The pathogenesis of rat virus infection in infant and juvenile rats after oronasal inoculation

Abstract

The pathogenesis of rat virus (RV) infection was studied in random-bred Sprague-Dawley rats after oronasal inoculation of a recent RV isolate designated RV-Yale (RV-Y). RV-Y was pathogenic for rats inoculated as infants (2 days) whereas rats inoculated as juveniles (4 weeks) had asymptomatic infection and no lesions. Rats inoculated as infants developed pantropic infection accompanied by hepatic necrosis, granuloprival cerebellar hypoplasia and hemorrhagic encephalopathy. Virological and serological studies showed that virus could persist in inoculated rats for at least 35 days and for at least 28 days after seroconversion was first detected. Immunohistochemical results indicated that RV-Y infects tissues conducive to virus excretion including kidney and lung. RV-Y also was found in genital tissues of some rats. Athymic juvenile rats inoculated intraperitoneally with RV-Y had a poor humoral immune response and harbored infectious virus for at least 3 weeks, whereas infection in euthymic control rats was detected for 1 week. These studies indicate that RV-Y can persists in the presence of humoral immunity and suggest that transmission of infection could occur for a substantial period after seroconversion. They also suggest that immunodeficient rats have increased susceptibility to persistent infection.

Pathogenesis of a Newly Isolated Rat Virus in Newborn and Juvenile Rats

“…Thus, we suspect that the different pathogenesis of UT-1 strain from the prototype strain of RV may be due to the altered HA pattern and antigenicity [5]. However, the clinical and histopathological findings in the juvenile and newborn rats presented here were essentially consistent with those of other strains of RV [2,4,7,11,17] . Although antibody production in the infected newborns was slightly delayed to that in the juveniles, the time and level of the peaks of the antibody titer were similar for both (Fig.…”

“…This fact indicates that the virus propagates at the primary infection sites in juvenilis as well as newborns. Jacoby, et al, [7] showed that the virus was re-isolated from most organs except for brain and blood at 5 to 7 days pi in oronasally inoculated juveniles, and that their viral titer was lower than that in newborns. In our study, the virus was recovered from the lung, spleen and kidneys of juveniles at 15 days pi, but the titer was low.…”

“…Rat virus (RV), a member of the family Parvoviridae, is one of the common viruses in laboratory rat colonies and often causes asymptomatic infections in adult rats, and severe diseases in fetal and newborn rats [1,7,11,[14][15][16] . Little attention, however, has been paid to the RV infection in laboratory rat colonies in Japan, since there has been no information about it.…”

Persistent Rat Virus Infection in Smooth Muscle of Euthymic and Athymic Rats

“…These effects have been attributed to the proclivity of autonomous parvoviruses for mitotically active cells (18). RV infection in fetal and infant rats, which have numerous cycling cells, can lead to severe tissue necrosis and clinical morbidity (30,34). The preference of RV for mitotically active cells is also thought to account for its ability to distort responses dependent on cell proliferation, including suppression of tumor growth (7) and immune responses to transplantable neoplasms (13) and tissue alloantigens (40).…”

Immune Responses to the Major Capsid Protein during Parvovirus Infection of Rats

“…It is known that rats develop antiviral antibodies and perivascular mononuclear cell infiltrates in infected tissues (10,14). Virusspecific antibodies have been shown to prevent establishment of RV infection but not to prevent or clear previously established infections.…”