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Abstract
The pathogenesis of ocular cytomegalovirus (CMV) infection in mice was studied in detail as a model of ocular involvement of human CMV infection. Smith strain of mouse CMV (MCMV) was inoculated into the anterior chamber of the eye and viral antigen was located by immunofluorescence. When salivary gland passaged MCMV (SG-MCMV) was inoculated into the 12- to 18-day-old ICR/Sic mice, it elicited transient uveitis, retinitis, and scleritis during the early phase of infection followed by spread into the lacrimal glands, extraocular muscles and salivary glands. Mouse embryonic fibroblasts (MEF) passaged attenuated MCMV (CC-MCMV) caused mild uveitis with a short duration even inoculated into young mice, and the viral antigen was detected only in salivary glands thereafter. SG-MCMV titer in the eye taken from the young mice decreased from 10(4.5) TCID50/0.1 g at 2 days postinfection (PI) to 10(3.0) TCID50/0.1 g at 21 days PI, whereas in the salivary glands, it became detectable at 5 days PI with a titer of 10(5.0) TCID50/0.1 g, which increased up to 10(8.7) TCID50/0.1 g at 21 days PI. CC-MCMV was detectable only in the young mice salivary glands ranging from 10(4.7) TCID50/0.1 g at 9 days PI to 10(7.3) TCID50/0.1 g at 21 days PI. When the lens capsule had been damaged during the inoculation procedure, the mice developed cataracts with evidence of viral growth in the lens. When SG-MCMV was inoculated onto the cornea, viral antigen was not detected during the period of the present experiment.(ABSTRACT TRUNCATED AT 250 WORDS)