Congenital reovirus, type 2 infections were produced after intraperitoneal inoculations of brood mothers on the 1st, 3rd, 6th, 10th, and 15th day of gestation. The offspring presented with a varied syndrome. About a quarter of a total of over 200 mice showed symptoms within the first 14 days of life; namely, lassitude, retarded growth, and roughening of fur. Some died, apparently of respiratory or renal failure. Post mortem examination showed marked interstitial pneumonia and subcortical renal tubular necrosis. Reovirus was isolated in high titer from the kidney and lungs as well as from blood, hearts, hind limbs, and brains in lesser titer.

At 3 wk of age over 50 apparently well mice were sacrificed, and virologic, serologic, and pathologic study was done. High titers of virus were again found in the kidney, lung, blood, brain, heart, and skeletal muscle, but all tissues appeared normal histologically. Type-specific serum antibody titers in these mice were approximately those of their mothers.

Another half of these mice showed decreased spontaneous activity and growth retardation which appeared between the 15th and 36th days of life. Three of these mice with late illnesses had marked proptosis and conjunctivitis. A subepidermal conjunctival and extraocular muscle lymphocytic infiltrate was observed on section, and reovirus was isolated from these eyes in tissue culture. Again blood, brain, kidney, liver, spleen, myocardium, and skeletal muscle were studied, and were found to be normal histologically and not to contain reovirus. Finally, the rest of the mice remain well to date.

At 3 months of age, 10 of them were sacrificed. All had lost their maternal antibody and contained no reovirus, type 2 hemagglutinating inhibiting antibodies.

No developmental abnormalities were observed.

These data suggest that prolonged reovirus infections may be established by means of congenital inoculation of the developing fetus. Tolerant infection with immune paralysis seems to have been established.

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