scholarly journals TRIM4 modulates type I interferon induction and cellular antiviral response by targeting RIG-I for K63-linked ubiquitination

2014 ◽  
Vol 6 (2) ◽  
pp. 154-163 ◽  
Author(s):  
J. Yan ◽  
Q. Li ◽  
A.-P. Mao ◽  
M.-M. Hu ◽  
H.-B. Shu
Keyword(s):  
Type I Interferon ◽  
Antiviral Response ◽  
Type I ◽  
Interferon Induction ◽  
Cellular Antiviral Response

scholarly journals Positive natural selection in primate genes of the type I interferon response

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Elena N. Judd ◽  
Alison R. Gilchrist ◽  
Nicholas R. Meyerson ◽  
Sara L. Sawyer
Keyword(s):  
Natural Selection ◽  
Positive Selection ◽  
Type I Interferon ◽  
Interferon Response ◽  
Type I ◽  
Sequence Alignments ◽  
Multiple Sequence ◽  
Multiple Sequence Alignments ◽  
Interferon Stimulated Genes ◽  
Interferon Induction

Abstract Background The Type I interferon response is an important first-line defense against viruses. In turn, viruses antagonize (i.e., degrade, mis-localize, etc.) many proteins in interferon pathways. Thus, hosts and viruses are locked in an evolutionary arms race for dominance of the Type I interferon pathway. As a result, many genes in interferon pathways have experienced positive natural selection in favor of new allelic forms that can better recognize viruses or escape viral antagonists. Here, we performed a holistic analysis of selective pressures acting on genes in the Type I interferon family. We initially hypothesized that the genes responsible for inducing the production of interferon would be antagonized more heavily by viruses than genes that are turned on as a result of interferon. Our logic was that viruses would have greater effect if they worked upstream of the production of interferon molecules because, once interferon is produced, hundreds of interferon-stimulated proteins would activate and the virus would need to counteract them one-by-one. Results We curated multiple sequence alignments of primate orthologs for 131 genes active in interferon production and signaling (herein, “induction” genes), 100 interferon-stimulated genes, and 100 randomly chosen genes. We analyzed each multiple sequence alignment for the signatures of recurrent positive selection. Counter to our hypothesis, we found the interferon-stimulated genes, and not interferon induction genes, are evolving significantly more rapidly than a random set of genes. Interferon induction genes evolve in a way that is indistinguishable from a matched set of random genes (22% and 18% of genes bear signatures of positive selection, respectively). In contrast, interferon-stimulated genes evolve differently, with 33% of genes evolving under positive selection and containing a significantly higher fraction of codons that have experienced selection for recurrent replacement of the encoded amino acid. Conclusion Viruses may antagonize individual products of the interferon response more often than trying to neutralize the system altogether.

PS1-122 Unraveling the complexity of the type I interferon antiviral response

Cytokine ◽  
2011 ◽  
Vol 56 (1) ◽  
pp. 48 ◽  
Author(s):  
John W. Schoggins ◽  
Sam J. Wilson ◽  
Maryline Panis ◽  
Mary Y. Murphy ◽  
Christopher T. Jones ◽  
...  
Keyword(s):  
Type I Interferon ◽  
Antiviral Response ◽  
Type I

Obesity worsens the outcome of influenza virus infection associated with impaired type I interferon induction in mice

2019 ◽  
Vol 513 (2) ◽  
pp. 405-411 ◽  
Author(s):  
Ho Namkoong ◽  
Makoto Ishii ◽  
Hideki Fujii ◽  
Takahiro Asami ◽  
Kazuma Yagi ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Type I Interferon ◽  
Influenza Virus Infection ◽  
Type I ◽  
Interferon Induction

scholarly journals A diverse range of gene products are effectors of the type I interferon antiviral response

Nature ◽  
2011 ◽  
Vol 472 (7344) ◽  
pp. 481-485 ◽  
Author(s):  
John W. Schoggins ◽  
Sam J. Wilson ◽  
Maryline Panis ◽  
Mary Y. Murphy ◽  
Christopher T. Jones ◽  
...  
Keyword(s):  
Type I Interferon ◽  
Antiviral Response ◽  
Type I ◽  
Gene Products ◽  
Diverse Range
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