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Reovirus Infection

Reoviruses that infect mice belong to the family Reovir- idae and subgroup 1 of the genus Orthoreovirus. The name reovirus (respiratory enteric orphan virus) was proposed for a group of viruses associated with respira­tory and enteric infections in humans.

Reoviruses have since been isolated from a wide variety of mammals, birds, reptiles, insects, and other species. In fact, reovirus infection has been documented in every mammalian species tested. Mammalian orthoreoviruses are divided into 3 serotypes, based upon hemagglutination inhibi­tion and neutralization tests. They are commonly referred to as reovirus 1, reovirus 2, and reovirus 3, although they actually represent a spectrum of viruses that are antigeni- cally cross-reactive and genetically related. Although dis­ease is rare, reovirus 3 has been incriminated as a pathogen in mice, and so it receives the most emphasis. Reoviruses frequently contaminate biological materials.

Epizootiology and Pathogenesis

Reovirus seroconversion is a frequent finding among wild mice and laboratory mice. Because reovirus 3 sero­types are the most common in laboratory mice, and only that serotype has been associated with natural disease in mice, reovirus 3 is emphasized and used as antigen. Seroconversion, however, reflects exposure to viruses from any of the serotypes. Reoviruses are transmitted by the orofecal route. Transmission among mice seems to occur primarily by direct contact among young mice. Contact transmission between adult mice is inefficient. Mice of all ages are susceptible to experimental infection by a variety of routes, but only mice infected as neonates develop disease. Strain-related differences in susceptibil­ity have not been reported. Following oral inoculation of neonatal mice, virus enters through the M cells of Peyer's patches with dissemination to multiple organs via hem­atogenous, lymphatic, and/or neural spread.

Reovirus 3 replication occurs in multiple organs of neonatal mice in the absence of significant lesions, until around day 10-12, when mice become clinically ill and develop lesions in multiple tissues, followed by recovery. This suggests an immune-mediated mechanism for develop­ment of lesions during the process of recovery, but this mechanism has not been defined. Pups born to immune dams do not develop disease. Oral inoculation of C.B-17- scid mice with reovirus 1 or 3 resulted in a lethal infec­tion due to necrotizing hepatitis, with virus, but not lesions, detectable in multiple other organs.

Pathology

Disease and lesions occur only in infant mice from colonies previously unexposed to reovirus. At around 2 weeks of age, mice may be runted, jaundiced, and uncoordinated and have matted hair due to steatorrhea, which has been termed “oily hair effect.” Surviving mice may remain runted and have transient dorsal alopecia. The most significant microscopic lesion is acute diffuse encephalitis that has a vascular distribution. Mice also develop focal necrotizing myocarditis, variable necrosis of lymphoid tissue, focal necrotizing hepatitis, portal hepatitis, acinar pancreatitis, and sialodacryoadenitis. C.B-17-scid mice infected with reovirus 1 or 3 developed progressive, necrotizing hepatitis, without lesions in other organs. Experimental inoculation of neonatal mice with prototype reovirus 1, 2, or 3 revealed different patterns of disease, but those differences do not neces­sarily reflect all members of each serotype.

Diagnosis

Reovirus infection is usually detected in a mouse popu­lation serologically, in the absence of disease, although outbreaks of disease have been reported among neo­nates. Some of the disease manifestations that have been reported in the early literature may be due to other infectious agents, such as MHV. Virus can be isolated from infected tissues, antigen can be visualized by immunohistochemistry, and tissues or biologic products can be tested by PCR. Lesions are nonspecific. Differen­tial diagnoses of neonatal disease with steatorrhea include MHV, EDIM virus, and Salmonella infections.

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Source: Barthold Stephen W., Griffey Stephen M., Percy Dean H.. Pathology of Laboratory Rodents and Rabbits. 4th Edition. — Wiley-Blackwell,2016. — 384 p.. 2016
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