Hemagglutinin (HA) of Influenza B virus Victoria lineage (HA (Victoria))

Hemagglutinin (HA) is the primary surface glycoprotein of Influenza B viruses belonging to the Victoria lineage, serving as a critical mediator of viral entry into host cells (Wikipedia, 2024). It functions as a homotrimer where each monomer consists of two subunits: HA1, which contains the receptor-binding site for sialic acids on the host cell surface, and HA2, which contains the fusion machinery (MDPI, 2020). Upon endocytosis, the acidic environment of the endosome triggers a dramatic conformational change in HA2, leading to the fusion of the viral and endosomal membranes and the release of the viral genome (NIH, 2022). As the immunodominant antigen on the virion surface, HA is the central component of seasonal influenza vaccines, which aim to induce neutralizing antibodies that block either receptor binding or the fusion process (NIH, 2024). However, the Victoria lineage HA is subject to continuous antigenic drift, particularly in the loops surrounding the receptor-binding site, which can lead to vaccine mismatch and reduced therapeutic efficacy (NIH, 2025). Recent developments focus on broadly neutralizing antibodies and universal vaccine candidates that target the more conserved stem region of the HA protein to provide broader protection against evolving strains (NIH, 2025).

Other names

Influenza B Victoria HAB/Victoria HemagglutininHemagglutinin glycoprotein (Victoria lineage)HA (Victoria)B/Victoria HA

The primary mechanism of action for drugs targeting the hemagglutinin of Influenza B/Victoria lineage strains is the neutralization of viral infectivity. Vaccines and monoclonal antibodies bind to the HA1 globular head to sterically hinder the interaction with host sialic acid receptors, thereby preventing viral attachment (NIH, 2020). Alternatively, antibodies and small-molecule inhibitors can target the conserved HA2 stem region to block the pH-dependent conformational change required for membrane fusion, effectively halting the release of the viral genome into the host cytoplasm (NIH, 2022; MDPI, 2020).