da Cunha Sousa Larissa Fonseca, Rachid Milene Alvarenga, Lima Graciela Kunrath, de Miranda Aline Silva, de Carvalho Vilela Márcia, Lacerda Queiroz Norinne, Rodrigues David Henrique, Campos Marco Antonio, Kroon Erna Geessien, Machado Fabiana Simão, Teixeira Antônio Lúcio
Laboratorio de Imunofarmacologia, Departamento de Bioquimica e Imunologia, Instituto de Ciências Biológicas (ICB), UFMG, Belo Horizonte, Brazil.
Laboratorio de Imunofarmacologia, Departamento de Bioquimica e Imunologia, Instituto de Ciências Biológicas (ICB), UFMG, Belo Horizonte, Brazil; Laboratorio de Apoptose, Departamento de Patologia Geral, Instituto de Ciências Biológicas (ICB), UFMG, Belo Horizonte, Brazil.
Brain Res Bull. 2016 Oct;127:164-170. doi: 10.1016/j.brainresbull.2016.09.011. Epub 2016 Sep 16.
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 10 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.
单纯疱疹病毒1型（HSV-1）感染最严重的表现是脑炎，其特征为觉醒障碍和癫痫发作，可发展为昏迷和死亡。先前的研究报道细胞因子信号转导抑制因子（SOCS）蛋白，特别是SOCS1和SOCS3参与了HSV-1感染，这表明该家族的其他成员可能参与了针对HSV-1的免疫反应。此前尚无研究报道SOCS2在HSV-1感染中的作用。在本研究中，将C57BL/6野生型小鼠（WT）和缺乏SOCS2基因的小鼠（SOCS2）进行颅内接种10个空斑形成单位（PFU）的HSV-1。评估生存曲线、神经炎症参数和神经病理学。与感染的WT动物相比，感染的SOCS2小鼠的存活率有所提高。这一较好的结果与白细胞浸润减少、细胞因子浓度降低以及大脑结构变化有关。SOCS2似乎在HSV-1脑炎中起有害作用。此外，控制HSV-1感染中的神经炎症反应对临床结果至关重要。
