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The SARS-CoV-2 virus replication process encompasses the series of molecular and cellular events by which SARS-CoV-2 copies its RNA genome and produces viral proteins necessary for assembly and release of infectious virus particles. The cycle starts with viral attachment to host cell surface receptors, mainly angiotensin-converting enzyme 2 (ACE2), followed by fusion and release of the viral RNA into the cytoplasm[1][2][3][5][6]. Viral proteins are translated, and viral RNA is replicated by the central replication complex, which includes RNA-dependent RNA polymerase (Nsp12), cofactors Nsp7 and Nsp8, and supporting non-structural proteins[1][2][3][5][6]. The replication steps involve proofreading, capping, and hijacking of host machinery; subgenomic RNAs are also produced to synthesize additional viral structural proteins[1][2][3][4][5]. Therapeutic interventions most often target key enzymes in these steps, such as the viral polymerase or protease[6][7]. Since "SARS-CoV-2 virus replication process" is a multicomponent process rather than a specific drug target or receptor, its use as a canonical target is structurally incorrect for molecular targeting and drug development databases[1][2][3][4][5][6][7].
Inhibition of RNA-dependent RNA polymerase activity; Blocking viral polyprotein cleavage via protease inhibition; Interference with viral entry proteins (e.g., spike protein-ACE2 interaction)
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