The innate immune system is the first line of host defense against pathogens. During viral infections, the host innate immune system acts as a first-line defense to prevent viral invasion or replication before more specific protection by the adaptive immune system ensues. Innate immune responses are not specific to a particular pathogen in the way that the adaptive immune responses are. They depend on a group of proteins and phagocytic cells that recognize conserved features of pathogens and become quickly activated to help destroy invaders. Upon infection, the invading pathogens are rapidly detected by the host pattern-recognition receptors (PRRs) such as Toll-like receptors (TLRs), C-type lectin-like receptors, a retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), and the nucleotide-binding oligomerization domain (NOD)-like receptor family proteins (NLRs). As a result, the activation of these receptors result in cytokine and chemokine production, phagocytosis as well as antigen presentation to the adaptive immune system. The PRRs detect specific viral components such as viral RNA or DNA or viral intermediate products and induce type I interferons (IFNs) and other pro-inflammatory cytokines in the infected cells and other immune cells. However, over-activation of the innate immune response can cause systemic inflammation and tissue damage. Viruses use different strategies to counter the antiviral state posed by the innate immune response by shutting down the PRR-induced pathways. Once the pathogen infection is established, it leads to the excessive production of proinflammatory cytokines that results in aggressive pro-inflammatory responses and insufficient control of anti-inflammatory responses that leads to “cytokine storm”, which is one of the reasons for the increased mortality during virus infections.
There is still a knowledge gap in how host innate immunity response varies for different viruses and which factors or events determine whether the infection may lead to the host tissue damage or not. Importantly, how viruses induce cytokine storms and cause severe inflammatory diseases like acute respiratory distress syndrome (ARDS). This Research Topic will further our understanding of host-virus interaction and its impact on host-pathogen biology by welcoming Original Research, Reviews and Mini-Reviews on virus-induced innate immune responses and inflammation.
The innate immune system is the first line of host defense against pathogens. During viral infections, the host innate immune system acts as a first-line defense to prevent viral invasion or replication before more specific protection by the adaptive immune system ensues. Innate immune responses are not specific to a particular pathogen in the way that the adaptive immune responses are. They depend on a group of proteins and phagocytic cells that recognize conserved features of pathogens and become quickly activated to help destroy invaders. Upon infection, the invading pathogens are rapidly detected by the host pattern-recognition receptors (PRRs) such as Toll-like receptors (TLRs), C-type lectin-like receptors, a retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), and the nucleotide-binding oligomerization domain (NOD)-like receptor family proteins (NLRs). As a result, the activation of these receptors result in cytokine and chemokine production, phagocytosis as well as antigen presentation to the adaptive immune system. The PRRs detect specific viral components such as viral RNA or DNA or viral intermediate products and induce type I interferons (IFNs) and other pro-inflammatory cytokines in the infected cells and other immune cells. However, over-activation of the innate immune response can cause systemic inflammation and tissue damage. Viruses use different strategies to counter the antiviral state posed by the innate immune response by shutting down the PRR-induced pathways. Once the pathogen infection is established, it leads to the excessive production of proinflammatory cytokines that results in aggressive pro-inflammatory responses and insufficient control of anti-inflammatory responses that leads to “cytokine storm”, which is one of the reasons for the increased mortality during virus infections.
There is still a knowledge gap in how host innate immunity response varies for different viruses and which factors or events determine whether the infection may lead to the host tissue damage or not. Importantly, how viruses induce cytokine storms and cause severe inflammatory diseases like acute respiratory distress syndrome (ARDS). This Research Topic will further our understanding of host-virus interaction and its impact on host-pathogen biology by welcoming Original Research, Reviews and Mini-Reviews on virus-induced innate immune responses and inflammation.
