期刊
JOURNAL OF VIROLOGY
卷 79, 期 3, 页码 1975-1980出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.3.1975-1980.2005
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资金
- NCRR NIH HHS [M01 RR000052, M01-RR00052] Funding Source: Medline
- NIAID NIH HHS [R01 AI043222, R37 AI051178, R01 AI051178, AI43222, AI51178] Funding Source: Medline
In vitro studies have shown that the host cytidine deaminase APOBEC3G causes lethal hypermutation in human immunodeficiency virus type 1 reverse transcripts unless its incorporation into virions is blocked by Vif. By examining stably archived sequences in resting CD4(+) T cells, we show that hypermutation occurs in most if not all infected individuals. Hypermutated sequences comprised >9% of archived species in resting CD4(+) T cells but were not found in plasma virus. Mutations occurred in predicted contexts, with notable hotspots. Thus, defects in Vif function in vivo give rise to hypermutated viral genomes that can be integrated but do not produce progeny viruses.
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