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“HIV-1 replication” describes the multi-step process by which Human Immunodeficiency Virus type 1 (HIV-1) infects a cell, converts its RNA genome into DNA via reverse transcriptase, integrates the DNA into the host genome using integrase, produces viral proteins and RNA by hijacking host cellular machinery, assembles new virions, and releases them from the host cell to perpetuate infection[4][6][8]. This process involves numerous viral proteins (gag, pol, env, tat, rev, nef, vif, vpr, vpu)[1][2][4], host factors, and complex viral-host interactions, and is broadly targeted by antiretroviral drugs. However, the term “HIV-1 replication” is not itself a singular molecular target and should be replaced by the specific HIV-1 gene products or host factors involved (e.g., HIV-1 reverse transcriptase, HIV-1 protease, CCR5 receptor, CXCR4 receptor) for structured biomedical records.
Inhibition of specific steps in the viral life cycle by targeting individual HIV-1 proteins (e.g., viral polymerase, protease, integrase) or viral entry receptors.
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