HIV mutation literature information.


  Molecular Modeling of Subtype-Specific Tat Protein Signatures to Predict Tat-TAR Interactions That May Be Involved in HIV-Associated Neurocognitive Disorders.
 PMID: 35464972       2022       Frontiers in microbiology
Discussion: From these energy important residues, Tat subtype C had mutations at residue 40 (K40T) and 57 (R57S).
Discussion: Our findings suggest that the R57S mutation found in Tat subtype C may influence lower TAR binding and this may be an initiating step to why we see less severe neuropathophysiological (e.g., dysregulated inflammation) features related to HIV-1C infection.
Discussion: The R57 signature in Tat subtype B is crucial for transactivation, and transactivation by Tat subtype B was significantly reduced by the R57S substitution which is present in Tat subtype C.


  HIV-1C and HIV-1B Tat protein polymorphism in Southern Brazil.
 PMID: 33462791       2021       Journal of neurovirology
Abstract: The frequency of the R57S substitution among the HIV-1C sequences from Brazil was 74% vs.


  A Naturally Occurring Polymorphism in the HIV-1 Tat Basic Domain Inhibits Uptake by Bystander Cells and Leads to Reduced Neuroinflammation.
 PMID: 30824746       2019       Scientific reports
Result: Tat-B* yielded higher levels of inflammatory cytokine gene transcripts IL-6, IL-8, IL-1beta and CXCL1 than Tat-B*-
Result: Next, we tested the effect of the R57S polymorphism on the cellular uptake of full-length Tat proteins.
Figure: At equivalent inputs, both Tat-B * and Tat-C proteins maximally transactivate only when R57 is present (a) Absorbance values from ELISA assay measuring the relative amounts of Tat protein in media samples from HeLa cells transfected with Tat-B*, Tat-B*R57S, Tat-C or Tat-CS57R expression constructs.



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