Viruses are intracellular obligate parasites that rely purely on the host cell for replication. The first step in initiating effective viral infection is breaking through the cytomembrane to enter the cell. Next, several adaptor proteins contribute to clathrin-mediated endocytosis of virus entry. After entering the cell, viruses are ultimately dependent on the host cell for their replication via altering cellular signal transduction pathways, including PI3K/Akt, mitogen-activated protein kinases, NF-kappaB, programmed cell death, autophagy, RIG-I-MAVS and cGAS-STING DNA sensing signals, and inflammasome activation signals. Research data documented on the involvement of various cellular proteins or molecules in the replication of viruses have provided essential insights into understanding the viral pathogenesis and have led to the development of antiviral therapeutics.
Increasing research data has shown that many cellular signal transduction pathways contribute to viral infection and replication. However, the underlying molecular pathogenesis will facilitate further revealing the molecular pathogenesis of virus infections, such as:
• How viruses trigger and maintain infection when binding with receptors and interacting with host cells
• How viruses interfere with the functions of the signalling factors that are responsible for the induction and maintenance of viral infection
• How the activation of the RIG-I-MAVS and cGAS-STING DNA sensing pathways contributes to virus replication and immune response
• How viruses alter the microRNAs and lncRNAs of host cells that regulate viral infection and pathogenicity
The following topics are welcomed but not limited to:
• Host cellular signal pathways during virus infection, including PI3K/Akt, mitogen-activated protein kinases, NF-kappaB signals
• Roles of adaptor proteins during endocytosis of virus entry
• Crosstalks between virus infection and programmed cell death/autophagy/inflammasome activation/immune response
• The activation of the RIG-I-MAVS and cGAS-STING DNA sensing pathways during virus infection
• Virus infection and replication regulated by miRNAs, lncRNAs, etc.
Viruses are intracellular obligate parasites that rely purely on the host cell for replication. The first step in initiating effective viral infection is breaking through the cytomembrane to enter the cell. Next, several adaptor proteins contribute to clathrin-mediated endocytosis of virus entry. After entering the cell, viruses are ultimately dependent on the host cell for their replication via altering cellular signal transduction pathways, including PI3K/Akt, mitogen-activated protein kinases, NF-kappaB, programmed cell death, autophagy, RIG-I-MAVS and cGAS-STING DNA sensing signals, and inflammasome activation signals. Research data documented on the involvement of various cellular proteins or molecules in the replication of viruses have provided essential insights into understanding the viral pathogenesis and have led to the development of antiviral therapeutics.
Increasing research data has shown that many cellular signal transduction pathways contribute to viral infection and replication. However, the underlying molecular pathogenesis will facilitate further revealing the molecular pathogenesis of virus infections, such as:
• How viruses trigger and maintain infection when binding with receptors and interacting with host cells
• How viruses interfere with the functions of the signalling factors that are responsible for the induction and maintenance of viral infection
• How the activation of the RIG-I-MAVS and cGAS-STING DNA sensing pathways contributes to virus replication and immune response
• How viruses alter the microRNAs and lncRNAs of host cells that regulate viral infection and pathogenicity
The following topics are welcomed but not limited to:
• Host cellular signal pathways during virus infection, including PI3K/Akt, mitogen-activated protein kinases, NF-kappaB signals
• Roles of adaptor proteins during endocytosis of virus entry
• Crosstalks between virus infection and programmed cell death/autophagy/inflammasome activation/immune response
• The activation of the RIG-I-MAVS and cGAS-STING DNA sensing pathways during virus infection
• Virus infection and replication regulated by miRNAs, lncRNAs, etc.
