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- W2895591204 abstract "Abstract Human APOBEC3H (A3H) is a single-stranded DNA cytosine deaminase that inhibits HIV-1. Seven haplotypes (I–VII) and four splice variants (SV154/182/183/200) with differing antiviral activities and geographic distributions have been described, but the genetic and mechanistic basis for variant expression and function remains unclear. Using a combined bioinformatic/experimental analysis, we find that SV200 expression is specific to haplotype II, which is primarily found in sub-Saharan Africa. The underlying genetic mechanism for differential mRNA splicing is an ancient intronic deletion [del(ctc)] within A3H haplotype II sequence. We show that SV200 is at least fourfold more HIV-1 restrictive than other A3H splice variants. To counteract this elevated antiviral activity, HIV-1 protease cleaves SV200 into a shorter, less restrictive isoform. Our analyses indicate that, in addition to Vif-mediated degradation, HIV-1 may use protease as a counter-defense mechanism against A3H in >80% of sub-Saharan African populations." @default.
- W2895591204 created "2018-10-12" @default.
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- W2895591204 date "2018-10-08" @default.
- W2895591204 modified "2023-10-16" @default.
- W2895591204 title "Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease" @default.
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- W2895591204 doi "https://doi.org/10.1038/s41467-018-06594-3" @default.
- W2895591204 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6175962" @default.
- W2895591204 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30297863" @default.
- W2895591204 hasPublicationYear "2018" @default.
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