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Altered cell cycle progression and aberrant mitosis in adenovirus-infected rodent cells
Abstract:
Actively growing mouse or rat embryo cells suffered structural chromosome damage, mitotic anomalies, and polyploidy after infection by human adenovirus type 5. Chromosome damage required expression of one or more early viral genes and showed regular periodicity in its frequency. The growth cycle time of some of the infected cells was reduced by about 5 hours due to a decrease in G1, and the interval between successive waves of chromosome damage corresponded to this reduced cycle time. After infection there was a decrease in cells with G1 DNA content and an increase in cells with G2 diploid, aneuploid, and polyploid DNA contents. We suggest these effects are due to the expression in semipermissive cells fo early viral gene(s), whose function in productive infection in vivo is to alter cell cycle controls in order to maximize the number of cells able to replicate viral DNA and the time such cells spend in DNA replication.
Insights
Human adenovirus type 5 infection causes chromosome damage and cell cycle changes in rodent embryo cells. Early viral gene expression alters cell cycle controls, impacting DNA replication and cell division.
Area of Science:
- Cell Biology
- Virology
- Genetics
Background:
- Human adenovirus type 5 (HAdV5) is a common human pathogen.
- Viral infections can impact host cell processes, including cell cycle regulation and genome integrity.
- Understanding viral-induced cellular changes is crucial for virology and cancer research.
Purpose of the Study:
- To investigate the effects of HAdV5 infection on actively growing mouse and rat embryo cells.
- To determine the role of early viral gene expression in HAdV5-induced cellular damage.
- To elucidate the impact of HAdV5 on cell cycle progression and DNA content.
Main Methods:
- Infection of rodent embryo cells with HAdV5.
- Microscopic analysis of chromosome structure and mitotic activity.
- Flow cytometry to assess DNA content and cell cycle distribution.
- Correlation of chromosome damage with viral gene expression.
Main Results:
- HAdV5 infection induced structural chromosome damage, mitotic anomalies, and polyploidy.
- Chromosome damage was dependent on the expression of early viral genes and occurred periodically.
- Infected cells exhibited a reduced cell cycle time (approx. 5 hours) due to a shortened G1 phase.
- A decrease in G1 DNA content and an increase in G2, aneuploid, and polyploid DNA content were observed.
Conclusions:
- Early viral gene expression in semipermissive cells alters host cell cycle controls.
- These alterations likely maximize viral DNA replication by increasing the pool of cells in S phase.
- HAdV5 infection disrupts normal cell cycle progression and genome stability in rodent embryo cells.