Influenza B virus is one of two types of influenza virus that cause substantial morbidity and mortality in humans, the other being influenza A virus. The inability to provide lasting protection to humans against influenza B virus infection is due, in part, to antigenic drift of the viral surface glycoprotein, haemagglutinin (HA). Studies of the antigenicity of the HA of influenza B virus have been hampered by lack of knowledge of its structure. To address this gap, two possible models have been inferred for this structure, based on two known structures of the homologous HA of the influenza A virus (subtypes H3 and H9). Statistical, structural and functional analyses of these models suggested that they matched important details of experimental observations and did not differ from each other in any substantive way. These models were used to investigate two HA sites at which viral variants appeared to carry a selective advantage. It was found that each of these sites coevolved with nearby sites to compensate for either size or charge changes.
Homology model of the structure of influenza B virus HA1.,Tung CS, Goodman JL, Lu H, Macken CA J Gen Virol. 2004 Nov;85(Pt 11):3249-59. PMID:15483238[1]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
References
↑ Tung CS, Goodman JL, Lu H, Macken CA. Homology model of the structure of influenza B virus HA1. J Gen Virol. 2004 Nov;85(Pt 11):3249-59. PMID:15483238 doi:85/11/3249
