Programmed cell death in the pathogenesis of rabbit hemorrhagic disease
Rabbit hemorrhagic disease is a rapidly lethal infection caused by a calicivirus, characterized by acute liver damage and disseminated intravascular coagulation (DIC). Following morphological criteria and using a specific in situ labeling technique, we have found that liver cell death induced upon infection is due to apoptosis, and that programmed cell death is a constant feature in rabbits experimentally infected with RHDV. The process affected mainly hepatocytes, but also macrophages and endothelial cells presented morphologic hallmarks of apoptosis, expressing all these cell types viral antigens as determined by immunohistochemistry. The occurrence of programmed cell death was correlated with the appearance of the RHDV induced pathology in tissues by DNA fragmentation detection in situ. Hepatocyte apoptosis produced extensive parenchymal destruction causing a lethal, acute fulminant hepatitis that is characteristic of RHD. Apoptosis of intravascular monocytes and endothelial cells was observed together with fibrin thrombi in blood vessels. Since apoptotic cells are known sites of enhanced procoagulant activity, apoptosis of these cell populations might constitute a first step in the pathogenesis of DIC and a common pathway to other viral hemorrhagic fevers. In conclusion, apoptosis in RHD may be determinant in the development of the pathogenesis of this disease.
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1998
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dig-inia-es-10261-2915432023-02-20T07:19:17Z Programmed cell death in the pathogenesis of rabbit hemorrhagic disease Alonso, C. Oviedo, J. M. Martín-Alonso, J. M. Díaz, E. Boga, J. A. Parra, F. Rabbit hemorrhagic disease is a rapidly lethal infection caused by a calicivirus, characterized by acute liver damage and disseminated intravascular coagulation (DIC). Following morphological criteria and using a specific in situ labeling technique, we have found that liver cell death induced upon infection is due to apoptosis, and that programmed cell death is a constant feature in rabbits experimentally infected with RHDV. The process affected mainly hepatocytes, but also macrophages and endothelial cells presented morphologic hallmarks of apoptosis, expressing all these cell types viral antigens as determined by immunohistochemistry. The occurrence of programmed cell death was correlated with the appearance of the RHDV induced pathology in tissues by DNA fragmentation detection in situ. Hepatocyte apoptosis produced extensive parenchymal destruction causing a lethal, acute fulminant hepatitis that is characteristic of RHD. Apoptosis of intravascular monocytes and endothelial cells was observed together with fibrin thrombi in blood vessels. Since apoptotic cells are known sites of enhanced procoagulant activity, apoptosis of these cell populations might constitute a first step in the pathogenesis of DIC and a common pathway to other viral hemorrhagic fevers. In conclusion, apoptosis in RHD may be determinant in the development of the pathogenesis of this disease. 2023-02-20T07:19:17Z 2023-02-20T07:19:17Z 1998 artículo Archives of Virology 143: 321-332 (1998) 0304-8608 http://hdl.handle.net/20.500.12792/5882 http://hdl.handle.net/10261/291543 10.1007/s007050050289 1432-8798 en none Springer Nature |
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Rabbit hemorrhagic disease is a rapidly lethal infection caused by a calicivirus, characterized by acute liver damage and disseminated intravascular coagulation (DIC). Following morphological criteria and using a specific in situ labeling technique, we have found that liver cell death induced upon infection is due to apoptosis, and that programmed cell death is a constant feature in rabbits experimentally infected with RHDV. The process affected mainly hepatocytes, but also macrophages and endothelial cells presented morphologic hallmarks of apoptosis, expressing all these cell types viral antigens as determined by immunohistochemistry. The occurrence of programmed cell death was correlated with the appearance of the RHDV induced pathology in tissues by DNA fragmentation detection in situ. Hepatocyte apoptosis produced extensive parenchymal destruction causing a lethal, acute fulminant hepatitis that is characteristic of RHD. Apoptosis of intravascular monocytes and endothelial cells was observed together with fibrin thrombi in blood vessels. Since apoptotic cells are known sites of enhanced procoagulant activity, apoptosis of these cell populations might constitute a first step in the pathogenesis of DIC and a common pathway to other viral hemorrhagic fevers. In conclusion, apoptosis in RHD may be determinant in the development of the pathogenesis of this disease. |
format |
artículo |
author |
Alonso, C. Oviedo, J. M. Martín-Alonso, J. M. Díaz, E. Boga, J. A. Parra, F. |
spellingShingle |
Alonso, C. Oviedo, J. M. Martín-Alonso, J. M. Díaz, E. Boga, J. A. Parra, F. Programmed cell death in the pathogenesis of rabbit hemorrhagic disease |
author_facet |
Alonso, C. Oviedo, J. M. Martín-Alonso, J. M. Díaz, E. Boga, J. A. Parra, F. |
author_sort |
Alonso, C. |
title |
Programmed cell death in the pathogenesis of rabbit hemorrhagic disease |
title_short |
Programmed cell death in the pathogenesis of rabbit hemorrhagic disease |
title_full |
Programmed cell death in the pathogenesis of rabbit hemorrhagic disease |
title_fullStr |
Programmed cell death in the pathogenesis of rabbit hemorrhagic disease |
title_full_unstemmed |
Programmed cell death in the pathogenesis of rabbit hemorrhagic disease |
title_sort |
programmed cell death in the pathogenesis of rabbit hemorrhagic disease |
publisher |
Springer Nature |
publishDate |
1998 |
url |
http://hdl.handle.net/20.500.12792/5882 http://hdl.handle.net/10261/291543 |
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