Cellular APOBEC3G restricts HIV-1 infection in resting CD4+ T cells

Ya-Lin Chiu, Vanessa B. Soros, Jason F. Kreisberg, Kim Stopak, Wes Yonemoto and Warner C. Greene ()
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Ya-Lin Chiu: Gladstone Institute of Virology and Immunology
Vanessa B. Soros: Gladstone Institute of Virology and Immunology
Jason F. Kreisberg: Gladstone Institute of Virology and Immunology
Kim Stopak: Gladstone Institute of Virology and Immunology
Wes Yonemoto: Gladstone Institute of Virology and Immunology
Warner C. Greene: Gladstone Institute of Virology and Immunology

Nature, 2005, vol. 435, issue 7038, 108-114

Abstract: Turning T cells against HIV Activated CD4 T cells are open to HIV attack, but HIV fails to infect resting cells. New work links this observation to the recently discovered cellular cytidine deaminase APOBEC3G (A3G), an innate antiretroviral that blocks the spread of HIV, if the virus lacks its Vif gene. A3G is now shown to exist in two forms — a large form that is ineffective in preventing cellular infection, and a shorter enzymatically active form that repels the virus. Activated T cells have the long form and are easily infected by HIV, but resting T cells carry the short form so are impervious to HIV infection. Blocking the small form of A3G in resting T cells suddenly makes them susceptible to HIV infection. The discovery suggests new strategies for preventing the spread of HIV infection, either by converting large A3G into the protective smaller form in activated CD4 T-cells, or by preventing the ‘small A3G’ from converting to the large form during T-cell activation.

Date: 2005
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DOI: 10.1038/nature03493

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