Influenza A virus subtype H3N2 (H3N2)

Influenza A virus subtype H3N2 is a major pathogen responsible for seasonal respiratory infections and significant global morbidity, historically known for causing the 1968 "Hong Kong flu" pandemic [1, 11]. As a member of the Orthomyxoviridae family, it features a segmented, negative-sense RNA genome and two primary surface glycoproteins: hemagglutinin (H3), which facilitates cell entry, and neuraminidase (N2), which enables the release of new virions [1, 2, 3]. The virus infects host cells by binding to sialic acid receptors on the respiratory epithelium [2, 9]. Therapeutic management involves annual vaccines targeting the hemagglutinin protein and antiviral medications that inhibit essential viral functions [4, 15]. Neuraminidase inhibitors like oseltamivir and zanamivir are used to prevent viral egress, while cap-dependent endonuclease inhibitors such as baloxavir marboxil target the viral polymerase complex to stop replication [12, 15]. H3N2 is characterized by rapid antigenic drift and has developed widespread resistance to older adamantane-based drugs, making it a persistent challenge for public health and vaccine development [13, 16, 17].

Other names

H3N2A/H3N2A(H3N2)Hong Kong flu virusSeasonal influenza A subtype H3N2Influenza A/H3N2

Inhibition of viral neuraminidase to prevent progeny release; inhibition of M2 ion channels to block viral uncoating; inhibition of cap-dependent endonuclease (PA subunit) to prevent viral RNA synthesis; and neutralization of hemagglutinin to block viral attachment and entry.