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Involvement of herpes simplex virus type 1 UL13 protein kinase in induction of SOCS genes, the negative regulators of cytokine signaling
Author(s) -
Sato Yuka,
Koshizuka Tetsuo,
Ishibashi Kei,
Hashimoto Koichi,
Ishioka Ken,
Ikuta Kazufumi,
Yokota Shinichi,
Fujii Nobuhiro,
Suzutani Tatsuo
Publication year - 2017
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12483
Subject(s) - socs3 , biology , suppressor of cytokine signaling 1 , suppressor of cytokine signalling , herpes simplex virus , enhancer , cytokine , socs5 , signal transduction , irf7 , socs6 , transcription factor , virology , microbiology and biotechnology , virus , gene , gene expression , stat3 , immunology , genetics , suppressor
The suppressor of cytokine signaling (SOCS) family has eight members and suppresses various cytokine signaling pathways, including IFN signaling. Therefore, some viruses have evolved molecular mechanisms for inducing SOCS proteins and thus escaping host immunity. Herpes simplex virus type 1 (HSV‐1) has a mechanism for escaping from type I IFN by induction of both SOCS1 and SOCS3. In this study, expression of the eight members of the SOCS family stimulated by HSV‐1 infection was comparatively analyzed by qRT‐PCR. It was found that SOCS1 and SOCS3 are induced by HSV‐1‐infection at 4 hr post infection. However, such induction was not observed in UL13 deficient virus‐infected cells, suggesting that UL13 protein kinase participates in induction of both genes. The transcription factor Sp1‐binding sites of SOCS3 promoter/enhancer region were identified as the regulatory elements for induction of SOCS3 in HSV‐1 infected cells. Accumulation of activated Sp1 was detectable in the nuclei of HSV‐1‐infected cells before induction of SOCS3. Taken together, these results suggest that HSV‐1 has a potent mechanism for escaping from the IFN system.