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Avian influenza virus (AIV) refers to a group of Influenza A viruses that primarily circulate among wild birds and poultry, occasionally crossing the species barrier to infect humans [1]. These viruses are not single molecular targets but are complex pathogens containing several distinct proteins that serve as therapeutic targets, including Hemagglutinin (HA), Neuraminidase (NA), and the M2 ion channel [2, 3]. HA facilitates viral attachment and entry into host cells by binding to sialic acid receptors, while NA is an enzyme essential for the release of progeny virions from the host cell surface [3]. Clinical management of infections often involves the use of NA inhibitors like oseltamivir or polymerase inhibitors like baloxavir marboxil to reduce viral load and symptom severity [4, 5]. However, the virus's high rate of genetic mutation, through processes like antigenic drift and shift, frequently leads to the emergence of drug-resistant strains and poses a significant threat for potential pandemics [1, 2]. Consequently, therapeutic development focuses on highly conserved regions of viral proteins to ensure broader and more durable efficacy [3].
Neuraminidase inhibition, Cap-dependent endonuclease inhibition, and M2 ion channel blockade
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