Anti-IBV Hemagglutinin Polyclonal antibody

Influenza A and B viruses show clear differences in their host specificity and pandemic potential. Recent studies have revealed that the host protease TMPRSS2 plays an essential role for proteolytic activation of H1, H3, and H7 subtype strains of influenza A virus (IAV) in vivo. IAV possessing a monobasic cleavage site in the haemagglutinin ( HA) protein replicates poorly in TMPRSS2 knockout mice owing to insufficient HA cleavage. In the present study, human isolates of influenza B virus (IBV) strains and a mouse-adapted IBV strain were analysed. The data showed that IBV successfully underwent HA cleavage in TMPRSS2 knockout mice, and that the mouse-adapted strain was fully pathogenic to these mice. The present data demonstrate a clear difference between IAV and IBV in their molecular mechanisms for spreading in vivo.

Influenza B virus (IBV) is one of the most important human respiratory viruses: it causes approximately one-third of the global influenza-related disease burden each year. However, compared with the several pathogenicity-related molecular markers that have been identified for influenza A virus (IAV), little is known about potential IBV pathogenicity-related markers. Here, although the IBV strain B/Anhui-Tunxi/1528/2014 (AH1528/14) exhibited a more efficient replication abilityin vitroand higher pathogenicityin vivocompared with IBV strain B/Anhui-Baohe/127/2015 (AH127/15), only three amino acids differences (HA(A390E), NA(N342D)and PB1(V212I)) were observed among their full genomes. The contributions of each amino acid difference to the virus pathogenicity were further investigated. Compared with the wild type IBV virus rAH127, the recombinant virus harbouring a single substitution of HA(A390E)had a similar phenotype, whereas the recombinant virus harbouring PB1(V212I)replicated to a moderately higher titre in both MDCK cells and in mice. Notably, the virus harbouring NA(N342D)showed significantly better growth properties in MDCK cells and higher fatality rates in mice. In addition, the presence of NA(N342D)dramatically enhanced the viral neuraminidase activity. In conclusion, our study identified a novel IBV molecular marker, NA(N342D), that could significantly increase the virulence of IBV in mice.