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Equine influenza virus (EIV) antigens, primarily the surface glycoproteins hemagglutinin (HA) and neuraminidase (NA), are the principal targets for both prophylactic vaccines and antiviral therapies in horses [1, 15]. Hemagglutinin facilitates viral entry by binding to sialic acid receptors on the host's respiratory epithelial cells and mediating the fusion of the viral envelope with the endosomal membrane [2, 19]. Neuraminidase is an enzyme essential for the release of newly formed viral particles from the host cell surface, preventing their aggregation and allowing the infection to spread [1, 19]. These antigens are highly susceptible to antigenic drift, particularly in the H3N8 subtype, which leads to the emergence of new lineages such as Florida Clade 1 and Clade 2, often necessitating updates to vaccine formulations [13, 18]. Therapeutic strategies include the use of neuraminidase inhibitors like oseltamivir and peramivir to limit viral replication and the administration of vaccines to stimulate a protective immune response [4, 12, 14]. Effective management of EIV is crucial due to its high transmissibility and the significant economic impact of outbreaks on the equine industry [6, 18].
Vaccines stimulate the production of neutralizing antibodies that bind to viral antigens, primarily hemagglutinin, to block viral entry into host cells [12, 19]. Neuraminidase inhibitors like oseltamivir and peramivir bind to and inhibit the viral neuraminidase enzyme, preventing the release of progeny virions from infected cells and limiting the spread of infection [4, 19].
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