What is it about?
The hemagglutinin (HA) protein of influenza virus mediates viral entry into cells. For this, HA needs to be cleaved by a cellular protease. Our previous research showed that the cellular serine protease TMPRSS2 can cleave HA and that TMPRSS2 activity is required for influenza A viruses to replicate in mice and to cause disease. Here, we shown that the TMPRSS2 related protease TMPRSS11A can also cleave HA in cell culture and we provide evidence that TMPRSS11A is expressed in viral target cells in mice. Finally, we demonstrate that an endogenous inhibitor of TMPRSS2 activity does not block TMPRSS11A.
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Why is it important?
Our results suggest that TMPRSS11A could support influenza A virus spread in case TMPRSS2 is not available.
Perspectives
TMPRSS2 activity is important for influenza A virus spread in mice and most likely also in humans and constitutes a potential target for antiviral intervention. Therefore, it is important to analyze whether certain influenza A viruses can employ related enzymes for spread if TMPRSS2 is not available.
Professor Stefan Pöhlmann
German Primate Center
Read the Original
This page is a summary of: TMPRSS11A activates the influenza A virus hemagglutinin and the MERS coronavirus spike protein and is insensitive against blockade by HAI-1, Journal of Biological Chemistry, July 2018, American Society for Biochemistry & Molecular Biology (ASBMB),
DOI: 10.1074/jbc.ra118.001273.
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