Hypermutation of HIV-1 DNA in the Absence of the Vif Protein
By D. Lecossier, F. Bouchonnet, F. Clavel, A. Hance. Science, 2003
702 citations recorded by the source corpus.
Subfields: Immunology, Infectious Diseases, Virology
View Paper: https://www.semanticscholar.org/paper/1dc0926434198dade14dd8b72cb8945ef7fac838
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In Immunology
In Virology
Citations in the corpus
- HIV-1 Vif protein binds the editing enzyme APOBEC3G and induces its degradation (2003, background): “It was recently shown that APOBEC3G causes cytidine deamination of HIV-1 negative-strand DNA during the process of reverse transcriptio”
- Species-specific exclusion of APOBEC3G from HIV-1 virions by Vif. (2003, result): “…are likely to be heavily mutated and not competent for further replication. reverse transcripts was consistent with the recent findings of Lecossier et al. (2003), Harris et al. (2003),Taken together, the data suggest that there is a small effect on preintegrative DNA, a larger effect…”
- Mechanisms of viral mutation (2016, background): “APOBEC3G was first shown to massively convert cytidines to uracils in the complementary HIV-1 DNA during or following reverse transcription [55] [56] [57] .”
- HIV-1 Vif blocks the antiviral activity of APOBEC3G by impairing both its translation and intracellular stability. (2003, background): “effect on the full-length genomic RNA packaged into the virion (Harris et al., 2003; Lecossier et al., 2003; Mariani et al. observed only a modest decrease in cellular APOBEC3G levels in the presence of Vif. We Mangeat et al., 2003; Zhang et al., 2003).”