Key result
Coxsackievirus B5 infection leads to a high number of empty capsids and decreased infective virions, a property dictated by structural proteins and not observed in the constructed chimera virus.
Why the study?
Enteroviruses cause severe diseases through lytic or persistent infections, making it essential to understand the mechanisms leading to efficient versus inefficient infections.
The structural proteins of coxsackievirus B5 dictate the production of empty capsids, which may be a mechanism leading to persistent rather than lytic infections.
High empty virus production may mark CVB5 persistence; leaves open structural-nonstructural determinants of enteroviral chronicity.
Enteroviruses cause several severe diseases, with lytic infections that lead to rapid cell death but also persistent infections that are more silent and lead to chronic states of infection. Our study compared a cytolytic echovirus 1 infection to persistent coxsackievirus B5 infection by making a chimera with the structural proteins of echovirus 1 and the nonstructural proteins of coxsackievirus B5. Coxsackievirus B5 infection was found to lead to the production of a high number of empty viruses (empty capsids) that do not contain genetic material and are unable to continue the infection. Coinciding with the high number of empty capsids, the amount of infective virions decreased. This characteristic property was not observed in the constructed chimera virus, suggesting that structural proteins are in charge of these phenomena. These results shed light on the mechanisms that may cause persistent infections. Understanding events leading to efficient or inefficient infections is essential in understanding virus-caused pathologies.
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Turkki et al. (2019) studied Enterovirus infection. Chimera with structural proteins of echovirus 1 and nonstructural proteins of coxsackievirus B5 vs. Cytolytic echovirus 1 and persistent coxsackievirus B5 was evaluated on Production of empty viruses (empty capsids) and infective virions. Coxsackievirus B5 infection leads to a high number of empty capsids and decreased infective virions, a property dictated by structural proteins and not observed in the constructed chimera virus.
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