Interestingly, in those adult cases of myocarditis in which the presence of virus was shown by detecting the viral RNA, rarely can an infectious virus be isolated. This is confusing: how can one detect viral RNA and not detect the virus? And indeed, this was a conundrum for many years.
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We decided to examine the entire viral RNA genome that was present in these mouse heart samples, asking the basic question: are there deletions anywhere else that might explain this odd phenomenon? When this was done, we discovered that one of the ends of the single strand of RNA that makes up the viral genome, was missing: these viral genomes were then called 'terminally deleted' or TD. What makes this discovery fascinating to virologists, is that the sequence which the virus naturally deletes, was hitherto thought to be absolutely essential for virus replication. Our results, however, showed that while this sequence was very important for efficient CVB replication, it could nonetheless be done away with, and yet have the virus survive.
The cost of this survival is, however, extremely slow replication. A further cost is that this survival can occur only in cell populations that do not divide anymore or divide very infrequently as in muscle tissue. It is this reason why we were able to find these novel virus populations in heart muscle of experimentally inoculated mice and later, in human heart.
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These results provided an answer to the conundrum of failing to find cytopathic virus in myocarditic heart samples despite the ability to find viral RNA. Indeed, virus (in TD form) does exist in such samples but because the TD populations replicate so slowly and produce so little virus, they are difficult to detect. However, because the defect is not in a part of the viral genome that makes viral proteins, they do make all the viral proteins and even virus particles. But what does the finding of TD genomes mean for HEV disease?
Source:
Human Enteroviruses and Chronic Infectious Disease, Steven Tracy and Nora M. Chapman.