Virus infection sensing by host cells is key for the induction of an anti-viral state in bystander cells and in the infected cells themselves as well as for the elicitation of both the innate and the adaptive immune responses, which are required to fight the virus. Host cells detect pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) that, when activated, lead to signal transduction events resulting in the expression of cytokines including type I interferons (IFNs). Type I IFNs act in autocrine and paracrine manners and elicit the expression of IFN-stimulated genes (ISGs) that lead to the establishment of a cellular anti-viral state. Along with the induction of IFNs/pro-inflammatory cytokines, virus-infected cells often present dramatic reorganization of their cytoskeleton and activation of stress pathways such as autophagy, the unfolded protein response (UPR), and cellular death.
The goal of this research topic is to allow authors to help clarify how actin/microtubule cytoskeleton remodeling as well as cell stress pathway engagement occur following virus infection and the innate immune sensing of viral PAMPs by PRRs and downstream secretion of type I IFNs and expression of ISGs. Although many groups have highlighted intense reorganizations of the cytoskeleton during virus infection, which can in some instances favor virus trafficking to cellular locations suitable for virus replication, the mechanism regulating these effects and their impact on cell anti-viral state remain to be clarified. Several studies highlighted that the induction of cell stress response such as the UPR and autophagy and even cellular death can directly or indirectly impact viral replication, but mechanism at play and the impacts of such stress pathways on the induction of type I IFN and pro-inflammatory cytokines by the infected cells remains to be better understood. Precise fine-tuning of cytoskeleton dynamics and of cell stress pathways experimentally during virus infection may help better understand the implications of these pathways on host cell responses to virus infection.
Manuscripts of interest would be the ones that describe, the following cell infection by DNA or RNA viruses:
• Changes in cytoskeleton organization
• The induction of cell stress or cell death pathways
• The acquisition of an anti-viral state in infected and/or bystander cells
• The impacts of cytoskeleton dynamics or cell stress pathway engagement on the anti-viral state establishment in cells
The experimental approaches of interest could be:
• Experimental models using novel genetical/chemical means of perturbing cytoskeleton dynamics and stress pathways in highly specific manners to demonstrate the impacts of such perturbations on anti-viral state acquisition in human or mouse cell lines or primary cells.
• In vivo mouse models within which stress/death pathways or cytoskeleton dynamics can be monitored and/or altered during virus infection. The alteration would allow the study of the impact of these pathways on the anti-viral immune response, including the priming of the adaptive immune response.
• In vitro/ex vivo only studies would be suitable too if mechanisms are well characterized.
Virus infection sensing by host cells is key for the induction of an anti-viral state in bystander cells and in the infected cells themselves as well as for the elicitation of both the innate and the adaptive immune responses, which are required to fight the virus. Host cells detect pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) that, when activated, lead to signal transduction events resulting in the expression of cytokines including type I interferons (IFNs). Type I IFNs act in autocrine and paracrine manners and elicit the expression of IFN-stimulated genes (ISGs) that lead to the establishment of a cellular anti-viral state. Along with the induction of IFNs/pro-inflammatory cytokines, virus-infected cells often present dramatic reorganization of their cytoskeleton and activation of stress pathways such as autophagy, the unfolded protein response (UPR), and cellular death.
The goal of this research topic is to allow authors to help clarify how actin/microtubule cytoskeleton remodeling as well as cell stress pathway engagement occur following virus infection and the innate immune sensing of viral PAMPs by PRRs and downstream secretion of type I IFNs and expression of ISGs. Although many groups have highlighted intense reorganizations of the cytoskeleton during virus infection, which can in some instances favor virus trafficking to cellular locations suitable for virus replication, the mechanism regulating these effects and their impact on cell anti-viral state remain to be clarified. Several studies highlighted that the induction of cell stress response such as the UPR and autophagy and even cellular death can directly or indirectly impact viral replication, but mechanism at play and the impacts of such stress pathways on the induction of type I IFN and pro-inflammatory cytokines by the infected cells remains to be better understood. Precise fine-tuning of cytoskeleton dynamics and of cell stress pathways experimentally during virus infection may help better understand the implications of these pathways on host cell responses to virus infection.
Manuscripts of interest would be the ones that describe, the following cell infection by DNA or RNA viruses:
• Changes in cytoskeleton organization
• The induction of cell stress or cell death pathways
• The acquisition of an anti-viral state in infected and/or bystander cells
• The impacts of cytoskeleton dynamics or cell stress pathway engagement on the anti-viral state establishment in cells
The experimental approaches of interest could be:
• Experimental models using novel genetical/chemical means of perturbing cytoskeleton dynamics and stress pathways in highly specific manners to demonstrate the impacts of such perturbations on anti-viral state acquisition in human or mouse cell lines or primary cells.
• In vivo mouse models within which stress/death pathways or cytoskeleton dynamics can be monitored and/or altered during virus infection. The alteration would allow the study of the impact of these pathways on the anti-viral immune response, including the priming of the adaptive immune response.
• In vitro/ex vivo only studies would be suitable too if mechanisms are well characterized.
