» Articles » PMID: 37090696

Current Progress on Innate Immune Evasion Mediated by N Protein of Pestiviruses

Overview
Journal Front Immunol
Date 2023 Apr 24
PMID 37090696
Authors
Affiliations
Soon will be listed here.
Abstract

Interferon (IFN), the most effective antiviral cytokine, is involved in innate and adaptive immune responses and is essential to the host defense against virus invasion. Once the host was infected by pathogens, the pathogen-associated molecular patterns (PAMPs) were recognized by the host pattern recognition receptors (PRRs), which activates interferon regulatory transcription factors (IRFs) and nuclear factor-kappa B (NF-κB) signal transduction pathway to induce IFN expression. Pathogens have acquired many strategies to escape the IFN-mediated antiviral immune response. Pestiviruses cause massive economic losses in the livestock industry worldwide every year. The immune escape strategies acquired by pestiviruses during evolution are among the major difficulties in its control. Previous experiments indicated that Erns, as an envelope glycoprotein unique to pestiviruses with RNase activity, could cleave viral ss- and dsRNAs, therefore inhibiting the host IFN production induced by viral ss- and dsRNAs. In contrast, Npro, the other envelope glycoprotein unique to pestiviruses, mainly stimulates the degradation of transcription factor IRF-3 to confront the IFN response. This review mainly summarized the current progress on mechanisms mediated by Npro of pestiviruses to antagonize IFN production.

Citing Articles

Network of Interactions between the Mut Domains of the E2 Protein of Atypical Porcine Pestivirus and Host Proteins.

Yang Y, Jiang G, He W, Tian X, Zheng H, Xiang B Genes (Basel). 2024; 15(8).

PMID: 39202352 PMC: 11354059. DOI: 10.3390/genes15080991.


Safety and DIVA Capability of Novel Live Attenuated Classical Swine Fever Marker Vaccine Candidates in Pregnant Sows.

Tong C, Mundt A, Meindl-Boehmer A, Haist V, Gallei A, Chen N Viruses. 2024; 16(7).

PMID: 39066207 PMC: 11281586. DOI: 10.3390/v16071043.

References
1.
Johns H, Doceul V, Everett H, Crooke H, Charleston B, Seago J . The classical swine fever virus N-terminal protease N(pro) binds to cellular HAX-1. J Gen Virol. 2010; 91(Pt 11):2677-86. DOI: 10.1099/vir.0.022897-0. View

2.
Honda K, Taniguchi T . IRFs: master regulators of signalling by Toll-like receptors and cytosolic pattern-recognition receptors. Nat Rev Immunol. 2006; 6(9):644-58. DOI: 10.1038/nri1900. View

3.
Li D, Dong H, Li S, Munir M, Chen J, Luo Y . Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus. J Virol. 2013; 87(10):5707-17. PMC: 3648164. DOI: 10.1128/JVI.03130-12. View

4.
Harman J, Loes A, Warren G, Heaphy M, Lampi K, Harms M . Evolution of multifunctionality through a pleiotropic substitution in the innate immune protein S100A9. Elife. 2020; 9. PMC: 7213983. DOI: 10.7554/eLife.54100. View

5.
Sakurai H, Chiba H, Miyoshi H, Sugita T, Toriumi W . IkappaB kinases phosphorylate NF-kappaB p65 subunit on serine 536 in the transactivation domain. J Biol Chem. 1999; 274(43):30353-6. DOI: 10.1074/jbc.274.43.30353. View