Identification of trypsin I as a candidate for influenza A virus and Sendai virus envelope glycoprotein processing protease in rat brain

@inproceedings{QuangLe2006IdentificationOT,
  title={Identification of trypsin I as a candidate for influenza A virus and Sendai virus envelope glycoprotein processing protease in rat brain},
  author={Trong Quang Le and Miki Kawachi and Hiroshi Yamada and Mayumi Shiota and Yuushi Okumura and Hiroshi Kido},
  booktitle={Biological chemistry},
  year={2006}
}
Abstract Extracellular cleavage of virus envelope fusion glycoprotein hemagglutinin (HA0) by host trypsin-like proteases is a prerequisite for the infectivity and pathogenicity of human influenza A viruses and Sendai virus. The common epidemic influenza A viruses are pneumotropic, but occasionally cause encephalopathy or encephalitis, although the HA0 processing enzyme in the brain has not been identified. In searching for the brain processing proteases, we identified a processing enzyme in rat… 
Host envelope glycoprotein processing proteases are indispensable for entry into human cells by seasonal and highly pathogenic avian influenza viruses
  • H. Kido, Y. Okumura, +5 authors M. Yano
  • Biology, Medicine
    Journal of molecular and genetic medicine : an international journal of biomedical research
  • 2008
TLDR
These proteases are discussed as new drug target molecules for IAV treatment acting by inhibition of IAV multiplication and prevention of multiple organ failure, other than anti-viral agents, viral neuraminidase inhibitors.
Role of host trypsin-type serine proteases and influenza virus-cytokine-trypsin cycle in influenza viral pathogenesis. Pathogenesis-based therapeutic options.
TLDR
Application of protease inhibitors and treatment of metabolic disorders that break these cycles and their interconnection is therefore a promising therapeutic approach against influenza.
Role of host cellular proteases in the pathogenesis of influenza and influenza-induced multiple organ failure.
TLDR
The roles of cellular proteases in the pathogenesis of IAV are discussed and the molecular mechanisms of upregulation of trypsins and matrix metalloproteinase-9 are highlighted as effective targets for the control of Iav infection.
Modifications to the Hemagglutinin Cleavage Site Control the Virulence of a Neurotropic H1N1 Influenza Virus
TLDR
An additional mutation in the P2 position of the WSN HA cleavage site (S328Y) that appears to control virus spread in a plasmin-dependent manner is identified and wild-type HA (Y328) was more efficiently cleaved by pl asmin than S328 HA.
Novel Type II Transmembrane Serine Proteases, MSPL and TMPRSS13, Proteolytically Activate Membrane Fusion Activity of the Hemagglutinin of Highly Pathogenic Avian Influenza Viruses and Induce Their Multicycle Replication
TLDR
It is reported here that ubiquitous type II transmembrane serine proteases, MSPL and its splice variant TMPRSS13, are novel candidates for proteases processing HA proteins of highly pathogenic avian influenza (HPAI) viruses, apart from the previously identified furin and proprotein convertases 5 and 6.
Changing the Protease Specificity for Activation of a Flavivirus, Tick-Borne Encephalitis Virus
TLDR
The results demonstrate that flaviviruses with altered protease specificities can be generated and suggest that this approach can be used for the construction of viral mutants or vectors that can be activated on demand and have restricted tissue tropism and virulence.
Influenza virus pathogenicity regulated by host cellular proteases, cytokines and metabolites, and its therapeutic options
  • H. Kido
  • Biology, Medicine
    Proceedings of the Japan Academy. Series B, Physical and biological sciences
  • 2015
TLDR
A new concept on the pathogenicity of MOF, the “influenza virus–cytokine–trypsin” cycle, has been proposed involving up-regulation of trypsin through pro-inflammatory cytokines, and potentiation of viral multiplication in various organs.
Up-regulation of ectopic trypsins in the myocardium by influenza A virus infection triggers acute myocarditis
TLDR
IAV-induced trypsins, particularly trypsin2, in the myocardium trigger acute viral myocarditis through stimulation of IAV replication, proMMP-9 activation, and cytokine induction, and aprotinin treatment suggest.
The Role of Secreted Serine Proteases of the Host in Influenza Viral Pathogenesis
TLDR
Application of protease inhibitors counteracting the effects of proinflammatory cytokines induced in influenza virus infections upregulate production of the proteases and enhance virus replication, tissue damage, and metabolic disorders.
IL-1β is a key cytokine that induces trypsin upregulation in the influenza virus–cytokine–trypsin cycle
TLDR
It is suggested that IL-1β plays a key role in trypsin upregulation and has a pathological role in multiple organ failure.
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