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Influenza A virus antigens are the primary molecular components of the virus recognized by the host immune system, serving as the fundamental targets for vaccines and immunotherapies [1, 4]. The most critical antigens are the surface glycoproteins Hemagglutinin (HA) and Neuraminidase (NA), which mediate viral entry into host cells and the release of progeny virions, respectively [1, 6]. Other important antigens include the Matrix 2 (M2) ion channel and the internal Nucleoprotein (NP), which are highly conserved and serve as targets for T-cell responses and universal vaccine development [8, 13]. These antigens are the basis for seasonal and pandemic influenza vaccines, which aim to elicit protective antibodies to prevent infection or reduce disease severity [2, 14]. While primarily viewed as immune targets, specific antigens like NA and M2 are also the direct targets of antiviral drugs such as oseltamivir and amantadine [10]. The rapid evolution of these antigens through antigenic drift and shift poses a significant challenge, requiring continuous surveillance and annual vaccine updates to maintain efficacy against circulating strains [3, 7].
Vaccines induce neutralizing antibodies against surface antigens (primarily HA) to prevent infection [4, 14]. Antiviral drugs inhibit specific antigenic functions: NA inhibitors prevent viral release, M2 blockers inhibit uncoating, and polymerase inhibitors block replication [10, 11].
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