TY - JOUR
T1 - TNFR1 plays a critical role in the control of severe HSV-1 encephalitis
AU - Vilela, Márcia Carvalho
AU - Lima, Graciela Kunrath
AU - Rodrigues, David Henrique
AU - Lacerda-Queiroz, Norinne
AU - Mansur, Daniel Santos
AU - Miranda, Aline Silva de
AU - Rachid, Milene Alvarenga
AU - Kroon, Erna Geessien
AU - Vieira, Leda Quercia
AU - Campos, Marco Antônio
AU - Teixeira, Mauro Martins
AU - Teixeira, Antônio Lúcio
PY - 2010/7
Y1 - 2010/7
N2 - 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 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.
AB - 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 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.
KW - Herpes simplex virus type 1
KW - Neuroinflammation
KW - TNFR1
UR - https://www.scopus.com/pages/publications/77953697695
UR - https://www.scopus.com/pages/publications/77953697695#tab=citedBy
U2 - 10.1016/j.neulet.2010.05.028
DO - 10.1016/j.neulet.2010.05.028
M3 - Article
C2 - 20478363
AN - SCOPUS:77953697695
SN - 0304-3940
VL - 479
SP - 58
EP - 62
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1
ER -