Journal
JOURNAL OF VIROLOGY
Volume 75, Issue 15, Pages 7114-7121Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.75.15.7114-7121.2001
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Funding
- NIEHS NIH HHS [T32 ES07141, T32 ES007141] Funding Source: Medline
- NINDS NIH HHS [R01 NS018596, R01 NS038932, R01 NS18596] Funding Source: Medline
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Virus infection of neurons leads to different outcomes ranging from latent and noncytolytic infection to cell death. Viruses kill neurons directly by inducing either apoptosis or necrosis or indirectly as a result of the host immune response. Sindbis virus (SV) is an alphavirus that induces apoptotic cell death both in vitro and in vivo. However, apoptotic changes are not always evident in neurons induced to die by alphavirus infection. Time lapse imaging revealed that SV-infected primary cortical neurons exhibited both apoptotic and necrotic morphological features and that uninfected neurons in the cultures also died. Antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors protected neurons from SV-induced death without affecting virus replication or SV-induced apoptotic cell death. These results provide evidence that SV infection activates neurotoxic pathways that result in aberrant NMDA receptor stimulation and damage to infected and uninfected neurons.
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