About this Research Topic
Given the success of Research Topic The Role of Inflammasome in Viral Infection and the rapidly evolving subject area, we are pleased to announce the launch of Volume II.
Pattern-recognition receptors (PRRs) are important cellular molecules that recognize foreign pathogens. Several families of PRRs function as components of the inflammasome complex, including the nucleotide-binding domain, leucine-rich repeat-containing proteins (also known as NOD-like receptors, NLRs) and the absent in melanoma 2 (AIM)-like receptors (ALRs) in both mice and humans. They sense certain stimuli such as mitochondrial factors released into the cytosol (mitochondrial ROS, mitochondrial DNA, or cardiolipin), and then oligomerize to assemble the inflammasome complex that activates caspase-1. The active caspase-1 cleaves IL-1/18 into the mature forms, or cleaves GSDMD to induce pyroptosis. Inflammasome has been proved to participate in a variety of autoimmune and autoinflammatory diseases. In recent years, it has been found that inflammasome plays an important role in viral infection and virus-induced inflammatory diseases including infectious hepatitis, pulmonitis, nephritis, myocarditis, and so on. Various viruses activate inflammasome in monocytes/macrophages through their proteins or other components, which subsequently trigger antiviral immune responses or infectious inflammation.
This Research Topic focuses on original findings about the biological role of inflammasome in viral infection and infectious diseases. Although the classical activation pathways of inflammasome are well defined, the pathways that viruses activate the assembly of inflammasome directly or indirectly need to be further clarified. Studies on how inflammasome participates and influences the acute or chronic pathogenic processes caused by viral infection in specific disease models deserve to be encouraged. Besides, developing intervention approaches targeting inflammasome to improve antiviral immunity or alleviate viral pathogenicity is appreciated.
We seek Original Research Articles, Reviews, Mini-Reviews, Perspectives, and Brief Research Reports that discuss the latest discoveries in inflammasome research upon viral infection. For details, we are committed to reporting studies on:
(1) The molecular mechanism that mediates inflammasome activation during the infection of viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Monkeypox virus (MPV), human immunodeficiency virus (HIV), Dengue virus (DENV), Zika virus (ZIKV), hepatitis B virus (HBV) and so on.
(2) The role of specific kinds of inflammasome (such as inflammasome of NLRP3, AIM2, NLRC4, NLRP6 and so on) in immune regulation or inflammation stimulation that drives viral infectious diseases.
(3) The intervention approaches targeting inflammasome via developing effective small molecule compounds, adapter DNA/RNA, siRNA, peptide or other biomaterials, aiming at therapeutic strategies for virus-related diseases.
Pattern-recognition receptors (PRRs) are important cellular molecules that recognize foreign pathogens. Several families of PRRs function as components of the inflammasome complex, including the nucleotide-binding domain, leucine-rich repeat-containing proteins (also known as NOD-like receptors, NLRs) and the absent in melanoma 2 (AIM)-like receptors (ALRs) in both mice and humans. They sense certain stimuli such as mitochondrial factors released into the cytosol (mitochondrial ROS, mitochondrial DNA, or cardiolipin), and then oligomerize to assemble the inflammasome complex that activates caspase-1. The active caspase-1 cleaves IL-1/18 into the mature forms, or cleaves GSDMD to induce pyroptosis. Inflammasome has been proved to participate in a variety of autoimmune and autoinflammatory diseases. In recent years, it has been found that inflammasome plays an important role in viral infection and virus-induced inflammatory diseases including infectious hepatitis, pulmonitis, nephritis, myocarditis, and so on. Various viruses activate inflammasome in monocytes/macrophages through their proteins or other components, which subsequently trigger antiviral immune responses or infectious inflammation.
This Research Topic focuses on original findings about the biological role of inflammasome in viral infection and infectious diseases. Although the classical activation pathways of inflammasome are well defined, the pathways that viruses activate the assembly of inflammasome directly or indirectly need to be further clarified. Studies on how inflammasome participates and influences the acute or chronic pathogenic processes caused by viral infection in specific disease models deserve to be encouraged. Besides, developing intervention approaches targeting inflammasome to improve antiviral immunity or alleviate viral pathogenicity is appreciated.
We seek Original Research Articles, Reviews, Mini-Reviews, Perspectives, and Brief Research Reports that discuss the latest discoveries in inflammasome research upon viral infection. For details, we are committed to reporting studies on:
(1) The molecular mechanism that mediates inflammasome activation during the infection of viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Monkeypox virus (MPV), human immunodeficiency virus (HIV), Dengue virus (DENV), Zika virus (ZIKV), hepatitis B virus (HBV) and so on.
(2) The role of specific kinds of inflammasome (such as inflammasome of NLRP3, AIM2, NLRC4, NLRP6 and so on) in immune regulation or inflammation stimulation that drives viral infectious diseases.
(3) The intervention approaches targeting inflammasome via developing effective small molecule compounds, adapter DNA/RNA, siRNA, peptide or other biomaterials, aiming at therapeutic strategies for virus-related diseases.
Keywords: inflammasome, virus, infectious disease, IL-1 family, pyroptosis
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
