Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/7085
Title: NFR1 plays a critical role in the control of severe HSV-1 encephalitis. TNFR1 plays a critical role in the control of severe HSV-1 encephalitis.
Authors: Vilela, Márcia Carvalho
Lima, Graciela Kunrath
Rodrigues, David Henrique
Queiroz, Norinne Lacerda
Mansur, Daniel Santos
Miranda, Aline Silva de
Rachid, Milene Alvarenga
Kroon, Erna Geessien
Vieira, Leda Quércia
Campos, Marco Antônio da Silva
Teixeira, Mauro Martins
Teixeira, Antônio Lúcio
Affilliation: Universidade Federal de Minas Gerais. Faculdade de Medicina. Departamento de Clínica Médica. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Microbiologia. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Faculdade de Medicina. Departamento de Clínica Médica. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Patologia Geral. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Microbiologia. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brazil.
Fundação Oswaldo Crz. Centro de Pesquisas René Rachou. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Insituto de Ciencias Biologicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brazil.
Universidade Federal de Minas Gerais. Faculdade de Medicina. Departamento de Clínica Médica. Belo Horizonte, MG, Brazil.
Abstract: Herpes simplex virus-1 (HSV-1) is a pathogen for humans that may cause severe encephalitis. Tumor necrosis factor (TNF- ) plays a role in several viral diseases of the central nervous system (CNS). The classic proinflammatory activities of TNF- are mediated mainly through activation of the receptor 1 for TNF- (TNFR1). However, when HSV-1 is inoculated in the periphery, TNF- 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 102 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.
Keywords: Herpes simplex virus type 1
TNFR1
Neuroinflammation
Issue Date: 2010
Publisher: Elsevier Ireland Ltd
Citation: VILELA, Márcia Carvalho et al. TNFR1 plays a critical role in the control of severe HSV-1 encephalitis. TNFR1 plays a critical role in the control of severe HSV-1 encephalitis. Neurosci Lett., v. 479, n. 1, p. 58-62, Jul. 2010.
DOI: 10.1016/j.neulet.2010.05.028
ISSN: 0304-3940
Copyright: restricted access
Appears in Collections:MG - IRR - Artigos de Periódicos

Files in This Item:
File Description SizeFormat 
130.2010.pdf710.84 kBAdobe PDFThumbnail
    Request a copy


FacebookTwitterDeliciousLinkedInGoogle BookmarksBibTex Format mendeley Endnote DiggMySpace

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.