TY - JOUR
T1 - Suppressor of cytokine signaling 2 (SOCS2) contributes to encephalitis in a model of Herpes infection in mice
AU - da Cunha Sousa, Larissa Fonseca
AU - Rachid, Milene Alvarenga
AU - Lima, Graciela Kunrath
AU - de Miranda, Aline Silva
AU - de Carvalho Vilela, Márcia
AU - Lacerda Queiroz, Norinne
AU - Rodrigues, David Henrique
AU - Campos, Marco Antonio
AU - Kroon, Erna Geessien
AU - Machado, Fabiana Simão
AU - Teixeira, Antônio Lúcio
N1 - Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/10/1
Y1 - 2016/10/1
N2 - The most severe manifestation of Herpes Simplex Type 1 virus (HSV-1) infection is encephalitis characterized by arousal impairment and seizures that can evolve to coma and death. Previous studies reported the involvement of suppressor of cytokine signaling (SOCS) proteins, specifically SOCS1 and SOCS3, in HSV-1 infection, suggesting that other members of this family could be involved in the immune response against HSV-1. No previous study has reported the role of SOCS2 in HSV-1 infection. In the current study, C57BL/6 wild-type mice (WT) and mice deficient in SOCS2 gene (SOCS2−/−) were subjected to intracranial inoculation with 102 plaque forming units (PFU) of HSV-1. Survival curve, neuroinflammatory parameters and neuropathology were evaluated. Infected SOCS2−/− mice had increased survival in comparison with infected WT animals. This better outcome was associated with reduced leukocyte infiltration, concentration of cytokines, and structural changes in the brain. SOCS2 seems to play a detrimental role in HSV-1 encephalitis. Moreover, the control of neuroinflammatory response in HSV-1 infection was of paramount importance to clinical outcome.
AB - The most severe manifestation of Herpes Simplex Type 1 virus (HSV-1) infection is encephalitis characterized by arousal impairment and seizures that can evolve to coma and death. Previous studies reported the involvement of suppressor of cytokine signaling (SOCS) proteins, specifically SOCS1 and SOCS3, in HSV-1 infection, suggesting that other members of this family could be involved in the immune response against HSV-1. No previous study has reported the role of SOCS2 in HSV-1 infection. In the current study, C57BL/6 wild-type mice (WT) and mice deficient in SOCS2 gene (SOCS2−/−) were subjected to intracranial inoculation with 102 plaque forming units (PFU) of HSV-1. Survival curve, neuroinflammatory parameters and neuropathology were evaluated. Infected SOCS2−/− mice had increased survival in comparison with infected WT animals. This better outcome was associated with reduced leukocyte infiltration, concentration of cytokines, and structural changes in the brain. SOCS2 seems to play a detrimental role in HSV-1 encephalitis. Moreover, the control of neuroinflammatory response in HSV-1 infection was of paramount importance to clinical outcome.
KW - Encephalitis
KW - HSV-1
KW - Neuroinflammation
KW - SOCS2
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U2 - 10.1016/j.brainresbull.2016.09.011
DO - 10.1016/j.brainresbull.2016.09.011
M3 - Article
C2 - 27646480
AN - SCOPUS:84988615529
SN - 0361-9230
VL - 127
SP - 164
EP - 170
JO - Brain Research Bulletin
JF - Brain Research Bulletin
ER -