Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 23, Pages 9822-9827Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0610352104
Keywords
antiviral response; interferon antagonists; interferon receptors; poxviruses; virus evasion
Categories
Funding
- MRC [G0501257] Funding Source: UKRI
- Medical Research Council [G0501257] Funding Source: Medline
- NIAID NIH HHS [R01 AI051139, AI057468, R01 AI057468] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Medical Research Council [G0501257] Funding Source: researchfish
Ask authors/readers for more resources
Type I (IFN-alpha/beta) and type III (IFN-lambda s) IFNs are important components of the host antiviral response. Although type III IFINs possess intrinsic antiviral activity similar to that of type I IFNs, they signal through a specific unique receptor complex, and their functional importance for antiviral resistance is largely uncharacterized. Here, we report the first virus defense mechanism that directly targets type III IFINs. Y136 from Yaba-like disease virus, a yatapoxvirus, is a secreted glycoprotein related to protein 1318 from Vaccinia virus, a known type III IFN-binding protein and a member of the Ig superfamily. Surprisingly, whereas B18 inhibits only type I IFNs, Y136 inhibits both type I and type III IFNs. Y136 inhibits IFN-induced signaling and suppresses IFIN-mediated biological activities including up-regulation of MHC class I antigen expression and induction of the antiviral state. These data demonstrate that poxviruses have developed unique strategies to counteract IFN-mediated antiviral protection and highlight the importance of type III IFNs in antiviral defense. These results suggest that type III IFNs may be an effective treatment for some poxviral infections.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available