107

Abstract

ABSTRACT Simian immunodeficiency virus (SIV) SIV smm naturally infects sooty mangabeys (SMs) and is the source virus of pathogenic infections with human immunodeficiency virus type 2 (HIV-2) and SIV mac of humans and macaques, respectively. In previous studies we characterized SIV smm diversity in naturally SIV-infected SMs and identified nine different phylogenetic subtypes whose genetic distances are similar to those reported for the different HIV-1 group M subtypes. Here we report that, within the colony of SMs housed at the Yerkes National Primate Research Center, at least four SIV smm subtypes cocirculate, with the vast majority of animals infected with SIV smm subtype 1, 2, or 3, resulting in the emergence of occasional recombinant forms. While SIV smm -infected SMs show a typically nonpathogenic course of infection, we have observed that different SIV smm subtypes are in fact associated with specific immunologic features. Notably, while subtypes 1, 2, and 3 are associated with a very benign course of infection and preservation of normal CD4 + T-cell counts, three out of four SMs infected with subtype 5 show a significant depletion of CD4 + T cells. The fact that virus replication in SMs infected with subtype 5 is similar to that in SMs infected with other SIV smm subtypes suggests that the subtype 5-associated CD4 + T-cell depletion is unlikely to simply reflect higher levels of virus-mediated direct killing of CD4 + T-cells. Taken together, this systematic analysis of the subtype-specific features of SIV smm infection in natural SM hosts identifies subtype-specific differences in the pathogenicity of SIV smm infection.

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

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