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Article

APOBEC3G-induced hypermutation of human immunodeficiency virus type-1 is typically a discrete "all or nothing" phenomenon.

PLoS genetics - 1 Jan 2012

Armitage Andrew E, Deforche Koen, Chang Chih-Hao, Wee Edmund, Kramer Beatrice, Welch John J, Gerstoft Jan, Fugger Lars, McMichael Andrew, Rambaut Andrew, Iversen Astrid K N

Abstract excerpt

The rapid evolution of Human Immunodeficiency Virus (HIV-1) allows studies of ongoing host-pathogen interactions. One key selective host factor is APOBEC3G (hA3G) that can cause extensive and inactivating Guanosine-to-Adenosine (G-to-A) mutation on HIV plus-strand DNA (termed hypermutation). HIV can inhibit this innate anti-viral defense through binding of the viral protein Vif to hA3G, but binding efficiency...

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Identifiers

PMID: 22457633
DOI: 10.1371/journal.pgen.1002550
PMCID: PMC3310730

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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APOBEC3G-induced hypermutation of human immunodeficiency virus type-1 is typically a discrete "all or nothing" phenomenon.PMID 22457633Read ↗

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