Key result
Group B coxsackieviruses infected human vascular endothelial cells in vitro, with CVB-3 and -5 causing persistent infections lasting >260 days associated with chronic TNF-alpha release.
Group B coxsackieviruses can persistently infect human vascular endothelial cells, leading to chronic TNF-alpha release, which may contribute to vascular disease and myocardial dysfunction.
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Suggests possible viral role in chronic vascular inflammation; leaves open relevance to human cardiovascular disease.
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.
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Conaldi et al. (1997) studied Group B coxsackievirus infection. Group B coxsackieviruses (CVB-1 to -6) was evaluated on Viral infection and replication. Group B coxsackieviruses infected human vascular endothelial cells in vitro, with CVB-3 and -5 causing persistent infections lasting >260 days associated with chronic TNF-alpha release.
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