HIV-1 has various subtypes and CRFs, each with unique genetic attributes that impact the virus's spread, disease development, and response to treatment in different populations. Determining V3 tropism is crucial for utilizing CCR5 antagonists and understanding why certain HIV-1 subtypes are more pathogenic than others are. Genotypic coreceptor usage of 603 major subtypes of A, B, C, AE, and CRF35-AD is investigated via five bioinformatics tools (PhenoSeq, WebPSSM, Geno2Pheno, Net charge, and the 11/25 rule). This study examined crown motifs, N-glycosylation sites, and T8V mutations in all subtypes. R5 viruses are common in subtypes A, B, C, and CRF35-AD. These data indicate that R5 viruses in subtypes A and B are more prone to crown motif formation. The first report assessed the tropism of common HIV-1 subtypes and reported that CCR5 inhibitors could help treat patients with all subtypes but not AE. WebPSSM is a suitable method for determining HIV-1 tropism in different subtypes. Finally, large cohorts to assess virological response to CCR5 inhibitors would provide deep insight into the practicality of genotypic methods in clinical settings.
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