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Human immunodeficiency virus (HIV) replication is the multi-stage biological process by which HIV infects host cells and generates new progeny (NIH, 2021). The cycle begins with the attachment of the viral gp120 protein to the host CD4 receptor and a co-receptor (CCR5 or CXCR4), followed by gp41-mediated membrane fusion (Nature Reviews Microbiology, 2018). Once the viral core enters the cytoplasm, reverse transcriptase converts the viral RNA genome into double-stranded DNA, which is then integrated into the host cell's genome by the enzyme integrase (StatPearls, 2023). The host's cellular machinery then transcribes and translates the integrated proviral DNA into viral RNA and polyproteins. These components assemble at the cell membrane to form immature virions that bud off; subsequently, the viral protease enzyme cleaves the polyproteins to produce mature, infectious virus particles (PubMed, 2020). Therapeutic strategies, collectively known as antiretroviral therapy (ART), target these specific enzymatic and entry steps to suppress viral load and prevent the progression to AIDS (NIH, 2021).
Inhibition of viral enzymes including reverse transcriptase, integrase, and protease; blockade of viral entry via CCR5 antagonism and fusion inhibition; and disruption of capsid assembly and disassembly (StatPearls, 2023; NIH, 2021).
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