Distinct genetic clusters in HIV-1 CRF01_AE-infected patients induced variable degrees of CD4 + T-cell loss.
Kang LiHuanhuan ChenJianjun LiYi FengShujia LiangAbdur RashidMeiliang LiuSisi LiQingfei ChuYuhua RuanHui XingGuanghua LanWentao QiaoYiming ShaoPublished in: mBio (2024)
T cells than other HIV-1 sub-types and CRF01_AE clusters. Its mechanisms are associated with increased CXCR4 tropism due to an envelope structure change favoring a tropism shift from CCR5 to CXCR4, thereby shaping viral phenotype features and impacting pathogenicity. This underscores the significance of consistently monitoring HIV-1 genetic evolution and phenotypic transfer to see whether selection bias across risk groups alters the delicate balance of transmissible versus toxic trade-offs, since virulent strains such as CRF01_AE clusters 1 and 2 could seriously compromise the efficacy of antiviral treatment. Only through such early warning and diagnostic services can precise antiviral treatments be administered to those infected with more virulent HIV-1 strains.
Keyphrases
- antiretroviral therapy
- hiv positive
- hiv testing
- hiv infected
- human immunodeficiency virus
- hepatitis c virus
- hiv aids
- men who have sex with men
- healthcare
- sars cov
- primary care
- dendritic cells
- regulatory t cells
- gene expression
- high glucose
- pseudomonas aeruginosa
- cystic fibrosis
- endothelial cells
- biofilm formation
- health insurance