980 CYTOMEGALOVIRUS (CMV) SPECIFIC CYTOTOXIC CELL-MEDIATED IMMUNITY (CMI) DURING PREGNANCY

Abstract

Maternal cytotoxic CMI functions may modify vertical CMV transmission₅₁ and/or disease manifestations but are ill defined. We performed Cr release cytotoxicity assays for CMV specific natural killer (NK), antibody dependent cell-mediated cy to toxicity (ADCC), and MHC-restricted CMV specific cytotoxic (MRCC) activities in uninfected and CMV infected inbred strain 2 guinea pigs during pregnancy. Animals were infected with 10⁵ TCID₅₀ tissue culture attenuated CMV during the first trimester (median gestation day 27).

CMV infected nonpregnant controls had augmented NK activity at two weeks (49.2 ± 11.7%) returning to baseline (22.9 ± 2.3) at 8 weeks, and had peak MRCC at six weeks (14.4 ± 5.5%). In contrast, NK augmentation in CMV infected pregnant (CIP) was delayed until two weeks postpartem (37.0 ± 2.5%). Uninfected pregnant (UP) animals had depressed NK activity during the second trimester, third trimester and two weeks postpartem (11.1 ± 1.5, 7.0 ± 1.1 and 9.9 ± 3.1%) compared to CIP (24.5 ± 7.2, 23.6 ± 7.1 and 27.9 ± 5.3%) (P < .05) and uninfected nonpregnant animals (UNP) (20.9 ± 4.8) (P <.05). Neither UNP nor UP animals expressed CMV specific MRCC or ADCC. CIP acquired CMV specific MRCC (11.0 ± 2.3, 4.0 ± 1.5, and 10.9 ± 2.3%). ADCC was not detected in plasma of CIP animals until two weeks postpartem (10.3 ± 4.2%).

Infection, pregnancy, and infection during pregnancy alter CMI to CMV. This model should allow investigation of the roles of each CMI function in the pathogenesis of congenital CMV infection.

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