TNFR1 plays a critical role in the control of severe HSV-1 encephalitis

Herpes simplex virus-1 (HSV-1) is a pathogen for humans that may cause severe encephalitis. Tumor necrosis factor α (TNF-α) plays a role in several viral diseases of the central nervous system (CNS). The classic proinflammatory activities of TNF-α are mediated mainly through activation of the recept...

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Veröffentlicht in:Neuroscience letters 2010-07, Vol.479 (1), p.58-62
Hauptverfasser: Vilela, Márcia Carvalho, Lima, Graciela Kunrath, Rodrigues, David Henrique, Lacerda-Queiroz, Norinne, Mansur, Daniel Santos, Miranda, Aline Silva de, Rachid, Milene Alvarenga, Kroon, Erna Geessien, Vieira, Leda Quercia, Campos, Marco Antônio, Teixeira, Mauro Martins, Teixeira, Antônio Lúcio
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Sprache:eng
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Zusammenfassung:Herpes simplex virus-1 (HSV-1) is a pathogen for humans that may cause severe encephalitis. Tumor necrosis factor α (TNF-α) plays a role in several viral diseases of the central nervous system (CNS). The classic proinflammatory activities of TNF-α are mediated mainly through activation of the receptor 1 for TNF-α (TNFR1). However, when HSV-1 is inoculated in the periphery, TNF-α 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-1 encephalitis 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.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2010.05.028