Transplacental infection of rats and hamsters induced by oral and parenteral inoculations of H‐1 and rat viruses (RV)

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An aim of the present investigations was to use recently isolated strains of H‐1 and RV, which had been subjected to a minimum of laboratory passages, to induce transplacental infection orally in order to replicate natural infections in rats, the natural hosts, as well as in hamsters, which are subject to “spontaneous” infection with these agents. H‐1 virus had a remarkable ability to penetrate both the gut wall and placental barrier and infect fetuses within 24 hours of oral inoculation of pregnant hamsters, whereas such infections could be induced in rats only by parenteral inoculation. However, rats were susceptible to fetal infection with RV given orally. The pathogenesis of infection was somewhat different with the two viruses. RV, in contradistinction to H‐1, proliferated in maternal organs and possibly in the placenta for several days before invading the fetus. Both H‐1 and RV were alike in being transported in the blood in close association with erythrocytes. All fetuses invaded by either agent developed widespread infections prior to death as shown by the presence of intranuclear inclusions and cytolytic effects. Placentas remained intact and viable even after resorption of attached fetuses. The health of all mother animals was unaffected. One special strain — HHP — was the only RV strain to induce transplacental infection orally in hamsters. The various attributes of these parvoviruses that make them particularly favorable agents for the study of transplacental infections are discussed.