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Cell cycle status affects coxsackievirus replication, persistence, and reactivation in vitro
Ralph Feuer1, Ignacio Mena, Robb Pagarigan
1Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.
Journal of Virology
|April 5, 2002
Summary
Enteroviruses like coxsackievirus B3 (CVB3) may persist by infecting quiescent cells. These cells harbor viral RNA, enabling reactivation when they divide, potentially causing chronic diseases.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Enteroviral persistence is linked to chronic diseases like dilated cardiomyopathy and diabetes.
- The mechanisms enabling long-term survival of cytolytic enteroviruses remain unclear.
Purpose of the Study:
- To investigate the role of cell cycle status in enterovirus persistence.
- To understand how coxsackievirus B3 (CVB3) survives in host cells.
Main Methods:
- Generated a recombinant enhanced green fluorescent protein-expressing coxsackievirus B3 (eGFP-CVB3).
- Infected quiescent and dividing tissue culture cells with CVB3 and eGFP-CVB3.
- Utilized cell cycle inhibitors to study viral replication at different cell cycle phases.
- Transfected viral RNA from non-productive cells into dividing cells.
Main Results:
- CVB3 replication and infectious virus production were significantly reduced in quiescent (G(0)) and G(2)/M phase cells.
- Quiescent cells retained CVB3 RNA without producing infectious virus, suggesting latency.
- Viral RNA from quiescent cells was infectious upon transfection into dividing cells.
- Wounding infected quiescent cells triggered viral protein expression in adjacent cells.
Conclusions:
- Cell cycle status dictates CVB3 distribution during acute infection.
- CVB3 persistence in vivo may involve infection of quiescent G(0) cells, which are not permissive for replication.
- Reactivation of CVB3 from latent G(0) cells upon cell cycle progression may trigger chronic pathology.