Abstract
Viruses are able to evolve in vitro by mutations after serial passages in cell cultures, which can lead to either a loss, or an increase, of virulence. Cyprinid herpesvirus 3 (CyHV-3), a 295-kb double-stranded DNA virus, is the etiological agent of the koi herpesvirus disease (KHVD). To assess the influence of serial passages, an isolate of CyHV-3 (KHV-T) was passaged 99 times onto common carp brain (CCB) cells, and virus virulence was evaluated during passages through the experimental infections of common carp. After 78 CCB passages, the isolate was much less virulent than the original form. A comparative genomic analysis of these three forms of KHV-T (P0, P78 and P99) revealed a limited number of variations. The largest one was a deletion of 1363 bp in the predicted ORF150, which was detected in P78, but not in P99. This unexpected finding was confirmed by conventional PCR and digital PCR. The results presented here primarily suggest that, CyHV-3 evolves, at least in vitro, through an assemblage of haplotypes that alternatively become dominant or under-represented.
Highlights
Common carp (Cyprinus carpio L.) is the most produced fish in the world
It is highly susceptible to the Cyprinid herpesvirus 3 (CyHV-3), called Koi Herpesvirus (KHV)
Common carp brain (CCB) cells [22] were grown at 20 ◦ C in minimal essential medium with Earls’
Summary
Common carp (Cyprinus carpio L.) is the most produced fish in the world. With its ornamental breed, the koi is one of the most expensive fish. 1), goldfish herpesvirus (Cyprinid herpesvirus 2), and eel herpesvirus (Anguillid herpesvirus 1), CyHV-3 clusters as a member of the genus Cyprinivirus in the family, Alloherpesviridae [5]. It causes mass mortality in carp aquaculture, often with more than 80% losses and severe symptoms. Persistent infected carp can shed the virus for the rest of their life Those carp or koi can infect naive fish and spread the virus. By successive passages on cell culture, has proven efficient [18], no genomic and/or transcriptomic comparisons, between original and attenuated viral strains, have been carried out so far, in view of understanding the molecular mechanisms of virus attenuation. The results presented below prove, for the first time, that CyHV-3 evolves, at least in vitro, through an assemblage of haplotypes that alternatively become dominant and under-represented
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