Chapter title |
The pattern of induction of apoptosis during infection with MHV-3 correlates with strain variation in resistance and susceptibility to lethal hepatitis.
|
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Chapter number | 80 |
Book title |
Coronaviruses and Arteriviruses
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Published in |
Advances in experimental medicine and biology, January 1998
|
DOI | 10.1007/978-1-4615-5331-1_80 |
Pubmed ID | |
Book ISBNs |
978-1-4613-7432-9, 978-1-4615-5331-1
|
Authors |
Belyavskyi, M, Levy, G A, Leibowitz, J L, Michail Belyavskyi, Gary A. Levy, Julian L. Leibowitz, Belyavskyi, Michail, Levy, Gary A., Leibowitz, Julian L. |
Abstract |
In the present study we have investigated the possibility that strain specific differences in the induction of apoptosis in macrophages could play a role in the resistance of strain A/J mice to MHV-3 induced hepatitis. MHV-3 infected macrophages from Balb/c and A/J mice were analyzed at various time points after infection. Apoptosis in A/J macrophages could be detected at 8 h post infection and increased significantly by 12 h, when almost 50-70% of the infected cells were undergoing apoptosis. In Balb/c macrophages, apoptotic changes were less pronounced and were observed in only 5-10% of the cells. MHV-3 induced apoptosis was inversely correlated with the ability of this virus to induce expression of fgl-2 prothrombinase protein and syncytia formation. Infected macrophages from A/J mice did not express fgl-2 protein and did not form syncytia. In contrast, infection of Balb/c derived macrophages resulted in fgl-2 expression and extensive syncytia formation. These data fit a model in which apoptosis of virally infected cells is a protective response which eliminates cells whose survival might be harmful for the whole organism. |
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Researcher | 1 | 17% |
Student > Bachelor | 1 | 17% |
Unknown | 1 | 17% |
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Unknown | 2 | 33% |