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Journal of Virology, May 2007, p. 5325-5330, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.02625-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Direct Evidence of Lower Viral Replication Rates In Vivo in Human Immunodeficiency Virus Type 2 (HIV-2) Infection than in HIV-1 Infection{triangledown}

Adam MacNeil,1 Abdoulaye Dieng Sarr,1 Jean-Louis Sankalé,1 Seema Thakore Meloni,1 Souleymane Mboup,2 and Phyllis Kanki1*

Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts,1 Laboratoire de Bacteriologie et Virologie, Universite Cheikh Anta Diop, Dakar, Senegal2

Received 28 November 2006/ Accepted 20 February 2007

Studies have shown that human immunodeficiency virus type 2 (HIV-2) is less pathogenic than HIV-1, with a lower rate of disease progression. Similarly, plasma viral loads are lower in HIV-2 infection, suggesting that HIV-2 replication is restricted in vivo in comparison to that of HIV-1. However, to date, in vivo studies characterizing replication intermediates in the viral life cycle of HIV-2 have been limited. In order to test the hypothesis that HIV-2 has a lower replication rate in vivo than HIV-1 does, we quantified total viral DNA, integrated proviral DNA, cell-associated viral mRNA, and plasma viral loads in peripheral blood samples from groups of therapy-naïve HIV-1-infected (n = 21) and HIV-2-infected (n = 18) individuals from Dakar, Senegal, with CD4+ T-cell counts of >200/µl. Consistent with our previous findings, total viral DNA loads were similar between HIV-1 and HIV-2 and plasma viral loads were higher among HIV-1-infected individuals. Proportions of DNA in the integrated form were also similar between these viruses. In contrast, levels of viral mRNA were lower in HIV-2 infection. Our study indicates that HIV-2 is able to establish a stable, integrated proviral infection in vivo, but that accumulation of viral mRNA is attenuated in HIV-2 infection relative to that in HIV-1 infection. The differences in viral mRNA are consistent with the differences in plasma viral loads between HIV-1 and HIV-2 and suggest that lower plasma viral loads, and possibly the attenuated pathogenesis of HIV-2, can be explained by lower rates of viral replication in vivo.


* Corresponding author. Mailing address: Department of Immunology and Infectious Diseases, Harvard School of Public Health, 651 Huntington Ave., Boston, MA 02115. Phone: (617) 432-1267. Fax: (617) 432-3575. E-mail: pkanki{at}hsph.harvard.edu

{triangledown} Published ahead of print on 28 February 2007.


Journal of Virology, May 2007, p. 5325-5330, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.02625-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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