Hospitalized patients with severe influenza infections develop an acute respiratory distress syndrome characterized by widespread alveolar-capillary damage, parenchymal hemorrhage, edema, pulmonary microvascular thrombosis, and hyper-inflammatory cytokine response. While compelling evidence indicates a critical role of an aggravated host-innate immune response, underlying mechanisms of innate immune regulation pathways contributing to these pathologic events remain unclear. Antiviral drug administration is not always effective in controlling mortality rates in severe influenza cases, as considerable lung pathology is mediated by host-related factors in addition to virus-inflicted cytotoxicity. However, there is a constant debate on the protection vs injury role of the innate immune response during influenza.
This Research Topic covers a wide range of topics on the role of host-innate immune regulation in response to the influenza virus pathogenesis. Researchers may contribute Reviews/Mini-Reviews, Original Research or Method articles in the following (but not limited to) topics:
- Studies on virus-host cell interactions and their impact on the host innate immune response in different animal species and in vitro culture systems
- Various highly influential signaling pathways in innate immune regulation and their role in influenza-induced acute lung injury (e.g. Toll-like receptors (TLRs), neutrophil extracellular traps (NETs)-mediated inflammation and inflammasome signaling pathways)
- Targeting innate immune regulation in influenza alone or in combination with antiviral agents– therapeutic strategies
- Regulation of innate immune response in different animal species, comparative pathology, and therapeutic intervention strategies
- Studies on the signaling events that interplay between innate and adaptive immunity
Hospitalized patients with severe influenza infections develop an acute respiratory distress syndrome characterized by widespread alveolar-capillary damage, parenchymal hemorrhage, edema, pulmonary microvascular thrombosis, and hyper-inflammatory cytokine response. While compelling evidence indicates a critical role of an aggravated host-innate immune response, underlying mechanisms of innate immune regulation pathways contributing to these pathologic events remain unclear. Antiviral drug administration is not always effective in controlling mortality rates in severe influenza cases, as considerable lung pathology is mediated by host-related factors in addition to virus-inflicted cytotoxicity. However, there is a constant debate on the protection vs injury role of the innate immune response during influenza.
This Research Topic covers a wide range of topics on the role of host-innate immune regulation in response to the influenza virus pathogenesis. Researchers may contribute Reviews/Mini-Reviews, Original Research or Method articles in the following (but not limited to) topics:
- Studies on virus-host cell interactions and their impact on the host innate immune response in different animal species and in vitro culture systems
- Various highly influential signaling pathways in innate immune regulation and their role in influenza-induced acute lung injury (e.g. Toll-like receptors (TLRs), neutrophil extracellular traps (NETs)-mediated inflammation and inflammasome signaling pathways)
- Targeting innate immune regulation in influenza alone or in combination with antiviral agents– therapeutic strategies
- Regulation of innate immune response in different animal species, comparative pathology, and therapeutic intervention strategies
- Studies on the signaling events that interplay between innate and adaptive immunity