Life Cycles and Reproduction

Varicella Zoster Virus is a virus completely unique to humans, therefore no other animal can host VZV and there is no animal equivalent. The virus is currently being studied by many biologist all over the world, but it is still unclear exactly what happens to the virus to make it go into latency and what triggers the virus to come out of latency. Because so little is known about the steps between latency and reactivation, it remains undetermined how exactly the life cycle of Varicella Zoster Virus works. There is an attempt to “recapitulate the full virus life cycle from primary infection to latency through to reactivation” according to M. Steain and his colleagues at the University of Sydney, though the attempts have not come through quite yet. M. Steain quotes “In order to elucidate the mechanisms which control the establishment of latency and reactivation as well as the effect of VZV replication on neuronal function, in vitro models of neuronal infection have been developed. Currently these models involve culturing and infecting dissociated human fetal neurons, with or without their supporting cells, an intact explant fetal dorsal root ganglia (DRG) model, neuroblastoma cell lines and rodent neuronal cell models. Each of these models has distinct advantages as well as disadvantages, and all have contributed towards our understanding of VZV neuronal infection”. What scientists do know is that the VZV operates the same way most viruses do, which is to attach to the host cells and reproduce with the injection and the multiplication of the viral chromosome.

An Average Virus Life Cycle


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