Viruses utilize ubiquitination systems to escape TLR/RLR-mediated innate immunity

Shanzhi Huang; Anchun Cheng; Mingshu Wang; Zhongqiong Yin; Juan Huang; Renyong Jia

doi:10.3389/fimmu.2022.1065211

Viruses utilize ubiquitination systems to escape TLR/RLR-mediated innate immunity

Front Immunol. 2022 Nov 25:13:1065211. doi: 10.3389/fimmu.2022.1065211. eCollection 2022.

Authors

Shanzhi Huang^{1

2}, Anchun Cheng^{1

2

3}, Mingshu Wang^{1

2

3}, Zhongqiong Yin³, Juan Huang^{1

2

3}, Renyong Jia^{1

2

3}

Affiliations

¹ Avian Disease Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.
² Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.
³ Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

Abstract

When the viruses invade the body, they will be recognized by the host pattern recognition receptors (PRRs) such as Toll like receptor (TLR) or retinoic acid-induced gene-I like receptor (RLR), thus causing the activation of downstream antiviral signals to resist the virus invasion. The cross action between ubiquitination and proteins in these signal cascades enhances the antiviral signal. On the contrary, more and more viruses have also been found to use the ubiquitination system to inhibit TLR/RLR mediated innate immunity. Therefore, this review summarizes how the ubiquitination system plays a regulatory role in TLR/RLR mediated innate immunity, and how viruses use the ubiquitination system to complete immune escape.

Keywords: E3 ubiquitin ligase; RLR; TLR; innate immune; ubiquitination; virus.

Publication types

Review

MeSH terms

Antiviral Agents
Immunity, Innate
Toll-Like Receptors*
Ubiquitination
Viruses*

Substances

Toll-Like Receptors
Antiviral Agents