Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Vilela, M.C. et al.

Márcia Carvalho Vilela, Graciela Kunrath Lima, David Henrique Rodrigues, Norinne Lacerda-Queiroz, Daniel Santos Mansur, Aline Silva de Miranda, Milene Alvarenga Rachid, Erna Geessien Kroon, Leda Quercia Vieira, Marco Antônio Campos, Mauro Martins Teixeira, Antônio Lúcio Teixeira,

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 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-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.[1]

References

TNFR1 plays a critical role in the control of severe HSV-1 encephalitis. Vilela, M.C., Lima, G.K., Rodrigues, D.H., Lacerda-Queiroz, N., Mansur, D.S., de Miranda, A.S., Rachid, M.A., Kroon, E.G., Vieira, L.Q., Campos, M.A., Teixeira, M.M., Teixeira, A.L. Neurosci. Lett. (2010) [Pubmed]

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