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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral proteins encompass a diverse group of structural, non-structural, and accessory proteins essential for the viral life cycle and pathogenesis of COVID-19 [1, 7]. The structural proteins include the Spike (S) protein, which mediates host cell entry via the ACE2 receptor; the Nucleocapsid (N) protein, which packages the viral RNA; and the Membrane (M) and Envelope (E) proteins, which are critical for viral assembly [6, 18]. Non-structural proteins (nsps), such as the main protease (Mpro) and RNA-dependent RNA polymerase (RdRp), facilitate viral replication and transcription within the host cell [13, 15]. These proteins serve as the primary targets for the global pharmaceutical response, including mRNA and viral vector vaccines that induce immunity against the Spike protein, and monoclonal antibodies that neutralize viral entry [1, 4]. Additionally, small-molecule antivirals have been developed to inhibit specific enzymatic functions, such as Mpro and RdRp, to halt viral progression [13, 22]. Understanding the structural and functional diversity of these antigens is crucial for addressing viral evolution and the emergence of variants that may evade existing therapeutic interventions [7, 23].
Neutralization of viral entry by blocking Spike-ACE2 interaction, inhibition of viral polyprotein cleavage by protease inhibitors, termination of viral RNA synthesis by polymerase inhibitors, and induction of adaptive humoral and cellular immune responses through vaccination [1, 6, 13].
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