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Journal of Virology, September 2008, p. 8619-8628, Vol. 82, No. 17
0022-538X/08/$08.00+0     doi:10.1128/JVI.00027-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Higher Homologous and Lower Cross-Reactive Gag-Specific T-Cell Responses in Human Immunodeficiency Virus Type 2 (HIV-2) Than in HIV-1 Infection{triangledown}

Wim Jennes,1* Makhtar Camara,2 Tandakha Dièye,2 Souleymane Mboup,2 and Luc Kestens1

Laboratory of Immunology, Department of Microbiology, Institute of Tropical Medicine, Antwerp, Belgium,1 Laboratory of Immunology, Centre Hospitalier Universitaire Le Dantec, Cheikh Anta Diop University, Dakar, Senegal2

Received 4 January 2008/ Accepted 9 June 2008

Human immunodeficiency virus type 2 (HIV-2) infection results in slower CD4+ T-cell decline, lower plasma viral load levels, and hence slower progression of the disease than does HIV-1 infection. Although the reasons for this are not clear, it is possible that HIV-2 replication is more effectively controlled by host responses. We used aligned pools of overlapping HIV-1 and HIV-2 Gag peptides in an enhanced gamma interferon enzyme-linked immunospot assay to compare the levels of homologous and cross-reactive Gag-specific T-cell responses between HIV-1- and HIV-2-infected patients. HIV-2-infected patients showed broader and stronger homologous Gag-specific T-cell responses than HIV-1-infected patients. In contrast, the cross-reactive T-cell responses in HIV-2-infected patients were both narrower and weaker than those in HIV-1-infected patients, in line with overall weaker correlations between homologous and heterologous T-cell responses among HIV-2-infected patients than among HIV-1-infected patients. Cross-reactive responses in HIV-2-infected patients tended to correlate directly with HIV-1/HIV-2 Gag sequence similarities; this was not found in HIV-1-infected patients. The CD4+ T-cell counts of HIV-2-infected patients correlated directly with homologous responses and inversely with cross-reactive responses; this was not found in HIV-1-infected patients. Our data support a model whereby high-level HIV-2-specific T-cell responses control the replication of HIV-2, thus limiting viral diversification and priming of HIV-1 cross-reactive T-cell responses over time. However, we cannot exclude the possibility that HIV-2 replication is controlled by other host factors and that HIV-2-specific T-cell responses are better maintained in the context of slow viral divergence and a less damaged immune system. Understanding the nature of immune control of HIV-2 infection could be crucial for HIV vaccine design.

* Corresponding author. Mailing address: Laboratory of Immunology, Department of Microbiology, Institute of Tropical Medicine, Nationalestraat 155, 2000 Antwerp, Belgium. Phone: 32 3 247 62 27. Fax: 32 3 247 62 31. E-mail: wjennes{at}itg.be

{triangledown} Published ahead of print on 18 June 2008.

Journal of Virology, September 2008, p. 8619-8628, Vol. 82, No. 17
0022-538X/08/$08.00+0     doi:10.1128/JVI.00027-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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