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Persistent infection of human vascular endothelial cells by group B coxsackieviruses
P G Conaldi1, C Serra, A Mossa
1Department of Clinical and Biological Sciences, University of Pavia, Varese, Italy.
Insights
Group B coxsackieviruses (CVBs) can persistently infect human vascular endothelial cells (ECs). These chronic infections, particularly with CVB-3 and CVB-5, may contribute to vascular disease development.
Area of Science:
- Virology
- Cardiovascular Biology
- Immunology
Background:
- Group B coxsackieviruses (CVBs) are significant causes of myocarditis and dilated cardiomyopathy.
- Limited information exists regarding the susceptibility of vascular cells to CVB infections.
Purpose of the Study:
- To investigate the in vitro interactions between Group B coxsackieviruses and human vascular endothelial cells (ECs).
- To determine the permissiveness of ECs to different CVB types and identify factors influencing viral persistence.
Main Methods:
- Infection of primary and immortalized human ECs with CVB types 1-6.
- Monitoring of viral replication, cytopathology, and cytokine production over extended periods (>260 days).
- Assessment of interferon-beta and tumor necrosis factor-alpha (TNF-α) levels in infected ECs.
Main Results:
- All 6 CVB types infected ECs without causing immediate cell death.
- CVB-3 and CVB-5 established persistent infections lasting over 260 days, unlike other CVB types.
- Constitutive interferon-beta production in ECs conferred resistance, while persistent CVB-3 and CVB-5 infections correlated with chronic TNF-α release.
Conclusions:
- Human vascular endothelial cells are permissive to CVB infection.
- CVB-3 and CVB-5 can establish chronic infections in ECs, potentially contributing to vascular pathology.
- Chronic endothelial CVB infection, associated with TNF-α, may play a role in vascular disease.
Abstract:
Group B coxsackieviruses (CVBs) cause >20% of the cases of myocarditis and dilated cardiomyopathy. Information on the permissiveness of vascular cells to CVBs is scant. Interactions of CVBs with human vascular endothelial cells (ECs) were investigated in vitro. All 6 CVBs (CVB-1 to -6) consistently infected primary EC cultures and an immortalized EC line without producing cytopathology. Whereas replication of types 1, 2, 4, and 6 ceased within 30-60 days after infection, CVB-3 and -5 caused a persistent infection. Replication of CVB-3 and -5 continued for >260 days. In ECs, the constitutive production of interferon-beta, but not of other cytokines, appeared to confer resistance to CVBs. Persistence of CVB-3 and -5 was associated with the chronic release of tumor necrosis factor-alpha, a cytotoxic cytokine that also has a negative inotropic effect on myocardial cells. The results suggest that chronic endothelial CVB infections may play a role in vascular disease.