Severe acute respiratory syndrome coronavirus spike glycoprotein (SARS-CoV S)

The **Severe acute respiratory syndrome coronavirus spike glycoprotein** is a large Class I viral fusion protein found on the surface of SARS coronaviruses, including SARS-CoV (causing SARS) and SARS-CoV-2 (causing COVID-19)[5][2][3]. This trimeric protein consists of two functional subunits: S1 (containing the receptor-binding domain or RBD) and S2 (responsible for membrane fusion)[2][3][5][6]. The spike glycoprotein mediates viral entry by binding to the host cell receptor angiotensin-converting enzyme 2 (ACE2), triggering conformational changes that allow fusion of the viral and cellular membranes[2][4][5][7]. The protein is highly glycosylated, both for proper folding and to evade immune detection[3][5][6]. It determines host range, tissue tropism, and is the principal antigen recognized by neutralizing antibodies, making it the main target for vaccine and therapeutic antibody development[5][8]. Variations in the spike's structure influence infectivity, transmission, and antigenicity, and mutations in the S protein are a major driver of viral evolution and immune escape[8]. The S protein is the largest structural protein in coronaviruses (SARS-CoV S: ~1255–1273 amino acids), makes up the distinctive surface spikes seen in electron micrographs, and is essential for pathogenesis[5]. Therapeutic agents targeting the S protein include neutralizing monoclonal antibodies, potential fusion inhibitors, and vaccines based on the S protein sequence[8][7]. For downstream structured data extraction, information regarding SARS-CoV-2 and SARS-CoV spike glycoproteins is widely applicable, as both share high structural and functional homology, with potential differences in certain epitopes or glycosylation sites influencing host range and antibody binding[3][4][7].

Other names

SARS coronavirus spike glycoproteinSpike proteinS proteinS glycoproteinE2 (historical name)

Neutralization (blocking receptor binding and/or fusion); Inhibition of spike-mediated membrane fusion; Receptor decoy (soluble ACE2 binds S, preventing cell entry); Preventing S protein cleavage/maturation