{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T07:34:58Z","timestamp":1761982498817,"version":"build-2065373602"},"reference-count":100,"publisher":"American Society for Microbiology","issue":"21","license":[{"start":{"date-parts":[[2014,11,1]],"date-time":"2014-11-01T00:00:00Z","timestamp":1414800000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2014,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Members of the apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like-3 (APOBEC3) innate cellular cytidine deaminase family, particularly APOBEC3F and APOBEC3G, can cause extensive and lethal G-to-A mutations in HIV-1 plus-strand DNA (termed hypermutation). It is unclear if APOBEC3-induced mutations\n            <jats:italic>in vivo<\/jats:italic>\n            are always lethal or can occur at sublethal levels that increase HIV-1 diversification and viral adaptation to the host. The viral accessory protein Vif counteracts APOBEC3 activity by binding to APOBEC3 and promoting proteasome degradation; however, the efficiency of this interaction varies, since a range of hypermutation frequencies are observed in HIV-1 patient DNA. Therefore, we examined \u201cfootprints\u201d of APOBEC3G and APOBEC3F activity in longitudinal HIV-1 RNA\n            <jats:italic>pol<\/jats:italic>\n            sequences from approximately 3,000 chronically infected patients by determining whether G-to-A mutations occurred in motifs that were favored or disfavored by these deaminases. G-to-A mutations were more frequent in APOBEC3G-disfavored than in APOBEC3G-favored contexts. In contrast, mutations in APOBEC3F-disfavored contexts were relatively rare, whereas mutations in contexts favoring APOBEC3F (and possibly other deaminases) occurred 16% more often than average G-to-A mutations. These results were supported by analyses of &gt;500 HIV-1\n            <jats:italic>env<\/jats:italic>\n            sequences from acute\/early infection.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Collectively, our results suggest that APOBEC3G-induced mutagenesis is lethal to HIV-1, whereas mutagenesis caused by APOBEC3F and\/or other deaminases may result in sublethal mutations that might facilitate viral diversification. Therefore, Vif-specific cytotoxic T lymphocyte (CTL) responses and drugs that manipulate the interplay between Vif and APOBEC3 may have beneficial or detrimental clinical effects depending on how they affect the binding of Vif to various members of the APOBEC3 family.\n          <\/jats:p>","DOI":"10.1128\/jvi.01460-14","type":"journal-article","created":{"date-parts":[[2014,8,28]],"date-time":"2014-08-28T01:28:45Z","timestamp":1409189325000},"page":"12882-12894","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["Possible Footprints of APOBEC3F and\/or Other APOBEC3 Deaminases, but Not APOBEC3G, on HIV-1 from Patients with Acute\/Early and Chronic Infections"],"prefix":"10.1128","volume":"88","author":[{"given":"Andrew E.","family":"Armitage","sequence":"first","affiliation":[{"name":"MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford, United Kingdom"}]},{"given":"Koen","family":"Deforche","sequence":"additional","affiliation":[{"name":"KU Leuven-University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium"}]},{"given":"John J.","family":"Welch","sequence":"additional","affiliation":[{"name":"Department of Genetics, University of Cambridge, Cambridge, United Kingdom"}]},{"given":"Kristel","family":"Van Laethem","sequence":"additional","affiliation":[{"name":"KU Leuven-University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium"}]},{"given":"Ricardo","family":"Camacho","sequence":"additional","affiliation":[{"name":"KU Leuven-University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium"},{"name":"Centro de Mal\u00e1ria e outras Doen\u00e7as Tropicais, Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, Lisbon, Portugal"}]},{"given":"Andrew","family":"Rambaut","sequence":"additional","affiliation":[{"name":"Institute of Evolutionary Biology. 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