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Hemagglutinin and neuraminidase of H2N3 influenza A virus (HA and NA (H2N3))

Target
HA and NA (H2N3)
Molecular classification
Hemagglutinin, Viral envelope glycoprotein, Fusion protein, Neuraminidase, Enzyme (sialidase)
01

Overview

Hemagglutinin and neuraminidase are the two principal surface glycoproteins of the influenza A virus, responsible for viral entry and release, respectively. Hemagglutinin (HA) binds to sialic acid-containing receptors on host cells and mediates membrane fusion after endocytosis, initiating infection. Neuraminidase (NA) cleaves sialic acid residues from host cell surfaces and viral glycoproteins, promoting the release and spread of progeny virions. The "H2N3" designation refers to an influenza A virus subtype expressing the second hemagglutinin and third neuraminidase proteins in the standard viral nomenclature system. Both proteins are critical determinants of host specificity, immune response, pathogenicity, and are established targets for antiviral therapy and vaccine development in influenza A infection[2][5][6][9].

Other names
HA (Hemagglutinin)NA (Neuraminidase)Influenza virus hemagglutininInfluenza virus neuraminidaseH2 (second hemagglutinin subtype)N3 (third neuraminidase subtype)
02

Mechanism of action

Neuraminidase inhibitors: prevent viral release by blocking NA’s sialidase activity[2] Hemagglutinin targeting antibodies or drugs: neutralize virus entry by blocking binding to the host-cell receptor or by preventing conformational changes needed for membrane fusion[6][9]

03

Biological functions

Hemagglutinin: Mediates viral attachment to host cell receptors (sialic acid-containing glycans)Hemagglutinin: Facilitates fusion of the viral and endosomal membranes during entry[6][9]Neuraminidase: Cleaves sialic acid residues to facilitate the release of newly formed viral particles from infected cells[2][9]
04

Disease associations

Infection (influenza A virus infection)Other (specifically zoonotic/avian-to-mammalian transmission potential due to rare subtype H2N3)
05

Safety considerations

Antigenic drift/mutation: rapid evolution leading to escape from therapeutics or vaccines[8][9]Resistance to neuraminidase inhibitors: due to NA mutations[2]Potential for zoonosis or pandemic potential (H2N3 is a rare, but experimentally zoonotic-capable strain)Vaccine mismatches: due to evolving HA/NA epitopes
06

Interacting drugs

Neuraminidase inhibitors: oseltamivir, zanamivir, peramivir[2]

1 more in the full profile.

07

Biomarkers

HA and NA subtype-specific serology/antibody detection as markers of infection or vaccine responseViral genetic sequencing for HA/NA variation or resistance mutations

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