Rabies is endemic to the Russian Federation. The disease incidence ranges between 2,000 and 4,000 cases annually. Between two and six cases in humans are also reported each year. Wild animals are the basic reservoir and vector of the virus, and the incidence of rabies in foxes and raccoon dogs amounts to 50% of the total number of disease cases. When outbreaks occur, the disease is also reported in domestic animals. To prevent the further spread of rabies, vaccination of domestic animals and oral immunisation of wildlife are practised. Unfortunately, vaccine coverage and disease prevention measures have not been sufficient to achieve a notable improvement in the rabies situation in the country.

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In the second half of the 20th century, fox rabies became unusually widespread in many European countries due to the adaptation of the rabies virus to a new natural host. Starting at the Polish-Russian border in 1939, a wave of fox rabies epizootic moved to the West at a rate of 30-60 km/year; state borders were not a barrier (Steck & Wandeler, 1980;Winkler, 1975). At the same time, fox rabies began to spread eastward in the former Soviet Union (Deviatkin et al., 2017;Winkler, 1975). In central and western Europe, this problem was managed through the implementation of expensive oral vaccination programs. As a result,

Porcine respiratory coronavirus is related genetically to porcine transmissible gastroenteritis virus with a large deletion in S protein. The respiratory virus is a mutated form that may be a consequence of the gastroenteritis virus's evolution. Intensive passages of the virus in its natural host may enhance the appearance of mutations and therefore may contribute to any attenuated form of the virus. The objective of this study was to characterize the porcine transmissible gastroenteritis virus TMK22 strain after passages in piglets from 1992 until 2007. A typical experimental infection, molecular characterization, and serological analysis were also carried out to further characterize and to evaluate any significant difference between strains. The sequence analysis showed two amino acid deletions and loss of an N-glycosylation site in transmissible gastroenteritis virus S protein after passages in piglets. Although these deletions were positioned at the beginning of the antigenic site B of S protein, no clinical differences were observed in piglets infected experimentally either with the native virus or the mutated one. Serological tests did not show any antibody reactivity difference between the two strains. In this article, we report that the S protein deletion did not affect the virus's pathogenicity. The variety of the virus's evolutionary forms may be a result, not only of the multiple passages in natural hosts, but also of other factors, such as different pathogens co-infection, nutrition, immunity, and others. Further studies need to be carried out to characterize the mutated strain.