Abstract
A flurry of new papers has shown that HIV reverse transcription is vulnerable to G-->A hypermutation. Apparently, cytidine bases in nascent DNA synthesis are lethally edited by the host cell molecule apolipoprotein B editing complex protein (APOBEC) 3G. This death mechanism is circumvented by the HIV viral infectivity factor protein, which prevents APOBEC3G from entering the virion.
MeSH terms
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APOBEC-3G Deaminase
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Base Sequence
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Cytidine Deaminase
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Gene Products, vif / genetics
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Gene Products, vif / physiology
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HIV / genetics
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Hepatitis B virus / genetics
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Humans
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Mutagenesis / genetics*
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Nucleoside Deaminases
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Proteins / antagonists & inhibitors
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Proteins / metabolism*
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Repressor Proteins
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Retroviridae / genetics*
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vif Gene Products, Human Immunodeficiency Virus
Substances
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Gene Products, vif
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Proteins
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Repressor Proteins
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vif Gene Products, Human Immunodeficiency Virus
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Nucleoside Deaminases
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APOBEC-3G Deaminase
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APOBEC3G protein, human
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Cytidine Deaminase