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• W2086518669 abstract "The role of nitric oxide synthase type-2 (NOS2)-derived nitric oxide (NO) in the pathogenesis of mouse hepatitis virus (MHV)-induced central nervous system disease was examined. Infection of NOS2 knockout ((-/-)) and NOS2(+/+) mice with MHV resulted in similar kinetics of viral clearance from the brain and comparable levels of demyelination. MHV-infected NOS2(-/-) mice displayed a marked decrease in mortality as compared to infected NOS2(+/+) mice that correlated with a significant decrease (P < or = 0.001) in the number of apoptotic cells (determined by TUNEL staining) present in the brain. Confocal microscopy revealed that the majority of cells (>70%) undergoing apoptosis were neurons. These studies indicate that NOS2-generated NO contributes to apoptosis of neurons but not demyelination following MHV infection." @default.
• W2086518669 created "2016-06-24" @default.
• W2086518669 creator A5002640166 @default.
• W2086518669 creator A5073553823 @default.
• W2086518669 date "2002-01-01" @default.
• W2086518669 modified "2023-09-26" @default.
• W2086518669 title "Lack of nitric oxide synthase type 2 (NOS2) results in reduced neuronal apoptosis and mortality following mouse hepatitis virus infection of the central nervous system" @default.
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• W2086518669 doi "https://doi.org/10.1080/135502802317247820" @default.
• W2086518669 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7094997" @default.
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