Viruses are usually classified according to structural principles and genetic homology. Agents causing zoonoses exist in various virus groups that have similarities in the disease patterns that they induce. There may also be similarities involved in hosts and vectors. In this we have chosen a sequential arrangement following viral classifications for the most part. This sequence makes it possible to point out similarities within individual virus groups. Viral zoonosis are also compared with nonviral zoonotic diseases.

Among the agents causing zoonotic disease, zoonotic viruses are the most abundant and the majority of zoonotic viruses have RNA as genetic material. DNA viruses, due to effective proofreading mechanisms of the DNA polymerases, have greater genetic stability, restricting their host range to a spectrum of closely interrelated host animals. Only proviruses and some representatives of the herpes virus family are able to cross species barriers and cause zoonotic infections.

RNA viruses on the other hand do not have proofreading mechanisms; consequently, every reproductive cycle will produce a great number of genetic variants, which may often be unable to reproduce in their original host cells. By chance, new variants may be produced with the ability to extend the host range to other hosts. Of course, all these variants will have to overcome a selection process that will, in most cases, restrict, or in some cases, even improve their reproductive success.

Single point mutation is not the only mechanism that is responsible for the variability of RNA viruses. In addition, some groups of RNA viruses have powerful mechanisms to use genetic recombination or genetic reassortment to extend their genetic variability enabling them to change or enlarge their host range, an ideal preposition for the life cycle of a zoonotic virus. Regarding the genetic variability of RNA- bacteriophages, von eigen has coined the term quasispecies, which offers an ideal understanding of the variability of zoonotic RNA viruses. In consequences of these developments, it has become more difficult to explain and to understand the relative stability that is observed in some none zoonotic RNA virus species, for example, in measles, mumps or rubella.

In most RNA viruses, the recognition of a “species” is defined by a great diversity of selection mechanisms or circumstances, too large to be discussed in this text. Some of these restrictions are due to human habits and to the mobility of human populations; others are due to human habits and to the mobility of human populations; others are due to geographic conditions. In many cases, the restricting circumstances are not understood to all. For example, the virus of Venezuelan horse encephalitis, an alpha virus, normally exists in enzootic cycles, where it is transmitted by mosquitoes. From time to time, variants of this virus appear which cause epizootic diseases in horses with a high rate of fatal encephalitis. Next to horses, humans are affected by the virus. These epizootic or epidemic variants of the virus are not detectable in the inter-epidemic periods, although the host reservoir of the enzootic variants is well known. In the same way, hitherto unknown viruses may by chance infect the human population and they cause outbreaks of severe disease.

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Regards,

John George

Journal of Zoonotic Diseases and Public Health

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