Abstract
Infection of inbred Strain-2 guinea pigs (GP) with CMV enhances cytotoxic CMI against CMV-infected syngeneic targets. We investigated this CMI during pregnancy of uninfected and CMV-infected females bred to uninfected strain-2 males. In uninfected dams with successful pregnancies, CMI was comparable to nonpregnant controls (19.2±5.9%) in 1st trimester (19.9±7.9), but suppressed during 2nd (12±7.6) and 3rd trimester (5.6±3.7) and up to 6 wks postpartum while breast feeding (6.2±2.3%). CMI was comparable to nonpregnant female controls by 10d after ceasing breastfeeding (17.8±8.2). Cytotoxic CMI did not decrease by trimester in CMV infected dams (40±15.4, 31±7.8, 42±18.8%) and increased postpartum (58±14.3%). Mean weights of pups from infected dams were less than from uninfected dams (68±21.4 vs 91±9.3 gm). Congenitally infected pups weighed less (54±17.3g) than those exposed but not infected (83.5±9.3 gm). Uninfected dams that resorbed fetuses or had >50% stillborns/litter had had more pregnancies than those with successful pregnancies (3.3±0.9 vs 1.6±0.9) whereas fetal loss in CMV-infected dams occurred with any pregnancy. Higher CMI was observed during 2nd and 3rd trimesters in uninfected (22±6.8 and 16.4±7.7%) and infected (39.1±7.1 and 48±8.8%) dams experiencing fetal wastage than in dams with successful pregnancy outcome. Thus lack of suppression of cytotoxic CMI to GPCMV in infected or multiparous GP was associated with increased fetal wastage.
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