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The **SARS-CoV-2 Beta variant spike protein** is a trimeric, surface-expressed glycoprotein of the SARS-CoV-2 virus variant B.1.351, classified as a class I viral fusion protein and critical determinant of viral infectivity, antigenicity, and immune escape[6][1][4][3]. The spike protein facilitates viral entry into host cells by binding to the ACE2 receptor via its receptor-binding domain (RBD), followed by membrane fusion mediated by its S2 subunit[2][4][1]. The Beta variant spike contains a constellation of substitutions—most notably K417N, E484K, and N501Y in the RBD—that alter its structure, stability, and affinity for ACE2, while also reducing susceptibility to neutralizing antibodies. As the principal target of vaccine- and infection-induced neutralizing antibodies, the spike protein is a major therapeutic target and a key antigen in all major COVID-19 vaccines, as well as the target of several monoclonal antibody therapeutics[6][1][2]. Variations in this protein among SARS-CoV-2 strains are closely linked to changes in transmission, vaccine effectiveness, and therapeutic response[6][1][5].
Inhibition of ACE2–spike protein interaction (by competitive binding of neutralizing antibodies) - Allosteric destabilization of prefusion conformation (some antibodies) - Vaccine-induced immunity targets spike to induce neutralizing antibody/immune responses
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