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- W2110365006 endingPage "3639" @default.
- W2110365006 startingPage "3628" @default.
- W2110365006 abstract "ABSTRACT After entering a host cell, retroviruses such as simian immunodeficiency virus (SIV) uncoat, disassembling the viral capsid. Rates of uncoating that are too high and too low can be detrimental to the efficiency of infection. Rapid uncoating typically leads to blocks in reverse transcription, but the basis for replication defects associated with slow uncoating is less clear. Here we characterize the phenotypes of two SIVmac239 mutants with changes, A87E and A87D, in the helix 4/5 loop of the capsid protein. These mutant viruses exhibited normal capsid morphology but were significantly attenuated for infectivity. The infectivity of wild-type and mutant SIVmac239 was not decreased by aphidicolin-induced growth arrest of the target cells. In the cytosol of infected cells, the A87E and A87D capsids remained in particulate form longer than the wild-type SIVmac239 capsid, suggesting that the mutants uncoat more slowly than the wild-type capsid. Both mutants exhibited much higher levels of autointegrated DNA forms than wild-type SIVmac239. Thus, some changes in the helix 4/5 loop of the SIVmac239 capsid protein result in capsid hyperstability and an increase in autointegration." @default.
- W2110365006 created "2016-06-24" @default.
- W2110365006 creator A5029567860 @default.
- W2110365006 creator A5071476197 @default.
- W2110365006 date "2013-04-01" @default.
- W2110365006 modified "2023-09-27" @default.
- W2110365006 title "Enhanced Autointegration in Hyperstable Simian Immunodeficiency Virus Capsid Mutants Blocked after Reverse Transcription" @default.
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- W2110365006 doi "https://doi.org/10.1128/jvi.03239-12" @default.
- W2110365006 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3624228" @default.
- W2110365006 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23345510" @default.
- W2110365006 hasPublicationYear "2013" @default.
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