The Molecular Mechanism of Herpes Simplex Virus 1 UL31 in Antagonizing the Activity of IFN-β

Gong, Lan; Ou, Xiaowen; Hu, Li; Zhong, Jiayi; Li, Jingjing; Deng, Shenyu; Pan, Lingxia; Wang, Liding; Hong, Xuejun; Luo, Wenqi; Zeng, Qiyuan; Zan, Jie; Peng, Tao; Cai, Mingsheng; Li, Meili

doi:10.1128/spectrum.01883-21

Cited by 8 publications

(8 citation statements)

References 87 publications

(108 reference statements)

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“…To determine whether gp110 can block the nuclear accumulation of IRF3, HeLa cells, which are suitable and widely used to observe the nuclear translocation of target proteins as its nucleus is relatively large ( 20 , 24 , 51 – 66 ), were transfected with vector or gp110 expression plasmid and infected with SeV. Immunofluorescence assays (IFAs) showed that in mock-treated cells, IRF3 was localized in the cytoplasm, and IRF3 was transferred to the nucleus when cells were infected with SeV.…”

Section: Resultsmentioning

confidence: 99%

“…Transfection and DLR assays were performed as previously described ( 66 , 86 ). HEK293T cells or Hone1-EBV cells plated in 24-well dishes (Corning) with a confluency of about 80% were cotransfected with 100 ng of reporter plasmid (IFN-β-Luc, [PRDIII]4-Luc, ISRE-Luc, or NF-κB-Luc) and 10 ng of pRL-TK ( Renilla luciferase reporter plasmid) to standardize transfection efficiency, along with the indicated amounts of expression plasmid(s).…”

Section: Methodsmentioning

confidence: 99%

“…Native PAGE was executed according to previous studies ( 20 , 66 ). HEK293T cells plated in 6-well plates (Corning) were transfected with the indicated expression plasmid(s).…”

Section: Methodsmentioning

confidence: 99%

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Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin

et al. 2023

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“…The small noncoding RNAs within HSV-1 latency-associated transcript also engage RIG-I to induce IFN expression [188]. Of note, the HSV-1 US11, US3 and UL31 γ134.5 proteins can suppress RIG-I signaling or IFN beta activity [189][190][191]. HSV-1 can evade the host innate immunity through complex mechanisms [192].…”

Section: Stimulation Of Rlr Signaling For Cancer Immunotherapy By Onc...mentioning

confidence: 99%

Exploiting RIG-I-like receptor pathway for cancer immunotherapy

et al. 2023

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RIG-I-like receptors (RLRs) are intracellular pattern recognition receptors that detect viral or bacterial infection and induce host innate immune responses. The RLRs family comprises retinoic acid-inducible gene 1 (RIG-I), melanoma differentiation-associated gene 5 (MDA5) and laboratory of genetics and physiology 2 (LGP2) that have distinctive features. These receptors not only recognize RNA intermediates from viruses and bacteria, but also interact with endogenous RNA such as the mislocalized mitochondrial RNA, the aberrantly reactivated repetitive or transposable elements in the human genome. Evasion of RLRs-mediated immune response may lead to sustained infection, defective host immunity and carcinogenesis. Therapeutic targeting RLRs may not only provoke anti-infection effects, but also induce anticancer immunity or sensitize “immune-cold” tumors to immune checkpoint blockade. In this review, we summarize the current knowledge of RLRs signaling and discuss the rationale for therapeutic targeting RLRs in cancer. We describe how RLRs can be activated by synthetic RNA, oncolytic viruses, viral mimicry and radio-chemotherapy, and how the RNA agonists of RLRs can be systemically delivered in vivo. The integration of RLRs agonism with RNA interference or CAR-T cells provides new dimensions that complement cancer immunotherapy. Moreover, we update the progress of recent clinical trials for cancer therapy involving RLRs activation and immune modulation. Further studies of the mechanisms underlying RLRs signaling will shed new light on the development of cancer therapeutics. Manipulation of RLRs signaling represents an opportunity for clinically relevant cancer therapy. Addressing the challenges in this field will help develop future generations of cancer immunotherapy.

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“…When a viral infection is encountered, PRR performs its vital function of antigen recognition and immune initiation at this moment. Immune signals are transmitted through a variety of different pathways, leading to the synthesis and release of a number of inflammatory factors, such as type I interferon (IFN-I) (Lin and Zheng, 2019;Zhu et al, 2022a;Li et al, 2022e;Gong et al, 2022).…”

Section: Direct Invasion and Lysis Of Cancer Cellsmentioning

confidence: 99%

HSV: The scout and assault for digestive system tumors

Li²,

Ren³

et al. 2023

Front. Mol. Biosci.

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More than 25% of all malignant tumors are digestive system tumors (DSTs), which mostly include esophageal cancer, gastric cancer, pancreatic cancer, liver cancer, gallbladder cancer and cholangiocarcinoma, and colorectal cancer. DSTs have emerged as one of the prominent reasons of morbidity and death in many nations and areas around the world, posing a serious threat to human life and health. General treatments such as radiotherapy, chemotherapy, and surgical resection can poorly cure the patients and have a bad prognosis. A type of immunotherapy known as oncolytic virus therapy, have recently shown extraordinary anti-tumor effectiveness. One of the viruses that has been the subject of the greatest research in this field, the herpes simplex virus (HSV), has shown excellent potential in DSTs. With a discussion of HSV-1 based on recent studies, we outline the therapeutic effects of HSV on a number of DSTs in this review. Additionally, the critical function of HSV in the detection of cancers is discussed, and some HSV future possibilities are shown.

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The Molecular Mechanism of Herpes Simplex Virus 1 UL31 in Antagonizing the Activity of IFN-β

Abstract: The innate immune system is the first line of host defense against the invasion of pathogens. Among its mechanisms, IFN-I is an essential cytokine in the antiviral response, which can help the host eliminate a virus.

Cited by 8 publications

References 87 publications

Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin

Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin

Exploiting RIG-I-like receptor pathway for cancer immunotherapy

HSV: The scout and assault for digestive system tumors

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