The Journal of Experimental Medicine
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Published online 10 April 2006 doi:10.1084/jem.20051856
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 4, 865-870
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BRIEF DEFINITIVE REPORT

 Endogenous factors enhance HIV infection of tissue naive CD4 T cells by stimulating high molecular mass APOBEC3G complex formation

Jason F. Kreisberg1,2, Wes Yonemoto1, and Warner C. Greene1,2,3

1 Gladstone Institute of Virology and Immunology, 2 Department of Microbiology and Immunology, and 3 Department of Medicine, University of California, San Francisco, San Francisco, CA 94158

CORRESPONDENCE Warner C. Greene: wgreene{at}gladstone.ucsf.edu

Human immunodeficiency virus (HIV) can infect resting CD4 T cells residing in lymphoid tissues but not those circulating in peripheral blood. The molecular mechanisms producing this difference remain unknown. We explored the potential role of the tissue microenvironment and its influence on the action of the antiviral factor APOBEC3G (A3G) in regulating permissivity to HIV infection. We found that endogenous IL-2 and -15 play a key role in rendering resident naive CD4 T cells susceptible to HIV infection. Infection of memory CD4 T cells also requires endogenous soluble factors, but not IL-2 or -15. A3G is found in a high molecular mass complex in HIV infection–permissive, tissue-resident naive CD4 T cells but resides in a low molecular mass form in nonpermissive, blood-derived naive CD4 T cells. Upon treatment with endogenous soluble factors, these cells become permissive for HIV infection, as low molecular mass A3G is induced to assemble into high molecular mass complexes. These findings suggest that in lymphoid tissues, endogenous soluble factors, likely including IL-2 and -15 and others, stimulate the formation of high molecular mass A3G complexes in tissue-resident naive CD4 T cells, thereby relieving the potent postentry restriction block for HIV infection conferred by low molecular mass A3G.


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