HIV-1 is an RNA retrovirus that infects immune cells through the envelope glycoprotein Env, whose mature gp120/gp41 trimer mediates viral entry into host cells
[1]. Mechanistically, gp120 binds CD4 and then the chemokine coreceptors CCR5 or CXCR4, while gp41 refolding brings viral and cellular membranes together for fusion
[2][3]. After entry, viral replication depends on reverse transcriptase, protease, and integrase, making these enzymes core targets for antiretroviral research
[4][5]. In disease relevance, untreated HIV replication causes progressive CD4
+ T-cell loss and immunological abnormalities, increasing infectious and oncological complications
[6]. Compared with related forms, HIV-1 remains the main focus because it is described as the most virulent and pathogenic subtype in diagnostic and treatment literature
[7]. For experimental applications, entry inhibitors target gp120, gp41, CCR5, or CXCR4, while enzyme inhibitors target reverse transcriptase, protease, or integrase to suppress distinct stages of the HIV life cycle
[4][8].