Abstract
APOBEC3 proteins are restriction factors that induce G→A hypermutation in retroviruses during replication as a result of cytidine deamination of minus-strand DNA transcripts. However, the mechanism of APOBEC inhibition of murine leukemia viruses (MuLVs) does not appear to be G→A hypermutation and is unclear. In this report, the incorporation of mA3 in virions resulted in a loss in virion reverse transcriptase (RT) activity and RT fidelity that correlated with the loss of virion-specific infectivity.
Copyright © 2014, American Society for Microbiology. All Rights Reserved.
Publication types
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Research Support, N.I.H., Intramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western
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Cytidine Deaminase / physiology*
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Knockout
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Moloney murine leukemia virus / enzymology*
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Moloney murine leukemia virus / pathogenicity
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RNA-Directed DNA Polymerase / metabolism*
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Retroviridae Infections / enzymology*
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Retroviridae Infections / virology
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Transfection
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Tumor Virus Infections / enzymology*
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Tumor Virus Infections / virology
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Virion / pathogenicity*
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Virus Assembly
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Virus Replication
Substances
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RNA-Directed DNA Polymerase
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Apobec3 protein, mouse
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Cytidine Deaminase