Severe acute respiratory syndrome coronavirus 2 viral protein (SARS-CoV-2 viral protein (for individual proteins, S, E, M, or N may be used; for the proteome as a whole, no standard abbreviation))

SARS-CoV-2 is the causative agent of COVID-19 and encodes a set of 29 known proteins, including four structural proteins (spike/S, envelope/E, membrane/M, and nucleocapsid/N), sixteen nonstructural proteins (nsps 1-16, derived from polyproteins), and multiple accessory proteins[1][2][4][5][6]. The **spike glycoprotein** mediates attachment and entry through binding to the ACE2 receptor, making it the primary target of neutralizing antibodies and vaccines[1][7]. The **membrane protein** organizes assembly and budding of virions[2][4]. The **envelope protein** functions as a viroporin (ion channel), contributing to virion assembly and pathogenesis[4][5]. The **nucleocapsid protein** packages the RNA genome and interacts with other structural proteins to facilitate virion formation[6]. Several nonstructural proteins, such as the main protease, papain-like protease, and RNA-dependent RNA polymerase, are essential for viral RNA replication and transcription, making them major antiviral drug targets[1][3]. Accessory proteins modulate the host immune response[1]. The SARS-CoV-2 proteome as a category is chemically and functionally heterogeneous; therefore, druggability, immune response, and clinical significance must be analyzed at the level of individual proteins. Note: For structured databases, each SARS-CoV-2 protein should ideally be annotated as a separate target (e.g., "Spike glycoprotein (S)", "RNA-dependent RNA polymerase (RdRp)", "Main protease (Mpro)") rather than using the collective term "SARS-CoV-2 viral proteins".

Other names

SARS-CoV-2 proteinsSARS-CoV-2 proteomeSARS-2 proteinsCOVID-19 viral proteinsCoronavirus structural proteins (when referring to S, E, M, N collectively)

Enzyme inhibition (protease inhibitors, polymerase inhibitors); Blocking receptor binding (spike/ACE2 interaction inhibition); Inhibiting viral membrane fusion (fusion inhibitors); Inducing error catastrophe in viral RNA synthesis (e.g., molnupiravir)