The interferon response circuit: Induction and suppression by pathogenic viruses
By O. Haller, G. Kochs, F. Weber. Virology, 2005
725 citations recorded by the source corpus.
Type I interferons (IFN-α/β) are potent antiviral cytokines and modulators of the adaptive immune system. They are induced by viral infection or by double-stranded RNA (dsRNA), a by-product of viral replication, and lead to the production of a broad range of antiviral proteins and immunoactive cytokines. Viruses, in turn, have evolved multiple strategies to counter the IFN system which would otherwise stop virus growth early in infection. Here we discuss the current view on the balancing act between virus-induced IFN responses and the viral counterplayers.
Subfields: Animal Science and Zoology, Immunology, Infectious Diseases
View Paper: https://www.semanticscholar.org/paper/6061714e53d28a6e22e1dd87c17104853ccb1da3
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In Animal Science and Zoology
In Immunology
In Infectious Diseases
Citations in the corpus
- SARS-Coronavirus Replication Is Supported by a Reticulovesicular Network of Modified Endoplasmic Reticulum (2008, background): “Both SARSCoV and MHV [72–74] were found to counteract the induction of interferon via cytoplasmic pattern recognition receptors that can sense the presence of viral dsRNA [9,10] and possibly also viral negative-strand RNAs carrying uncapped 59-triphosphates [75].”
- Influenza A virus NS1 targets the ubiquitin ligase TRIM25 to evade recognition by RIG-I (2009, background): “Specifically, virus-encoded IFN antagonists inhibit host innate antiviral responses by targeting IFN gene expression or IFN-induced host effector molecules (Garcia-Sastre and Biron, 2006; Haller et al., 2006).”
- The cytokine storm in COVID-19: An overview of the involvement of the chemokine/chemokine-receptor system (2020, positive): “by the first contact with a virus can slow down viral multiplication and “buy time” for the organism to establish a more efficient adaptive immune response [56].”