| Literature DB >> 25673722 |
Kouji Sakai1, Tsuyoshi Sekizuka2, Yasushi Ami3, Noriko Nakajima4, Minori Kitazawa5, Yuko Sato4, Katsuhiro Nakajima5, Masaki Anraku6, Toru Kubota6, Katsuhiro Komase6, Kazuaki Takehara7, Hideki Hasegawa4, Takato Odagiri8, Masato Tashiro8, Makoto Kuroda2, Makoto Takeda6.
Abstract
The host protease TMPRSS2 plays an essential role in proteolytic activation of the influenza A virus (IAV) hemagglutinin (HA) protein possessing a monobasic cleavage site. However, after passages in TMPRSS2 knockout mice, an H3N2 subtype IAV began to undergo cleavage activation of HA, showing high virulence in the mice due to the loss of an oligosaccharide at position 8 in the HA stalk region. Thus, the H3N2 IAV acquired cleavability by an alternative HA activation mechanism/protease(s).Entities:
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Year: 2015 PMID: 25673722 PMCID: PMC4403495 DOI: 10.1128/JVI.00124-15
Source DB: PubMed Journal: J Virol ISSN: 0022-538X Impact factor: 5.103