When viruses infect cells, their nucleic acids can often be detected by the host cell's pattern recognition receptors (PRRs). The sensing of non-self nucleic acids activates various host signaling pathways, one of which culminates in the production of a group of proteins termed type I interferons (IFN-I). IFNs act in an autocrine and paracrine manner to induce antiviral defense mechanisms which restrict viral spread and preserve organismal tissue integrity.
In recent years, a number of immune disorders associated with mutations in host genes involved in the modification or degradation of host nucleic acids, or/and mutations associated with the auto-activation of PRRs have been described. Many of these disease-causing mutations lead to chronic activation of PRRs and the constitutive production of IFN-I. This dysregulation of the IFN-I response leads to hyper-inflammation and tissue destruction, resulting in diseases referred to as type I interferonopathies. Studies of interferonopathies have contributed key insights into the molecular regulation of nucleic acid sensing, providing unique models for understanding homeostatic mechanisms the host employs to limit sensing of self but still mount robust anti-viral immune responses during viral infection.
The goal of this Research Topic is to understand how eukaryotic cells molecularly distinguish between self and non-self nucleic acids. This direction is important not only for developing new strategies for antiviral therapies, but also to understand the role of nucleic acid recognition pathways in metabolism, the etiology of autoimmune diseases, and antiviral immunity.
We encourage authors to submit papers on viral sensing mechanisms deployed by the host to prevent infectious disease, with an emphasis on the regulation of IFN-I signaling. We also welcome manuscripts on the genes involved in nucleic acid metabolism which contribute to sterile inflammation when mutated.
When viruses infect cells, their nucleic acids can often be detected by the host cell's pattern recognition receptors (PRRs). The sensing of non-self nucleic acids activates various host signaling pathways, one of which culminates in the production of a group of proteins termed type I interferons (IFN-I). IFNs act in an autocrine and paracrine manner to induce antiviral defense mechanisms which restrict viral spread and preserve organismal tissue integrity.
In recent years, a number of immune disorders associated with mutations in host genes involved in the modification or degradation of host nucleic acids, or/and mutations associated with the auto-activation of PRRs have been described. Many of these disease-causing mutations lead to chronic activation of PRRs and the constitutive production of IFN-I. This dysregulation of the IFN-I response leads to hyper-inflammation and tissue destruction, resulting in diseases referred to as type I interferonopathies. Studies of interferonopathies have contributed key insights into the molecular regulation of nucleic acid sensing, providing unique models for understanding homeostatic mechanisms the host employs to limit sensing of self but still mount robust anti-viral immune responses during viral infection.
The goal of this Research Topic is to understand how eukaryotic cells molecularly distinguish between self and non-self nucleic acids. This direction is important not only for developing new strategies for antiviral therapies, but also to understand the role of nucleic acid recognition pathways in metabolism, the etiology of autoimmune diseases, and antiviral immunity.
We encourage authors to submit papers on viral sensing mechanisms deployed by the host to prevent infectious disease, with an emphasis on the regulation of IFN-I signaling. We also welcome manuscripts on the genes involved in nucleic acid metabolism which contribute to sterile inflammation when mutated.
