Influenza B Virus Victoria Group with a New Glycosylation Site Was Epidemic in Japan in the 2002-2003 Season

Abstract

In the 2002-2003 season, influenza B virus Victoria strains were epidemic after a 6-year absence in Kobe City, Japan. They reacted poorly to the immune ferret sera prepared for use against the previous strain. An amino acid substitution in the HA1 region caused them to acquire an N-linked glycosylation site

Structural basis for receptor specificity of influenza B virus hemagglutinin

“…Thus, the growth environment of chicken eggs imposes a strong selective pressure on influenza B virus toward losing the glycans at residue 194, with concomitant enhanced affinity for ␣(2,3)-linked sialic acids (40). Interestingly, the gain or loss of a glycosylation site at residue 194 seems to be an effective tool used by naturally occurring influenza B virus to modify its antigenicity (55,56). Similar strategy was also found by egg-adapted influenza A virus (2,40).…”

Discovery of the Neutralizing Epitope Common to Influenza B Virus Victoria Group Isolates in Japan

“…In the 1996/1997 season, there was a B/Victoria epidemic in Japan after almost 10 years' absence of the strain. Then, the next one was in the 2002/2003 season (8,11,12). The antigenicities of B/Victoria isolates in these seasons were distinct from those of the isolates in the mid-1980s.…”

“…The antigenicities of B/Victoria isolates in these seasons were distinct from those of the isolates in the mid-1980s. The first variants appeared in the 1996/1997 season with an extra oligosaccharide chain near the receptor binding region, and they became predominant in the 2002/2003 season (11). Then, the second variants appeared with variation in the conserved epitope of B/Victoria isolates, at the "tip" of the hemagglutinin (HA) molecule (12).…”

“…Escape mutants were induced by incubating virus with 9B2, by a modification of the method previously described (1,4,10). The nucleotide sequences of the escape mutants were analyzed as described previously (8)(9)(10)(11)(12).…”

Universal Influenza B Vaccine Based on the Maturational Cleavage Site of the Hemagglutinin Precursor

“…Since HA and NA readily undergo point mutations to evade the immune system (antigenic drift) (39,41), the vaccine formulations need to be evaluated on a yearly basis and accordingly, vaccination must be performed annually. For influenza B virus, the emergence of new variants (36), coupled with the cocirculation of the different viral lineages (30,46), makes the annual World Health Organization designation of the type B vaccine strain particularly problematic (48).…”