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Severe acute respiratory syndrome coronavirus (SARS-CoV) is an enveloped, positive-sense, single-stranded RNA virus that causes a severe respiratory illness in humans [WHO, 2003]. It belongs to the genus Betacoronavirus and was the causative agent of the 2002-2004 global outbreak [CDC, 2004]. The virus initiates infection by binding its surface Spike (S) protein to the human Angiotensin-converting enzyme 2 (ACE2) receptor, facilitating membrane fusion and entry [Nature, 2003]. Inside the host cell, the viral genome is translated into polyproteins that are cleaved by viral proteases, such as the main protease (Mpro), to form functional replication complexes [Science, 2003]. Therapeutic interventions typically target these viral enzymes or the entry mechanism to halt the progression of the infection [FEBS Journal, 2014]. Although the original SARS-CoV is no longer circulating in humans, it remains a significant focus of research for pandemic preparedness and broad-spectrum antiviral development [Nature Reviews Microbiology, 2013].
Antiviral agents target various stages of the viral life cycle, including RNA-dependent RNA polymerase (RdRp) inhibition, viral protease inhibition (3CLpro and PLpro), and blocking of viral entry into host cells by interfering with the Spike-ACE2 interaction.
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