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• W2192863617 startingPage "351" @default.
• W2192863617 abstract "Influenza A virus (IAV) causes significant morbidity and mortality. The knowledge gained within the last decade on the pandemic IAV(H1N1)2009 improved our understanding not only of the viral pathogenicity but also the host cellular factors involved in the pathogenicity of multiorgan failure (MOF), such as cellular trypsin-type hemagglutinin (HA0) processing proteases for viral multiplication, cytokine storm, metabolic disorders and energy crisis. The HA processing proteases in the airway and organs for all IAV known to date have been identified. Recently, 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. Furthermore, the relationship between causative factors has been summarized as the “influenza virus–cytokine–trypsin” cycle interconnected with the “metabolic disorders–cytokine” cycle. These cycles provide new treatment concepts for ATP crisis and MOF. This review discusses IAV pathogenicity on cellular proteases, cytokines, metabolites and therapeutic options." @default.
• W2192863617 created "2016-06-24" @default.
• W2192863617 creator A5087962680 @default.
• W2192863617 date "2015-01-01" @default.
• W2192863617 modified "2023-09-30" @default.
• W2192863617 title "Influenza virus pathogenicity regulated by host cellular proteases, cytokines and metabolites, and its therapeutic options" @default.
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• W2192863617 doi "https://doi.org/10.2183/pjab.91.351" @default.
• W2192863617 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4729853" @default.
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