Version 1
: Received: 1 July 2024 / Approved: 2 July 2024 / Online: 2 July 2024 (14:49:16 CEST)
How to cite:
Ringo, R. S.; Choonnasard, A.; Okabayashi, T.; Saito, A. Conserved Antagonization of Type I Interferon Signaling by Arterivirus GP5 Proteins. Preprints2024, 2024070166. https://doi.org/10.20944/preprints202407.0166.v1
Ringo, R. S.; Choonnasard, A.; Okabayashi, T.; Saito, A. Conserved Antagonization of Type I Interferon Signaling by Arterivirus GP5 Proteins. Preprints 2024, 2024070166. https://doi.org/10.20944/preprints202407.0166.v1
Ringo, R. S.; Choonnasard, A.; Okabayashi, T.; Saito, A. Conserved Antagonization of Type I Interferon Signaling by Arterivirus GP5 Proteins. Preprints2024, 2024070166. https://doi.org/10.20944/preprints202407.0166.v1
APA Style
Ringo, R. S., Choonnasard, A., Okabayashi, T., & Saito, A. (2024). Conserved Antagonization of Type I Interferon Signaling by Arterivirus GP5 Proteins. Preprints. https://doi.org/10.20944/preprints202407.0166.v1
Chicago/Turabian Style
Ringo, R. S., Tamaki Okabayashi and Akatsuki Saito. 2024 "Conserved Antagonization of Type I Interferon Signaling by Arterivirus GP5 Proteins" Preprints. https://doi.org/10.20944/preprints202407.0166.v1
Abstract
Arterivirus can establish persistent infection in animals such as equids, pigs, nonhuman primates, rodents, and possums. Some Arterivirus can even cause overt and severe diseases such as Equine Arteritis in horses and Porcine Reproductive and Respiratory Syndrome in pigs, leading to huge economic losses. Arterivirus have evolved viral proteins to antagonize the host cell’s innate immune responses by inhibiting type I interferon (IFN) signaling, assisting viral evasion and persistent infection. So far, the role of the Arterivirus glycoprotein 5 (GP5) protein in IFN signaling inhibition remains unclear. Here, we investigated the inhibitory activity of 47 Arterivirus GP5 proteins derived from various hosts. We demonstrated that all GP5 proteins showed conserved activity for antagonizing TIR-domain-containing adapter protein inducing interferon-β (TRIF)-mediated IFN- signaling through TRIF degradation. In addition, Arterivirus GP5 proteins showed conserved inhibitory activity against IFN-β signaling, induced by either pig or human TRIF. Furthermore, certain Arterivirus GP5 proteins could inhibit the induction of IFN-stimulated genes. These findings highlight the role of Arterivirus GP5 proteins in supporting persistent infection.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
