About this Research Topic
As part of the first line of innate defense, hosts are equipped with a set of sensors called pattern recognition receptors (PRRs). They recognize conserved features of microorganisms called pathogen-associated molecular patterns (PAMPs), including microbial nucleic acid, proteins, and so on. So far, researchers have discovered five classes of PRRs. The Toll-like receptors (TLRs) and the C-type lectin receptors (CLRs) are both localized to the cell or endosomal membranes and recognize extracellular PAMPs, while intracellular PRRs including the cytoplasmic NOD-like receptors (NLRs), retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), and cytoplasmic DNA sensors, such as cyclic GMP-AMP synthase (cGAS) and interferon-γ (IFNγ)-inducible protein 16(IFI16) are found in the cytoplasm or nucleus. Although PRR-PAMP was initially thought to play a crucial role in bacterial invasion, we now understand that PRRs can also recognize viral structures and activate immune responses to defend against viruses.
The detection of viral nucleic acids was the main way for the host to sense viruses, mainly through different PRRs, including cGAS and IFI16 which recognize cytosolic viral dsDNA, RLRs that detect viral RNA, and different nucleic acid sensing TLRs. Activation of PRR signals is essential for establishing an antiviral state, followed by antiviral cytokines production and adaptive immune response. Viruses have also developed effective mechanisms to counteract or bypass PRRs. The past few decades have seen tremendous advances in our understanding of the interaction between viruses and host innate immune sensing. However, the repertoire of viral ligands targeting PRRs along with the downstream immunological events they initiated is still expanding, and some new concepts like inhibitory PRRs (iPRRs) emerging recently add another layer of complexity to this sensing and acting system. A better understanding of the PRRs in viral infection is of great significance for antiviral strategies.
Herein, by gathering novel evidence of human or animal PRRs (including those with inhibitory ability) on the control of viral infection and the mechanism of viral manipulation of PRRs, we hope to inform the development of next-generation antiviral therapeutics. Submissions, including but not limited to the following, are welcome:
• Novel membranous or cytosolic PRRs in viral infection
• Novel viral ligands detection
• PRRs related gene expression pattern upon viral stimuli
• Gene regulation coordination and metabolism
• Viral-PRRs’ impact on adaptive immunity
• PRRs related inborn errors (preferable clinical cases)
• Viral evasion strategies targeting PRRs
• Vaccines/therapeutic approaches targeting PRRs
• Context-dependent PRRs responses
• Viruses encoding TIR domain-containing proteins (bacteria equivalent is also acceptable in this case)
The detection of viral nucleic acids was the main way for the host to sense viruses, mainly through different PRRs, including cGAS and IFI16 which recognize cytosolic viral dsDNA, RLRs that detect viral RNA, and different nucleic acid sensing TLRs. Activation of PRR signals is essential for establishing an antiviral state, followed by antiviral cytokines production and adaptive immune response. Viruses have also developed effective mechanisms to counteract or bypass PRRs. The past few decades have seen tremendous advances in our understanding of the interaction between viruses and host innate immune sensing. However, the repertoire of viral ligands targeting PRRs along with the downstream immunological events they initiated is still expanding, and some new concepts like inhibitory PRRs (iPRRs) emerging recently add another layer of complexity to this sensing and acting system. A better understanding of the PRRs in viral infection is of great significance for antiviral strategies.
Herein, by gathering novel evidence of human or animal PRRs (including those with inhibitory ability) on the control of viral infection and the mechanism of viral manipulation of PRRs, we hope to inform the development of next-generation antiviral therapeutics. Submissions, including but not limited to the following, are welcome:
• Novel membranous or cytosolic PRRs in viral infection
• Novel viral ligands detection
• PRRs related gene expression pattern upon viral stimuli
• Gene regulation coordination and metabolism
• Viral-PRRs’ impact on adaptive immunity
• PRRs related inborn errors (preferable clinical cases)
• Viral evasion strategies targeting PRRs
• Vaccines/therapeutic approaches targeting PRRs
• Context-dependent PRRs responses
• Viruses encoding TIR domain-containing proteins (bacteria equivalent is also acceptable in this case)
Keywords: Pattern Recognition Receptors (PRRs), Pathogen-associated Molecular Patterns (PAMPs), Viral sensing, Inhibitory PRRs (iPRRs), Primary Immunodeficiencies
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