{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T17:01:42Z","timestamp":1791219702727,"version":"4.1.0"},"reference-count":61,"publisher":"American Society for Microbiology","issue":"18","license":[{"start":{"date-parts":[[2010,9,15]],"date-time":"2010-09-15T00:00:00Z","timestamp":1284508800000},"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":[[2010,9,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Genomic hypermutation of RNA viruses, including human immunodeficiency virus type 1 (HIV-1), can be provoked by intrinsic and extrinsic pressures, which lead to the inhibition of viral replication and\/or the progression of viral diversity. Human APOBEC3G was identified as an HIV-1 restriction factor, which edits nascent HIV-1 DNA by inducing G-to-A hypermutations and debilitates the infectivity of\n            <jats:italic>vif<\/jats:italic>\n            -deficient HIV-1. On the other hand, HIV-1 Vif protein has the robust potential to degrade APOBEC3G protein. Although subsequent investigations have revealed that lines of APOBEC3 family proteins have the capacity to mutate HIV-1 DNA, it remains unclear whether these endogenous APOBEC3s, including APOBEC3G, contribute to mutations of\n            <jats:italic>vif<\/jats:italic>\n            -proficient HIV-1 provirus\n            <jats:italic>in vivo<\/jats:italic>\n            and, if so, what is the significance of these mutations. In this study, we use a human hematopoietic stem cell-transplanted humanized mouse (NOG-hCD34 mouse) model and demonstrate the predominant accumulation of G-to-A mutations in\n            <jats:italic>vif<\/jats:italic>\n            -proficient HIV-1 provirus displaying characteristics of APOBEC3-mediated mutagenesis. Notably, the APOBEC3-associated G-to-A mutation of HIV-1 DNA that leads to the termination of translation was significantly observed. We further provide a novel insight suggesting that HIV-1 G-to-A hypermutation is independently induced by individual APOBEC3 proteins. In contrast to the prominent mutation in intracellular proviral DNA, viral RNA in plasma possessed fewer G-to-A mutations. Taken together, these results provide the evidence indicating that endogenous APOBEC3s are associated with G-to-A mutation of HIV-1 provirus\n            <jats:italic>in vivo<\/jats:italic>\n            , which can result in the abrogation of HIV-1 infection.\n          <\/jats:p>","DOI":"10.1128\/jvi.00823-10","type":"journal-article","created":{"date-parts":[[2010,7,8]],"date-time":"2010-07-08T03:10:42Z","timestamp":1278558642000},"page":"9546-9556","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":74,"title":["Remarkable Lethal G-to-A Mutations in\n            <i>vif-<\/i>\n            Proficient HIV-1 Provirus by Individual APOBEC3 Proteins in Humanized Mice"],"prefix":"10.1128","volume":"84","author":[{"given":"Kei","family":"Sato","sequence":"first","affiliation":[{"name":"Laboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, Kyoto 606-8507, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taisuke","family":"Izumi","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, 54 Shogoinkawara-cho, Sakyo-ku, Kyoto, Kyoto 606-8507, Japan"},{"name":"Japanese Foundation for AIDS Prevention, 1-3-12 Misaki-cho, Chiyoda-ku, Tokyo 101-0061, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naoko","family":"Misawa","sequence":"additional","affiliation":[{"name":"Laboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, Kyoto 606-8507, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoko","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Laboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, Kyoto 606-8507, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshiki","family":"Yamashita","sequence":"additional","affiliation":[{"name":"Department of Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki, Osaka 569-8686, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masahide","family":"Ohmichi","sequence":"additional","affiliation":[{"name":"Department of Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki, Osaka 569-8686, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mamoru","family":"Ito","sequence":"additional","affiliation":[{"name":"Central Institute for Experimental Animals, 1430 Nogawa, Miyamae-ku, Kawasaki, Kanagawa 216-0001, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akifumi","family":"Takaori-Kondo","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, 54 Shogoinkawara-cho, Sakyo-ku, Kyoto, Kyoto 606-8507, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshio","family":"Koyanagi","sequence":"additional","affiliation":[{"name":"Laboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, Kyoto 606-8507, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1017\/S1462399409001343"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2004.06.057"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/nsmb0509-454"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.26.021607.090350"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.80.3.1067-1076.2006"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.01123-06"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2005.06.005"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/20.18.4933"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1089\/aid.1993.9.833"},{"key":"e_1_3_2_11_2","first-page":"1971","volume":"2","year":"2001","unstructured":"Freed, E. 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