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• W2032202436 startingPage "147" @default.
• W2032202436 abstract "Virion infectivity factor (Vif) facilitates HIV infection by counteracting APOBEC3G late in replication in virus-producer cells. Here, we show that early after infection of new target cells Vif is part of the HIV reverse transcription machinery and acts as an accessory factor for reverse transcription. Vif protein was present in gradient fractions containing reverse transcription complexes (RTCs), and anti-Vif antibody immunoprecipitated HIV reverse transcription products from these gradient fractions. To investigate a role for Vif in RTCs independent of APOBEC3G, we created an intracellular environment that would restrict reverse transcription by pre-treating permissive target cells with 5-Fluoro 2-deoxyuridine, a thymidylate synthetase inhibitor, prior to infection with virus from permissive cells. Infectivity assays and quantitation of reverse transcription products demonstrated that replication of HIV lacking Vif was inhibited to a greater degree than wild type, without concurrent mutation of reverse transcription products, suggesting compromised reverse transcription in the absence of Vif." @default.
• W2032202436 created "2016-06-24" @default.
• W2032202436 creator A5041774185 @default.
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• W2032202436 date "2008-03-01" @default.
• W2032202436 modified "2023-09-23" @default.
• W2032202436 title "Human immunodeficiency virus 1 (HIV-1) virion infectivity factor (Vif) is part of reverse transcription complexes and acts as an accessory factor for reverse transcription" @default.
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• W2032202436 doi "https://doi.org/10.1016/j.virol.2007.10.041" @default.
• W2032202436 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18037155" @default.
• W2032202436 hasPublicationYear "2008" @default.
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