tetano
Editor, Senior Moderator
J Virol. 2015 Feb 11. pii: JVI.00124-15. [Epub ahead of print]
[h=1]A Mutant H3N2 Influenza Virus Uses an Alternative Activation Mechanism in TMPRSS2 Knockout Mice by Loss of an Oligosaccharide in the Hemagglutinin Stalk Region.[/h] Sakai K[SUP]1[/SUP], Sekizuka T[SUP]2[/SUP], Ami Y[SUP]3[/SUP], Nakajima N[SUP]4[/SUP], Kitazawa M[SUP]5[/SUP], Sato Y[SUP]4[/SUP], Nakajima K[SUP]5[/SUP], Anraku M[SUP]6[/SUP], Kubota T[SUP]6[/SUP], Komase K[SUP]6[/SUP], Takehara K[SUP]7[/SUP], Hasegawa H[SUP]4[/SUP], Odagiri T[SUP]8[/SUP], Tashiro M[SUP]8[/SUP], Kuroda M[SUP]2[/SUP], Takeda M[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The host protease TMPRSS2 plays an essential role for proteolytic activation of influenza A virus (IAV) HA protein possessing a monobasic cleavage site. However, after passages in TMPRSS2 knockout mice, an H3N2 subtype IAV became to undergo cleavage activation of HA showing high virulence for the mice by loss of an oligosaccharide at position 8 in the HA stalk region. Thus, the H3N2 IAV acquired the cleavability by an alternative activation mechanism/protease(s) for HA.
Copyright ? 2015, American Society for Microbiology. All Rights Reserved.
PMID: 25673722 [PubMed - as supplied by publisher]
[h=1]A Mutant H3N2 Influenza Virus Uses an Alternative Activation Mechanism in TMPRSS2 Knockout Mice by Loss of an Oligosaccharide in the Hemagglutinin Stalk Region.[/h] Sakai K[SUP]1[/SUP], Sekizuka T[SUP]2[/SUP], Ami Y[SUP]3[/SUP], Nakajima N[SUP]4[/SUP], Kitazawa M[SUP]5[/SUP], Sato Y[SUP]4[/SUP], Nakajima K[SUP]5[/SUP], Anraku M[SUP]6[/SUP], Kubota T[SUP]6[/SUP], Komase K[SUP]6[/SUP], Takehara K[SUP]7[/SUP], Hasegawa H[SUP]4[/SUP], Odagiri T[SUP]8[/SUP], Tashiro M[SUP]8[/SUP], Kuroda M[SUP]2[/SUP], Takeda M[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The host protease TMPRSS2 plays an essential role for proteolytic activation of influenza A virus (IAV) HA protein possessing a monobasic cleavage site. However, after passages in TMPRSS2 knockout mice, an H3N2 subtype IAV became to undergo cleavage activation of HA showing high virulence for the mice by loss of an oligosaccharide at position 8 in the HA stalk region. Thus, the H3N2 IAV acquired the cleavability by an alternative activation mechanism/protease(s) for HA.
Copyright ? 2015, American Society for Microbiology. All Rights Reserved.
PMID: 25673722 [PubMed - as supplied by publisher]