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Journal of Virology, March 2009, p. 2686-2696, Vol. 83, No. 6
0022-538X/09/$08.00+0     doi:10.1128/JVI.02237-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Partial Protection of Simian Immunodeficiency Virus (SIV)-Infected Rhesus Monkeys against Superinfection with a Heterologous SIV Isolate{triangledown}

Wendy W. Yeh,1 Pimkwan Jaru-ampornpan,1 Daiva Nevidomskyte,1 Mohammed Asmal,1 Srinivas S. Rao,2 Adam P. Buzby,1 David C. Montefiori,3 Bette T. Korber,4,5 and Norman L. Letvin1*

Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215,1 Vaccine Research Center, National Institutes of Health, Bethesda, Maryland 20892,2 Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710,3 Los Alamos National Laboratory, Los Alamos, New Mexico 87545,4 Santa Fe Institute, Santa Fe, New Mexico 8750155

Received 23 October 2008/ Accepted 23 December 2008

Although there is increasing evidence that individuals already infected with human immunodeficiency virus type 1 (HIV-1) can be infected with a heterologous strain of the virus, the extent of protection against superinfection conferred by the first infection and the biologic consequences of superinfection are not well understood. We explored these questions in the simian immunodeficiency virus (SIV)/rhesus monkey model of HIV-1/AIDS. We infected cohorts of rhesus monkeys with either SIVmac251 or SIVsmE660 and then exposed animals to the reciprocal virus through intrarectal inoculations. Employing a quantitative real-time PCR assay, we determined the replication kinetics of the two strains of virus for 20 weeks. We found that primary infection with a replication-competent virus did not protect against acquisition of infection by a heterologous virus but did confer relative control of the superinfecting virus. In animals that became superinfected, there was a reduction in peak replication and rapid control of the second virus. The relative susceptibility to superinfection was not correlated with CD4+ T-cell count, CD4+ memory T-cell subsets, cytokine production by virus-specific CD8+ or CD4+ cells, or neutralizing antibodies at the time of exposure to the second virus. Although there were transient increases in viral loads of the primary virus and a modest decline in CD4+ T-cell counts after superinfection, there was no evidence of disease acceleration. These findings indicate that an immunodeficiency virus infection confers partial protection against a second immunodeficiency virus infection, but this protection may be mediated by mechanisms other than classical adaptive immune responses.

* Corresponding author. Mailing address: Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, CLS 1043, 3 Blackfan Circle, Boston, MA 02115. Phone: (617) 735-4400. Fax: (617) 735-4527. E-mail: nletvin{at}bidmc.harvard.edu

{triangledown} Published ahead of print on 7 January 2009.

Journal of Virology, March 2009, p. 2686-2696, Vol. 83, No. 6
0022-538X/09/$08.00+0     doi:10.1128/JVI.02237-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



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