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Infect Immun. 1970 Sep;2(3):298-303. doi: 10.1128/iai.2.3.298-303.1970.

Pathogenesis and transmission of kilham rat virus infection in rats.

Infection and immunity

J F Novotny, F M Hetrick

Affiliations

  1. Department of Microbiology, University of Maryland, College Park, Maryland 20742.

PMID: 16557835 PMCID: PMC416005 DOI: 10.1128/iai.2.3.298-303.1970

Abstract

The Kilham rat virus (RV) was found to produce mortality in newborn rats after intracerebral, intravenous, or subcutaneous administration of virus. Both infectious virus and viral hemagglutinins were detected in a variety of tissues and in the blood and urine of experimentally infected rats. Contact control rats housed with infected littermates did not develop disease but did produce antibody to RV. Horizontal virus transmission was also evidenced by the seroconversion of antibody-negative mothers whose litters were infected with RV. The level of maternal antibody was found to be the determining factor in the susceptibility or refractiveness of newborn rats to RV infection. If the mother had no detectable hemagglutination-inhibiting (HI) antibody titer (less than 10) or a low antibody titer (10 or 20), her offspring were highly susceptible to RV. However, the litters of rats with HI titers of 40 or greater were afforded protection when challenged with RV; the higher the maternal antibody level the more solid was the protection conferred. Vertical transmission of RV was also demonstrated. Litters born of mothers infected with RV several days before delivery died within 7 to 9 days of a disease identical to that seen in infected newborns and virus was recovered from a variety of tissues. Results of mother-litter exchange experiments also indicated vertical transmission (rather than transmission through milk) occurs, since litters of infected mothers developed the disease when nursed by normal mothers, whereas litters of normal mothers remained normal although they were nursed by infected mothers.

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