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Review
. 2024 Jun 12:17:3737-3752.
doi: 10.2147/JIR.S455035. eCollection 2024.

Host Factors Modulate Virus-Induced IFN Production via Pattern Recognition Receptors

Jingjing Wang  1 , Yirui Dong  1 , Xuewei Zheng  1 , Haodi Ma  1 , Mengjiao Huang  1 , Dongliao Fu  1 , Jiangbo Liu  2 , Qinan Yin  1   3
Affiliations
Review

Host Factors Modulate Virus-Induced IFN Production via Pattern Recognition Receptors

Jingjing Wang et al. J Inflamm Res. .

Abstract

Innate immunity is the first line of defense in the human body, and it plays an important role in defending against viral infection. Viruses are identified by different pattern-recognition receptors (PRRs) that activate the mitochondrial antiviral signaling protein (MAVS) or transmembrane protein 173 (STING), which trigger multiple signaling cascades that cause nuclear factor-κB (NF-κB) and interferon regulatory factor 3 (IRF3) to produce inflammatory factors and interferons (IFNs). PRRs play a pivotal role as the first step in pathogen induction of interferon production. Interferon elicits antiviral activity by inducing the transcription of hundreds of IFN-stimulated genes (ISGs) via the janus kinase (JAK) - signal transducer and activator of transcription (STAT) pathway. An increasing number of studies have shown that environmental, pathogen and host factors regulate the IFN signaling pathway. Here, we summarize the mechanisms of host factor modulation in IFN production via pattern recognition receptors. These regulatory mechanisms maintain interferon levels in a normal state and clear viruses without inducing autoimmune disease.

Keywords: host factors; interferon-signaling pathway; pattern recognition receptors.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
The regulator of the RIG-I signaling pathway. RIG-I recognizes RNA derived from actively replicating RNA viruses. RIG-I contains CARD-like structures that mediate interactions with the adaptor MAVS. MAVS initiates signaling pathways leading to IRF3 and IRF7 via TBK1. Activated IRF3 and IRF7 form dimers and translocate to the nucleus to induce the production of type I IFN. RIG-I is regulated by various mechanisms, such as PTMs (phosphorylation, ubiquitylation, SUMOylation and ISGylation) and small non-coding RNAs.
Figure 2
Figure 2
The regulator of the MDA5 signaling pathway. MDA5 recognizes RNA derived from actively replicating RNA viruses. MDA5 contains CARD-like structures that mediate interactions with the adaptor MAVS. MAVS initiates signaling pathways leading to IRF3 and IRF7 via TBK1. Activated IRF3 and IRF7 form dimers and translocate to the nucleus to induce the production of type I IFN. RIG-I is regulated by various mechanisms, such as PTMs (phosphorylation, ubiquitylation, SUMOylation and ISGylation) and small non-coding RNAs.
Figure 3
Figure 3
The regulator of the TLR3 signaling pathway. TLR3 recognizes viral dsRNA. TLR3 mediates the interaction with the adaptor TRIF. TRIF initiates signaling pathways leading to IRF3 via TBK1. Activated IRF3 dimerizes and translocates to the nucleus to induce the production of type I IFN. TLR3 is regulated by various mechanisms, such as PTMs.
Figure 4
Figure 4
The regulator of the cGAS signaling pathway. cGAS recognizes viral dsRNA and activates a STING-dependent signaling pathway. STING initiates signaling pathways leading to IRF3 via TBK1. Activated IRF3 dimerizes and translocates to the nucleus to induce the production of type I IFN. cGAS is regulated by various mechanisms, such as PTMs (phosphorylation, ubiquitylation, SUMOylation, glutamylation and acetylation) and small non-coding RNAs.
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