Influenza’s Newest Trick

ABSTRACT Influenza A viruses are important pathogens for humans and for many birds and mammals. Hemagglutinin and neuraminidase are the major surface proteins of this enveloped RNA virus. Hemagglutinin requires proteolytic cleavage for activation, but because the viral genome does not encode its own...

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Autor principal: Jeffery K. Taubenberger
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Lenguaje:EN
Publicado: American Society for Microbiology 2019
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Acceso en línea:https://doaj.org/article/397776b880824575b5af27c9efa39876
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spelling oai:doaj.org-article:397776b880824575b5af27c9efa398762021-11-15T15:54:48ZInfluenza’s Newest Trick10.1128/mBio.02854-192150-7511https://doaj.org/article/397776b880824575b5af27c9efa398762019-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.02854-19https://doaj.org/toc/2150-7511ABSTRACT Influenza A viruses are important pathogens for humans and for many birds and mammals. Hemagglutinin and neuraminidase are the major surface proteins of this enveloped RNA virus. Hemagglutinin requires proteolytic cleavage for activation, but because the viral genome does not encode its own protease, an exogenous serine protease must be provided by host cells. A novel, neuraminidase-dependent mechanism for hemagglutinin activation was described, in which a thrombin-like protease allows an influenza A/H7N6 virus, isolated from a mallard duck, to replicate systemically and induce enhanced disease in avian and mammalian model animals and to replicate in vitro in the absence of trypsin. Thrombin-like protease activation required the N6 neuraminidase, but also required the presence of a thrombin-like cleavage motif in the H7 hemagglutinin. This novel example of neuraminidase-dependent hemagglutinin activation demonstrates the extraordinary evolutionary flexibility of influenza A viruses and is a fascinating example of epistasis between the hemagglutinin and neuraminidase genes.Jeffery K. TaubenbergerAmerican Society for Microbiologyarticlehemagglutinininfluenzaneuraminidasepandemicviral pathogenesisMicrobiologyQR1-502ENmBio, Vol 10, Iss 6 (2019)
institution DOAJ
collection DOAJ
language EN
topic hemagglutinin
influenza
neuraminidase
pandemic
viral pathogenesis
Microbiology
QR1-502
spellingShingle hemagglutinin
influenza
neuraminidase
pandemic
viral pathogenesis
Microbiology
QR1-502
Jeffery K. Taubenberger
Influenza’s Newest Trick
description ABSTRACT Influenza A viruses are important pathogens for humans and for many birds and mammals. Hemagglutinin and neuraminidase are the major surface proteins of this enveloped RNA virus. Hemagglutinin requires proteolytic cleavage for activation, but because the viral genome does not encode its own protease, an exogenous serine protease must be provided by host cells. A novel, neuraminidase-dependent mechanism for hemagglutinin activation was described, in which a thrombin-like protease allows an influenza A/H7N6 virus, isolated from a mallard duck, to replicate systemically and induce enhanced disease in avian and mammalian model animals and to replicate in vitro in the absence of trypsin. Thrombin-like protease activation required the N6 neuraminidase, but also required the presence of a thrombin-like cleavage motif in the H7 hemagglutinin. This novel example of neuraminidase-dependent hemagglutinin activation demonstrates the extraordinary evolutionary flexibility of influenza A viruses and is a fascinating example of epistasis between the hemagglutinin and neuraminidase genes.
format article
author Jeffery K. Taubenberger
author_facet Jeffery K. Taubenberger
author_sort Jeffery K. Taubenberger
title Influenza’s Newest Trick
title_short Influenza’s Newest Trick
title_full Influenza’s Newest Trick
title_fullStr Influenza’s Newest Trick
title_full_unstemmed Influenza’s Newest Trick
title_sort influenza’s newest trick
publisher American Society for Microbiology
publishDate 2019
url https://doaj.org/article/397776b880824575b5af27c9efa39876
work_keys_str_mv AT jefferyktaubenberger influenzasnewesttrick
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