SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis

Alston, Christine I.; Dix, Richard D.

doi:10.3389/fimmu.2019.00732

Cited by 26 publications

(19 citation statements)

References 262 publications

(384 reference statements)

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“…Though miR-155 is upregulated, strong expression of SOCS1 can be observed in EBV-infected cells (46). Simultaneous upregulation of SOCS1 and miR-155 has become an important controversy for researchers who study herpesviruses (47). It might be possible that miR-155 may target another gene expressed higher than SOCS1 in NPC cells.…”

Section: Host Mirna-mediated Evasion Of the Immune System By Ebv-infementioning

confidence: 99%

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

et al. 2020

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Epstein-Barr virus (EBV) is an oncogenic human herpes virus that was discovered in 1964. Viral non-coding RNAs, such as BamHI-A rightward fragment-derived microRNAs (BART miRNAs) or BamHI-H rightward fragment 1-derived miRNAs (BHRF1 miRNA) in EBV-infected cells have been recently reported. Host miRNAs are also upregulated upon EBV infection. Viral and host miRNAs are important in maintaining viral infection and evasion of host immunity. Although miRNAs in EBV-infected cells often promote cell proliferation by targeting apoptosis or cell cycle, this review focuses on the regulation of the recognition of the host immune system. This review firstly describes the location and organization of two clusters of viral miRNAs, then describes evasion from host immune surveillance systems by modulating viral gene expression or inhibiting innate and acquired immunity by viral miRNAs as well as host miRNAs. Another topic is the enigmatic depletion of viral miRNAs in several types of EBV-infected tumor cells. Finally, this review introduces the strong correlation of nasopharyngeal cancer cases with a newly identified single nucleotide polymorphism that enhances BART miRNA promoter activity.

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Section: Host Mirna-mediated Evasion Of the Immune System By Ebv-infementioning

confidence: 99%

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

et al. 2020

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“…Various viruses suppress IFN-driven immunity by inducing SOCS1 and SOCS3, thereby evading immune responses [2]. SOCS proteins can be quickly induced by IFN signaling and inhibit the specific JAK/STAT signaling pathway [25,26].…”

Section: Discussionmentioning

confidence: 99%

“…Enterovirus 71 (EV71), a member of the Picornavirus family, is notable for its role in epidemics of hand, foot, and mouth disease (HFMD) in children, which is a global infectious disease that affects millions of people [1]. Currently, the pathogenic mechanisms underlying EV71 are unclear, and there are no effective treatments for diseases caused by EV71 [2].…”

Section: Introductionmentioning

confidence: 99%

Induction of SOCS Expression by EV71 Infection Promotes EV71 Replication

Gao

Huang

Liu

et al. 2020

BioMed Research International

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Enterovirus 71 (EV71) is the causative pathogen of hand, foot, and mouth disease (HFMD). However, no effective antiviral therapy is currently available. Some viruses could escape the host’s innate immunity by upregulating suppressor of cytokine signaling (SOCS) proteins. Until now, whether EV71 evades the host immune system by regulating the expression of SOCS proteins remains unknown. In this study, we found that EV71 infection promoted SOCS expression at both mRNA and protein levels in vitro and in vivo. Consistently, the infectivity of EV71 was decreased significantly in the SOCS3 or SOCS1 knockdown cells, suggesting that SOCS1 and especially SOCS3 are crucial for EV71 infection. Further investigation showed that SOCS3 promoted virus infection by inhibiting interferon-induced STAT3 phosphorylation. SOCS1 and SOCS3 mRNA expressions were independent on virus-induced type I interferon expression but were blocked by the inhibitor of NF-κB. Therefore, EV71 infection stimulates the expression of SOCS proteins in an interferon-independent way and negatively regulates the JAK/STAT signaling pathway, thus escaping host immunity. All these results may add new information to the mechanism of EV71 in fighting against type I interferon responses.

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“…All in all, the negative feedback loop of cells plays a vital role in maintaining the close relationship between cytokine secretion and inhibition. Therefore, the SOCS proteins with negative feedback regulation ability prevents the excessive secretion of cytokines from harming the host ( 6 ). An intracellular protein family is constituted by SOCS1-7 proteins and cytokine-inducible SRC homology 2 (SH2) domain-containing proteins (CIS; also known as CISH), some of which play an essential role in regulating the response of immune cells to cytokines ( 7 – 9 ).…”

Section: Introductionmentioning

confidence: 99%

SOCS Proteins Participate in the Regulation of Innate Immune Response Caused by Viruses

et al. 2020

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The host immune system has multiple innate immune receptors that can identify, distinguish and react to viral infections. In innate immune response, the host recognizes pathogen-associated molecular patterns (PAMP) in nucleic acids or viral proteins through pathogen recognition receptors (PRRs), especially toll-like receptors (TLRs) and induces immune cells or infected cells to produce type I Interferons (IFN-I) and pro-inflammatory cytokines, thus when the virus invades the host, innate immunity is the earliest immune mechanism. Besides, cytokine-mediated cell communication is necessary for the proper regulation of immune responses. Therefore, the appropriate activation of innate immunity is necessary for the normal life activities of cells. The suppressor of the cytokine signaling proteins (SOCS) family is one of the main regulators of the innate immune response induced by microbial pathogens. They mainly participate in the negative feedback regulation of cytokine signal transduction through Janus kinase signal transducer and transcriptional activator (JAK/STAT) and other signal pathways. Taken together, this paper reviews the SOCS proteins structures and the function of each domain, as well as the latest knowledge of the role of SOCS proteins in innate immune caused by viral infections and the mechanisms by which SOCS proteins assist viruses to escape host innate immunity. Finally, we discuss potential values of these proteins in future targeted therapies.

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SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis

Cited by 26 publications

References 262 publications

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

Induction of SOCS Expression by EV71 Infection Promotes EV71 Replication

SOCS Proteins Participate in the Regulation of Innate Immune Response Caused by Viruses

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