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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Herpes simplex virus-1 (HSV-1) is a pathogen for humans that may cause severe encephalitis.Tumor necrosis factor alpha (TNF-alpha) plays a role in several viral diseases of the central nervous system (CNS).The classic proinflammatory activities of TNF-alpha are mediated mainly through activation of the receptor 1 for TNF-alpha (TNFR1).However, when HSV-1 is inoculated in the periphery, TNF-alpha seems to protect C57Bl/6 mice against encephalitis by a mechanism independent of TNFR1.This study aims to investigate the role of TNFR1 in HSV-1encephalitis induced by the inoculation of the virus into the brain.Wild-type C57BL/6 (WT) and TNFR1(-/-) were inoculated with 10(2) plaque-forming units of HSV-1 by the intracranial route.Infection with HSV-1 was lethal in TNFR1(-/-) mice in early times after infection.TNFR1(-/-) mice had reduced expression of the chemokines CCL3 and CCL5, and decreased leukocyte adhesion in the brain vasculature compared to WT mice 4 days post-infection (dpi).At this time point TNFR1(-/-) infected mice also had higher HSV-1 viral replication and more injuries in the brain, especially in the hippocampus.In conclusion, TNFR1 seems to play a relevant role in the control of viral replication in the CNS when HSV-1 is inoculated by intracranial route.