DNA deamination mediates innate immunity to retroviral infection

Reuben S. Harris, Kate N. Bishop, Ann M. Sheehy, Heather M. Craig, Svend K. Petersen-Mahrt, Ian N. Watt, Michael S. Neuberger, Michael H. Malim

Research output: Contribution to journalArticle

1065 Scopus citations

Abstract

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).

Original languageEnglish (US)
Pages (from-to)803-809
Number of pages7
JournalCell
Volume113
Issue number6
DOIs
StatePublished - Jun 13 2003

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    Harris, R. S., Bishop, K. N., Sheehy, A. M., Craig, H. M., Petersen-Mahrt, S. K., Watt, I. N., Neuberger, M. S., & Malim, M. H. (2003). DNA deamination mediates innate immunity to retroviral infection. Cell, 113(6), 803-809. https://doi.org/10.1016/S0092-8674(03)00423-9