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The primary surface antigens of Influenza B virus are the envelope glycoproteins hemagglutinin (HA) and neuraminidase (NA), which are embedded in the viral lipid envelope[2][4][5]. Hemagglutinin mediates virus attachment to host cell sialic acid receptors and catalyzes fusion of the viral and cellular membranes during entry[1][4]. Neuraminidase removes sialic acid residues from glycoproteins, facilitating release of new virions from infected cells and preventing viral self-aggregation[5]. Both proteins are the main targets of host neutralizing antibodies and are subject to immune-driven antigenic variation[1][5]. These structures serve as the basis for subtype nomenclature and as targets for licensed antivirals and vaccines for influenza B.
Inhibition of neuraminidase enzymatic activity blocks viral particle release from infected cells and limits spread[5]. Monoclonal antibodies prevent hemagglutinin-mediated cell entry and membrane fusion[1].
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