Your browser version may not work well with NCBI's Web applications. More information here...
1: Cell. 2003 Jun 13;113(6):803-9.Click here to read Links
Erratum in:
Cell. 2004 Feb 20;116(4):629.

DNA deamination mediates innate immunity to retroviral infection.

Harris RS, Bishop KN, Sheehy AM, Craig HM, Petersen-Mahrt SK, Watt IN, Neuberger MS, Malim MH.

Medical Research Council Laboratory of Molecular Biology, Hills Road, CB2 2QH, Cambridge, United Kingdom. rharris@mrc-lmb.cam.ac.uk

CEM15/APOBEC3G is a cellular protein required for resistance to infection by virion infectivity factor (Vif)-deficient human immunodeficiency virus (HIV). Here, using a murine leukemia virus (MLV)-based system, we provide evidence that CEM15/APOBEC3G is a DNA deaminase that is incorporated into virions during viral production and subsequently triggers massive deamination of deoxycytidine to deoxyuridine within the retroviral minus (first)-strand cDNA, thus providing a probable trigger for viral destruction. Furthermore, HIV Vif can protect MLV from this CEM15/APOBEC3G-dependent restriction. These findings imply that targeted DNA deamination is a major strategy of innate immunity to retroviruses and likely also contributes to the sequence variation observed in many viruses (including HIV).

PMID: 12809610 [PubMed - indexed for MEDLINE]