Role of the suppressor of cytokine signaling 2 (SOCS2) during meningoencephalitis caused by Bovine herpesvirus 5 (BoHV-5)

Barbosa, Aline Aparecida Silva; Versiani, Alice F.; Sousa, Larissa Fonseca da Cunha; Miranda, Aline Silva de; Gasparini, Marcela Ribeiro; Brant, Fátima; Silva, Daniele Gonçalves; Quintino-de-Carvalho, Iracema Luisa; Soriani, Frederico Marianetti; Fonseca, Flávio Guimarães da; Vasconcelos, A.C.; Barcelos, Lucíola da Silva; Teixeira, Mauro Martins; Teixeira, Antônio Lúcio; Machado, Fabiana S.; Barbosa-Stancioli, Edel Figueiredo

doi:10.1016/j.cimid.2016.05.003

Cited by 8 publications

(7 citation statements)

References 24 publications

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“…Some recent studies have also explored the effects of SOCS2 gene knockout on viral infection during viral infections such as HSV-1 ( 157 ), HSV-2 ( 158 ), or bovine herpesvirus type 5 (BHV-5) ( 159 ). For example, under the same infection with HSV-1, SOCS2 gene-deficient mice showed less severe immune cell infiltration, encephalitis and neuroinflammation than wild-type C57BL/6 mice ( 157 ).…”

Section: Socs Proteins Regulate Innate Immunity Caused By Virusesmentioning

confidence: 99%

“…For example, under the same infection with HSV-1, SOCS2 gene-deficient mice showed less severe immune cell infiltration, encephalitis and neuroinflammation than wild-type C57BL/6 mice ( 157 ). Unlike HSV-1 infection, SOCS2 KO mice have worsened meningoencephalitis compared to wild-type animals during BHV-5 infection, indicating that SOCS2 protein has a protective effect on intracranial BHV-5 infection ( 159 ). There are also reports on SOCS5 in the regulation of influenza virus infection.…”

Section: Socs Proteins Regulate Innate Immunity Caused By Virusesmentioning

confidence: 99%

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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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Section: Socs Proteins Regulate Innate Immunity Caused By Virusesmentioning

confidence: 99%

Section: Socs Proteins Regulate Innate Immunity Caused By Virusesmentioning

confidence: 99%

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

et al. 2020

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“…In addition to HSV-1, these include the human herpesviruses VZV (17), HCMV (14), and KSHV (13), as well as the animal herpesviruses MDV (15, 19), PRV (20), MCMV (11, 16, 18, 21, 23), and MHV-68 (22) (Table 2). In addition to these, recent reports discuss the effects of SOCS2 gene knockout during infection with HSV-1 (171), HSV-2 (172), or BHV-5 (173). It is likely that still more viruses affecting SOCS proteins will be discovered in the future.…”

Section: Herpesviruses Affecting Host Socs Proteinsmentioning

confidence: 99%

“…In LTEP-α-2 and SPC-α-1 human lung cancer cell lines experimentally infected with HSV-2, the virally-encoded microRNA Hsv2-miR-H9-5p targets and inhibits SOCS2, thereby driving experimental tumor metastasis in these cell lines (172). BHV-5 in the Varicellovirus genus natively infects cattle but can establish productive infection in rabbits and mice, which are frequently used as animal models to study neurological disease caused by this virus (173). Unlike HSV-1 infection, infection with BHV-5 exacerbates meningoencephalitis in SOCS2-knockout mice compared with wild type animals (173), suggesting a protective role during intracranial BHV-5 infection.…”

Section: Herpesviruses Affecting Host Socs Proteinsmentioning

confidence: 99%

“…BHV-5 in the Varicellovirus genus natively infects cattle but can establish productive infection in rabbits and mice, which are frequently used as animal models to study neurological disease caused by this virus (173). Unlike HSV-1 infection, infection with BHV-5 exacerbates meningoencephalitis in SOCS2-knockout mice compared with wild type animals (173), suggesting a protective role during intracranial BHV-5 infection. Although it remains unknown whether HSV-1 or BHV-5 stimulates or dampens host SOCS2 expression in these models, SOCS2 nevertheless plays a multivariate role in the pathologies of these herpesviruses.…”

Section: Herpesviruses Affecting Host Socs Proteinsmentioning

confidence: 99%

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SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis

Alston

Dix

2019

Front. Immunol.

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Suppressor of cytokine signaling (SOCS) proteins provide selective negative feedback to prevent pathogeneses caused by overstimulation of the immune system. Of the eight known SOCS proteins, SOCS1 and SOCS3 are the best studied, and systemic deletion of either gene causes early lethality in mice. Many viruses, including herpesviruses such as herpes simplex virus and cytomegalovirus, can manipulate expression of these host proteins, with overstimulation of SOCS1 and/or SOCS3 putatively facilitating viral evasion of immune surveillance, and SOCS suppression generally exacerbating immunopathogenesis. This is particularly poignant within the eye, which contains a diverse assortment of specialized cell types working together in a tightly controlled microenvironment of immune privilege. When the immune privilege of the ocular compartment fails, inflammation causing severe immunopathogenesis and permanent, sight-threatening damage may occur, as in the case of AIDS-related human cytomegalovirus (HCMV) retinitis. Herein we review how SOCS1 and SOCS3 impact the virologic, immunologic, and/or pathologic outcomes of herpesvirus infection with particular emphasis on retinitis caused by HCMV or its mouse model experimental counterpart, murine cytomegalovirus (MCMV). The accumulated data suggests that SOCS1 and/or SOCS3 can differentially affect the severity of viral diseases in a highly cell-type-specific manner, reflecting the diversity and complexity of herpesvirus infection and the ocular compartment.

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Susceptibility of mice to bovine herpesvirus type 5 infection in the central nervous system

et al. 2017

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Bovine herpesvirus type 5 (BoHV-5) is an important pathogen that causes meningoencephalitis in cattle. Few studies have used the mouse as a model for BoHV-5 infection. Despite the fact that BoHV-5 can infect mice with immune deficiencies, little is known about viral replication, immune response, and the course of infection in the central nervous system (CNS) of wild-type mice. Therefore, the aim of this study was to evaluate the response in the CNS of BALB/c mice acutely infected with BoHV-5 at different days post-inoculation (dpi). BoHV-5, when inoculated intracranially, was able to infect and replicate within the CNS of BALB/c mice. Until 15 dpi, the mice were able to survive without showing prominent neurological signs. The infection was accompanied by a Th1 immune response, with a significant expression of the cytokines IFN-γ and TNF-α and chemokine CCL-2. The expression of these cytokines and chemokines was most significant in the early course of infection (3 and 4 dpi), and it was followed by meningoencephalitis with perivascular cuffing and periventriculitis, composed mainly of macrophages and lymphocytes. After the expression of cytokines and chemokine, the mice were able to curb BoHV-5 acute infection in the brain, since there was a decrease in the number of BoHV-5 DNA copies after 3 dpi and viable viral particles were not detected after 6 dpi. Importantly, BoHV-5 was able to infect the trigeminal ganglia during acute infection, since a large number of BoHV-5 DNA copies were detected on 1 and 2 dpi.

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Role of the suppressor of cytokine signaling 2 (SOCS2) during meningoencephalitis caused by Bovine herpesvirus 5 (BoHV-5)

Cited by 8 publications

References 24 publications

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

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

SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis

Susceptibility of mice to bovine herpesvirus type 5 infection in the central nervous system

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