Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A family of three white-faced saki monkeys (Pithecia pithecia pithecia) died 48-96 hours after the onset of anorexia, nasal discharge, pyrexia and oral ulceration. One animal also had clonic seizures. Lesions found post-mortem consisted of oral and esophageal ulcers, hepatic and intestinal necrosis, meningoencephalitis and sporadic neuronal necrosis. Intranuclear inclusion bodies and syncytial cells were present in oral lesions and affected areas of liver. Herpes simplex virus 1 (HSV-1) was identified as the etiology of disease by virus isolation, polymerase chain reaction, or in situ hybridization in all three animals. Immunohistochemistry for detection of apoptotic DNA and activated caspase-3 showed significant levels of apoptosis in oral and liver lesions and occasional apoptotic neurons in the brain. These findings demonstrate the vulnerability of white-faced saki monkeys to HSV-1 and provide initial insight into the pathogenesis of fatal HSV-1-induced disease, indicating that apoptosis plays a significant role in cell death.
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PMID:Naturally occurring fatal herpes simplex virus 1 infection in a family of white-faced saki monkeys (Pithecia pithecia pithecia). 1273 97

Peste des petits ruminant (PPR), a highly contagious viral disease of small ruminants, is characterized by erosive stomatitis and pneumo-enteritis. However, its neurovirulence potential as observed with other morbilliviruses has not been fully investigated. The present study describes the neuropathological alterations induced by PPR virus through apoptotic pathway. A total number of 12 carcasses of local breed goat kids of either sex were received for postmortem examination. The clinical history was described as symptoms of mucopurulent nasal discharge, high to low grade fever, erosive stomatitis, dyspnoea and profuse watery diarrhoea followed by mortality of 35 goat kids within a week. The pathoanatomical lesions and immunohistochemical demonstration of PPRV antigen in lungs, intestine, spleen and lymph nodes confirmed PPR disease in goats. Grossly, five brain specimens showed moderate to severe leptomeningeal congestion during necropsy. Microscopically, brain sections showed leptomeningitis and nonsuppurative encephalitis characterized by vascular congestion, haemorrhages in the parenchyma, perivascular cuffing with mild to moderate mononuclear cells (mainly lymphocytes and few macrophages), focal to diffuse microgliosis, neuronal degeneration, satellitosis and neuronophagia. Immunolabelling of viral antigen was observed in the cytoplasm of neurons and glial cells. The RT-PCR amplification of N gene fragment also confirmed the presence of PPRV in the brain. The strong immunoreactivity of Caspase-3, Caspase-8 and comparatively lower expression of caspase-9 along with the absence of any reactivity for Apaf-1 antigen in the brain sections indicated the role of caspase dependent extrinsic pathway in inducing neuropathological changes. The presence of apoptotic neurons in the brain by TUNEL assay further confirmed the apoptosis and strong immunoreactivity of iNOS in neurons which suggested the generation of oxidative stress, that might have induced the apoptosis. The overall findings confirm the neurovirulence potential of PPR virus, via the extrinsic pathway of apoptosis, in natural cases of PPR disease in goat kids.
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PMID:Neuropathology mediated through caspase dependent extrinsic pathway in goat kids naturally infected with PPRV. 3187 17