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Influenza Virus Propagation in Embryonated Chicken Eggs
Published on: March 19, 2015
Influenza virus overcomes apoptosis by rapid multiplication
M Kurokawa1, A H Koyama, S Yasuoka
1Department of Nursing, School of Medical Sciences, The University of Tokushima, Tokushima 770-8503, Japan.
International Journal of Molecular Medicine
|April 15, 1999
Abstract:
The kinetics of apoptotic fragmentation of the chromosomal DNA was determined in the influenza virus-infected MDCK, HeLa and KB cells, respectively. Comparison of these kinetics with the kinetics of virus multiplication revealed that the multiplication of influenza virus was observed only when apoptosis was induced after the production of progeny virus in the infected cells. The extent of apoptotic response was reversely correlated with the permissiveness of the cells.
Insights
Influenza virus multiplication occurs only after progeny virus production, coinciding with induced apoptosis. Cell permissiveness inversely correlates with the apoptotic response in infected cells.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Apoptosis, or programmed cell death, is a critical cellular process.
- Influenza virus infection can trigger various cellular responses, including apoptosis.
- Understanding the interplay between viral replication and host cell apoptosis is crucial.
Purpose of the Study:
- To investigate the kinetics of chromosomal DNA fragmentation during influenza virus infection in different cell lines.
- To compare the timing of apoptosis with viral multiplication.
- To determine the relationship between cellular permissiveness and the apoptotic response.
Main Methods:
- Determining the kinetics of apoptotic DNA fragmentation in MDCK, HeLa, and KB cells infected with influenza virus.
- Monitoring and comparing the kinetics of viral multiplication alongside DNA fragmentation.
- Assessing the correlation between the extent of apoptotic response and cell permissiveness.
Main Results:
- Apoptotic fragmentation of chromosomal DNA was observed in infected MDCK, HeLa, and KB cells.
- Influenza virus multiplication was detected exclusively when apoptosis induction followed progeny virus production.
- A negative correlation was found between the degree of the apoptotic response and the permissiveness of the cells for viral replication.
Conclusions:
- The timing of apoptosis relative to viral replication is critical for influenza virus multiplication.
- Cell permissiveness influences the host cell's apoptotic response during influenza virus infection.
- These findings provide insights into the complex interactions between influenza virus and host cell death pathways.
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