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18th World Congress on Heart Disease



Nora M. Chapman, M.D., University of Nebraska Medical Center, Omaha, NE, USA


Human enteroviruses like the group B coxsackieviruses (CVB) are known to cause human inflammatory cardiomyopathies but until recently, the CVB were thought to be acute infections, rapidly cleared by the host's immune system. We discovered that CVB can persist for weeks to months following either experimental inoculation (in cell cultures or mice) or natural infection (humans) through a mechanism that involves the loss of the 5' terminal genomic sequence. These 5' terminally deleted (TD) viruses replicate very slowly because the deleted region is key to efficient viral genome replication. Although isolation of CVB-TD from experimentally inoculated mouse hearts revealed a strain with a 49 nucleotide deletion, containing nearly all the domain I structure at the 5' end, we have now deleted the remainder of domain I with a 77 nucleotide deletion. This viable CVB3 strain shows that domain I, previously thought required for virus replication, can be entirely deleted. Slow persistent replication of an enterovirus in heart muscle has been proposed as one mechanism by which heart function can be progressively and deleteriously impacted following an enterovirus infection. The discovery of naturally occurring enteroviral terminal deletions provides a mechanism by which the virus can persist in the host cardiomyocyte, producing viral proteases which can cleave host proteins.




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