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Journal of Virology, January 2006, p. 634-642, Vol. 80, No. 2
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.2.634-642.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Perturbations of Cell Cycle Control in T Cells Contribute to the Different Outcomes of Simian Immunodeficiency Virus Infection in Rhesus Macaques and Sooty Mangabeys

M. Paiardini,1,2*,{dagger} B. Cervasi,1,2,{dagger} B. Sumpter,1 H. M. McClure,3 D. L. Sodora,4 M. Magnani,2 S. I. Staprans,1,5 G. Piedimonte,6 and G. Silvestri1,3

Division of Infectious Diseases and Emory Vaccine Center, Emory University, Atlanta, Georgia,1 Department of Biochemistry, University of Urbino, Urbino, Italy,2 Yerkes National Primate Research Center, Atlanta, Georgia,3 Division of Infectious Diseases, University of Texas Southwestern, Dallas, Texas,4 Department of Microbiology and Immunology, Emory University, Atlanta, Georgia,5 Department of Public Health, University of Messina, Messina, Italy6

Received 1 August 2005/ Accepted 25 October 2005

In contrast to human immunodeficiency virus (HIV) infection of humans and experimental simian immunodeficiency virus (SIV) infection of rhesus macaques (RMs), SIV infection of sooty mangabeys (SMs), a natural host African monkey species, is typically nonpathogenic and associated with preservation of CD4+ T-cell counts despite chronic high levels of viral replication. In previous studies, we have shown that the lack of SIV disease progression in SMs is related to lower levels of immune activation and bystander T-cell apoptosis compared to those of pathogenic HIV/SIV infection (G. Silvestri, D. Sodora, R. Koup, M. Paiardini, S. O’Neil, H. M. McClure, S. I. Staprans, and M. B. Feinberg, Immunity 18:441-452, 2003; G. Silvestri, A. Fedanov, S. Germon, N. Kozyr, W. J. Kaiser, D. A. Garber, H. M. McClure, M. B. Feinberg, and S. I. Staprans, J. Virol. 79:4043-4054, 2005). In HIV-infected patients, increased T-cell susceptibility to apoptosis is associated with a complex cell cycle dysregulation (CCD) that involves increased activation of the cyclin B/p34-cdc2 complex and abnormal nucleolar structure with dysregulation of nucleolin turnover. Here we report that CCD is also present during pathogenic SIV infection of RMs, and its extent correlates with the level of immune activation and T-cell apoptosis. In marked contrast, naturally SIV-infected SMs show normal regulation of cell cycle control (i.e., normal intracellular levels of cyclin B and preserved nucleolin turnover) and a low propensity to apoptosis in both peripheral blood- and lymph node-derived T cells. The absence of significant CCD in the AIDS-free, non-immune-activated SMs despite high levels of viral replication indicates that CCD is a marker of disease progression during lentiviral infection and supports the hypothesis that the preservation of cell cycle control may help to confer the disease-resistant phenotype of SIV-infected SMs.

* Corresponding author. Mailing address: Division of Infectious Diseases and Emory Vaccine Center, Emory University, 954 Gatewood Rd. NE, Atlanta, GA 30329. Phone: (404) 712-8113. Fax: (404) 727-8199. E-mail: gsilves{at}rmy.emory.edu.

{dagger} These authors contributed equally to this work.

Journal of Virology, January 2006, p. 634-642, Vol. 80, No. 2
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.2.634-642.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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