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Hemagglutinin and neuraminidase are the two principal surface glycoproteins of the influenza A virus, responsible for viral entry and release, respectively. Hemagglutinin (HA) binds to sialic acid-containing receptors on host cells and mediates membrane fusion after endocytosis, initiating infection. Neuraminidase (NA) cleaves sialic acid residues from host cell surfaces and viral glycoproteins, promoting the release and spread of progeny virions. The "H2N3" designation refers to an influenza A virus subtype expressing the second hemagglutinin and third neuraminidase proteins in the standard viral nomenclature system. Both proteins are critical determinants of host specificity, immune response, pathogenicity, and are established targets for antiviral therapy and vaccine development in influenza A infection[2][5][6][9].
Neuraminidase inhibitors: prevent viral release by blocking NA’s sialidase activity[2] Hemagglutinin targeting antibodies or drugs: neutralize virus entry by blocking binding to the host-cell receptor or by preventing conformational changes needed for membrane fusion[6][9]
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