HIV-1 is characterized by substantial genetic diversity, resulting in different subtypes and circulating recombinant forms (CRFs). This section provides an overview of the genetic diversity of HIV-1 and the significance of sub-subtype A6, CRF02_AG, and subtype B in the context of this article [3-5]. HIV-1 subtypes can exhibit variations in their replication capacities, influencing viral load, disease progression, and transmission dynamics. This section discusses the replication capacity of sub-subtype A6, CRF02_AG, and subtypes B. Female sex hormones, including estradiol and progesterone, have been shown to modulate the replication of HIV-1. This section explores the mechanisms by which sex hormones interact with the viral replication cycle. The interplay between sex hormones and HIV-1 replication may have implications for preventive interventions, such as Pre-Exposure Prophylaxis (PrEP) and microbicides. This section explores the potential to tailor prevention strategies based on subtype-specific hormone interactions.
Recent studies have highlighted the contrasting effects of female sex hormones on the replication activity of HIV-1 sub-subtype A6, CRF02_AG, and subtype B. This section examines the specific findings and their implications for HIV-1 pathogenesis and transmission [6].