Differential Sensitivity of “Old” versus “New” APOBEC3G to Human Immunodeficiency Virus Type 1 Vif
Author:
Affiliation:
1. Laboratory of Molecular Microbiology, Viral Biochemistry Section, National Institute of Allergy and Infectious Diseases, NIH, Building 4, Room 310, 4 Center Drive, MSC 0460, Bethesda, Maryland 20892-0460
Abstract
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Link
https://journals.asm.org/doi/pdf/10.1128/JVI.01734-08
Reference27 articles.
1. Chiu, Y. L., V. B. Soros, J. F. Kreisberg, K. Stopak, W. Yonemoto, and W. C. Greene. 2005. Cellular APOBEC3G restricts HIV-1 infection in resting CD4+ T cells. Nature435:108-114.
2. Conticello, S. G., R. S. Harris, and M. S. Neuberger. 2003. The Vif protein of HIV triggers degradation of the human antiretroviral DNA deaminase APOBEC3G. Curr. Biol.13:2009-2013.
3. Goila-Gaur, R., M. Khan, E. Miyagi, S. Kao, S. Opi, H. Takeuchi, and K. Strebel. 2008. HIV-1 Vif promotes the formation of high molecular mass APOBEC3G complexes. Virology372:136-146.
4. Harris, R. S., K. N. Bishop, A. M. Sheehy, H. M. Craig, S. K. Petersen-Mahrt, I. N. Watt, M. S. Neuberger, and M. H. Malim. 2003. DNA deamination mediates innate immunity to retroviral infection. Cell113:803-809.
5. Kao, S., R. Goila-Gaur, E. Miyagi, M. A. Khan, S. Opi, H. Takeuchi, and K. Strebel. 2007. Production of infectious virus and degradation of APOBEC3G are separable functional properties of human immunodeficiency virus type 1 Vif. Virology369:329-339.
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