Caspase-3 activation is required for reovirus-induced encephalitis in vivo.

Journal of Neurovirology
J David BeckhamKenneth L Tyler

Abstract

Reovirus infection of neonatal mice provides a classic experimental system for understanding the molecular pathogenesis of central nervous system (CNS) viral infection. CNS tissue injury, caused by many human neurotropic viruses, including herpes viruses and West Nile virus, is associated with caspase-dependent apoptotic neuronal cell death. We have previously shown that reovirus-induced CNS tissue injury results from apoptosis and is associated with activation of both death-receptor and mitochondrial apoptotic pathways culminating in the activation of the downstream effector caspase, caspase-3. In order to directly investigate the role of caspase-3 in virus-induced neuronal death and CNS tissue injury during encephalitis, we have compared the pathogenesis of reovirus CNS infection in mice lacking the caspase-3 gene (caspase-3 (-/-)) to syngeneic wild-type mice. Prior studies of antiapoptotic treatments for reovirus-infected mice have indicated that protection from reovirus-induced neuronal injury can occur without altering the viral titer in the brains of infected mice. We now show that reovirus infection of caspase-3 (-/-) mice was associated with dramatic reduction in severity of CNS tissue injury, decreased viral antigen an...Continue Reading

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Citations

May 25, 2012·Journal of Virology·Stephanie A SchittonePenny Clarke
May 16, 2013·MBio·Angela K Berger, Pranav Danthi
Aug 1, 2015·Virology·Bradley E HillerPranav Danthi
Oct 12, 2013·The American Journal of Pathology·Sandra PaciosDana T Graves
Jan 1, 2016·Journal of Virology·Erica L BeatmanJ David Beckham
Aug 28, 2020·Journal of Virology·Roxana M Rodríguez StewartBernardo A Mainou
Dec 21, 2019·Neurobiology of Learning and Memory·YunLei WangTong Zhang

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