Induction of suppressor of cytokine signaling-3 by herpes simplex virus type 1 confers efficient viral replication

Yokota, Shinichi; Yokosawa, Noriko; Okabayashi, Tamaki; Suzutani, Tatsuo; Fujii, Nobuhiro

doi:10.1016/j.virol.2005.04.028

Cited by 52 publications

(61 citation statements)

References 40 publications

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“…In addition, Wang et al found that trout SOCS-3 gene is higher expression induced by two cytokines in the monocyte/macrophage RTS-11 cell line than in fibroid RTG-2 cell line [18], and previous reports have also indicated that SOCS-3 is induced in T cells, B cells, neutrophils, macrophages and DCs by a variety of agents both in vitro and in vivo [3,7,42,43], which may explain why the induced expression of carp SOCS-3 gene was significantly up-regulated in the immune organs in this study. Noteworthily, in human, the inhibition of the IFN system by virus (HSV-1)-induced SOCS-3 can confer efficient viral replication, and SOCS-3 is up-regulated via activated STAT3 and it efficiently inhibits IFN-a/b signalling [38]. Thereby, it is possible to use a Jak3 inhibitor to suppress SOCS-3 expression and treat viral diseases.…”

Section: Discussionmentioning

confidence: 99%

Cloning of common carp SOCS-3 gene and its expression during embryogenesis, GH-transgene and viral infection

Xiao

Hong

et al. 2010

Fish & Shellfish Immunology

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Section: Discussionmentioning

confidence: 99%

Cloning of common carp SOCS-3 gene and its expression during embryogenesis, GH-transgene and viral infection

Xiao

Hong

et al. 2010

Fish & Shellfish Immunology

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“…Interestingly, SOCS proteins have been shown to contribute to HSV-1 immune evasion in multiple ways. SOCS3 is induced by HSV-1 in a number of cell lines through a mechanism that involves the viral tegument proteins UL41 and UL13 and STAT3 (76,77). In cells which are capable of expressing SOCS3, HSV-1 is sufficient to inhibit IFN-␣-induced STAT1 phosphorylation and downstream OAS production and establish a rapidly propagating infection (76).…”

Section: Virally Exploited Functions Of Socs Proteinsmentioning

confidence: 99%

“…SOCS3 is induced by HSV-1 in a number of cell lines through a mechanism that involves the viral tegument proteins UL41 and UL13 and STAT3 (76,77). In cells which are capable of expressing SOCS3, HSV-1 is sufficient to inhibit IFN-␣-induced STAT1 phosphorylation and downstream OAS production and establish a rapidly propagating infection (76). However, in cells that do not express SOCS3 in response to HSV-1, or when SOCS3 expression is inhibited with STAT3 or SOCS3 antagonists, viral replication is attenuated.…”

Section: Virally Exploited Functions Of Socs Proteinsmentioning

confidence: 99%

“…However, in cells that do not express SOCS3 in response to HSV-1, or when SOCS3 expression is inhibited with STAT3 or SOCS3 antagonists, viral replication is attenuated. This attenuation is rescued following treatment with IFN-␣/␤-neutralizing antibodies, indicating that HSV-1-induced SOCS3 is sufficient to inhibit antiviral type I IFN signaling, thereby enhancing viral replication (76). Notably, in addition to targeting IFN signaling, HSV-1-induced SOCS3 has also been shown to inhibit IFN-␣ production.…”

Section: Virally Exploited Functions Of Socs Proteinsmentioning

confidence: 99%

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Viral Exploitation of Host SOCS Protein Functions

Akhtar

Benveniste

2011

J Virol

107

100

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Over the past decade, a family of host proteins known as suppressors of cytokine signaling (SOCS) have emerged as frequent targets of viral exploitation. Under physiologic circumstances, SOCS proteins negatively regulate inflammatory signaling pathways by facilitating ubiquitination and proteosomal degradation of pathway machinery. Their expression is tightly regulated to prevent excessive inflammation while maintaining protective antipathogenic responses. Numerous viruses, however, have developed mechanisms to induce robust host SOCS protein expression following infection, essentially "hijacking" SOCS function to promote virus survival. To date, SOCS proteins have been shown to inhibit protective antiviral signaling pathways, allowing viruses to evade the host immune response, and to ubiquitinate viral proteins, facilitating intracellular viral trafficking and progeny virus assembly. Importantly, manipulation of SOCS proteins not only facilitates progression of the viral life cycle but also powerfully shapes the presentation of viral disease. SOCS proteins can define host susceptibility to infection, contribute to peripheral disease manifestations such as immune dysfunction and cancer, and even modify the efficacy of therapeutic interventions. Looking toward the future, it is clear that a better understanding of the role of SOCS proteins in viral diseases will be essential in our struggle to modulate and even eliminate the pathogenic effects of viruses on the host.

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“…Another SOCS family member has also been reported to regulate HSV-1 infection. Yokota et al 47,48 showed that induction of SOCS3 was required for efficient replication of wild-type HSV-1 (strain RV3) in human cell lines. Similar to our study, these authors found that the upregulation of SOCS3 was important to determine virus sensitivity.…”

Section: Discussionmentioning

confidence: 99%

Molecular analysis of human cancer cells infected by an oncolytic HSV-1 reveals multiple upregulated cellular genes and a role for SOCS1 in virus replication

Sakthivel

et al. 2008

Cancer Gene Ther

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Oncolytic herpes simplex viruses (oHSVs) are promising anticancer therapeutics. We sought to characterize the functional genomic response of human cancer cells to oHSV infection using G207, an oHSV previously evaluated in a phase I trial. Five human malignant peripheral nerve sheath tumor cell lines, with differing sensitivity to oHSV, were infected with G207 for 6 h. Functional genomic analysis of virus-infected cells demonstrated large clusters of downregulated cellular mRNAs and smaller clusters of those upregulated, including 21 genes commonly upregulated in all five lines. Of these, 7 are known to be HSV-1 induced and 14 represent novel virus-regulated genes. Gene ontology analysis revealed that a majority of G207-upregulated genes are involved in Janus kinase/signal transducer and activator of transcription signaling, transcriptional regulation, nucleic acid metabolism, protein synthesis and apoptosis. Ingenuity networks highlighted nodes for AP-1 subunits and interferon signaling via STAT1, suppressor of cytokine signaling-1 (SOCS1), SOCS3 and RANTES. As biological confirmation, we found that virus-mediated upregulation of SOCS1 correlated with sensitivity to G207 and that depletion of SOCS1 impaired virus replication by 410-fold. Further characterization of roles provided by oHSV-induced cellular genes during virus replication may be utilized to predict oncolytic efficacy and to provide rational strategies for designing next-generation oncolytic viruses.

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Induction of suppressor of cytokine signaling-3 by herpes simplex virus type 1 confers efficient viral replication

Cited by 52 publications

References 40 publications

Cloning of common carp SOCS-3 gene and its expression during embryogenesis, GH-transgene and viral infection

Cloning of common carp SOCS-3 gene and its expression during embryogenesis, GH-transgene and viral infection

Viral Exploitation of Host SOCS Protein Functions

Molecular analysis of human cancer cells infected by an oncolytic HSV-1 reveals multiple upregulated cellular genes and a role for SOCS1 in virus replication

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