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Objectives: To assess the association between maternal parvovirus B19 infection and fetal death, birthweight and length of gestation., Design: Case-control study., Setting: Population based., Population: Cases were all 281 women with fetal death within a cohort of 35 940 pregnant woxmen in Norway. The control group consisted of a random sample of 957 women with a live born child., Method: Information on pregnancy outcome was obtained from the Medical Birth Registry of Norway. First trimester serum samples were tested for antibodies against parvovirus B19 (IgM and IgG). In seronegative women, further serum was analysed to detect seroconversion during pregnancy., Main Outcome Measures: Fetal death, length of gestation and birthweight., Results: Two of 281 (0.7%) of the women who experienced fetal death and nine of 957 (0.9%) of the controls had presence of IgM antibodies, crude odds ratio 0.8; 95% CI (0.2-3.5). In initially, seronegative women, 3.1% (2/65) with fetal death and 2.6% (8/307) with a live birth seroconverted, crude odds ratio 1.2; 95% CI (0.2-5.7). Presence of maternal parvovirus-specific IgG or IgM antibodies in the first trimester, or seroconversion during pregnancy were not associated with lower birthweight or reduced length of gestation in live born children, but was associated with low birthweight in stillborn offspring., Conclusion: Maternal parvovirus B19 infection was not associated with fetal death in our study. Very few cases of fetal death may be attributed to maternal parvovirus B19 infection.

Objectives: To study the association between Epstein-Barr virus (EBV) antibody status in early pregnancy and pregnancy outcomes including fetal death, length of gestation and fetal weight and length at birth., Design: Nested control study., Setting: Population based health registers., Population: The source population comprised 35,940 pregnant women. Cases were all (280) women with fetal death and a random sample of 940 women with a live born child., Method: Information on pregnancy outcome was obtained from the Norwegian Medical Birth Registry. Serum samples from the first trimester were tested for EBV antibodies. In women seronegative for EBV, further serum from late pregnancy was analysed to detect seroconversion. Main outcome measures Vital status, length of gestation, weight and length at birth., Results: There was no association between EBV antibody status and fetal death. Women with significant EBV reactivation had a significantly shorter duration of pregnancy, and associated lighter babies, compared with women without significant reactivation (stillborn: 176 vs 197 days, P=0.16, and live born: 271 vs 279 days, P=0.03, respectively)., Conclusion: Significant reactivation of EBV infection during pregnancy may influence pregnancy duration.

Problem: Pediatric human immunodeficiency virus (HIV) infection is largely a result of transplacental transmission, and pregnancy perturbation is more frequent in HIV-infected women. Dysregulation of placental immunology may occur during HIV infection, possibly facilitating HIV vertical transfer and miscarriage. The (FIV)-infected cat is a useful small-animal model for HIV pathogenesis because the viruses share common biological and clinical features. Transplacental transmission is readily achieved experimentally, resulting in a high proportion of infected offspring and frequent reproductive failure., Method of Study: We are using this model to examine lentivirus-induced placental immunopathology to determine the role aberrant immunology plays in intrauterine transmission and pregnancy perturbation., Results: Kittens were cesarean delivered from FIV-B-2542-infected and control queens at week 8 gestation (1 week short of term), and placental and fetal specimens were collected. On average, control queens delivered 3.8 kittens/litter, and 1 of 31 kittens (3.2%) was non-viable. FIV-infected queens produced 2.7 kittens/litter with 15 of 25 fetuses (60%) non-viable. The virus was detected in 14 of 15 placentas (93%) and 21 of 22 fetuses (95%) using polymerase chain reaction (PCR). Using a one-step, real time reverse transcriptase (RT)-PCR, we measured expression of representative placental T helper 1 (Th1) cytokines, interleukin (IL)-1beta and interferon (IFN)-gamma, a Th2 cytokine, IL-10, and chemokine receptor CXCR4. A comparison of placental cytokine expression between infected and control queens did not reveal differences between the two groups. However, elevated expression of Th1 cytokines and increased Th1/Th2 ratios (IL-1beta/IL-10) occurred in placentas from resorptions, indicating that increased placental Th1 cytokine expression was associated with pregnancy failure in the FIV-infected cat., Conclusion: The potential to establish efficient FIV in utero transmission, coupled with the parallels in immunopathology between FIV-infected cats and HIV-infected humans, suggests the usefulness of the FIV-infected cat as a cost-effective, small-animal model to study lentivirus-induced immunopathology, transplacental infection, and reproductive failure.

Objective: The aim of this study was to assess the association of fetal death with herpes simplex virus type-2 (HSV-2) antibody status during pregnancy: 1. presence of antibodies in first trimester; 2. appearance of antibodies (incident infection); 3. increase in antibody titre; and 4. loss of antibodies., Design: Prospective study., Population: The source population was a cohort of 35,940 pregnant women in Norway., Methods: Nested case-control study within the cohort. Cases were all women in the study population who experienced a fetal death after the 16th weeks of gestation (n = 281), and controls were 961 randomly selected women with a live born child., Main Outcome Measures: HSV-2 antibody status., Results: Twenty-nine percent (82/281) of women with a fetal death and 27% (256/961) of the controls had of HSV-2 antibodies present in the first trimester (odds ratio 1.1, 95% CI 0.8-1.5). HSV-2 antibodies appeared in 2% (3/136) of initially seronegative cases and 3% (16/623) of the controls during pregnancy (odds ratio 0.9, 95% CI 0.2-3.0). An increase in HSV-2 antibodies occurred in 4% (2/55) of initially seropositive cases and 7% (16/231) of the controls (odds ratio 0.5, 95% CI 0.1-2.3). Loss of HSV-2 antibodies in initially seropositive women was not associated with fetal death, 42% (23/55) of the cases and 45% (104/231) of the controls seroreverted (odds ratio 0.8, 95% CI 0.5-1.6). Differences in follow up time, age and parity were controlled and did not influence the comparisons between cases and controls., Conclusion: This study provides no evidence of an association between HSV-2 infection during pregnancy and fetal death.

Objective: To identify the presence of parvovirus B19 infection as a possible cause of fetal loss in the third trimester., Design: Prospective study of women experiencing third-trimester intrauterine fetal death (IUFD)., Setting: All cases of IUFD at Danderyd Hospital from 1992 to 1998., Population: Ninety-three women with IUFD in 33,759 deliveries (0.3%)., Methods: Detection of B19 DNA by polymerase chain reaction (PCR) in placental and fetal tissue. Placental pathology and B19-specific immunohistochemistry. Maternal serology in consecutive samples., Results: Among 93 cases of IUFD, seven (7.5%) had detectable B19 DNA in freshly-frozen placental tissue. The detection of B19 DNA in these tissues was confirmed by detection of B19 DNA in six separately stored paraffin-embedded placental tissues. No other explanations for the fetal deaths were found. None of the women had experienced any clinical signs of infection prior to fetal demise. None of the seven fetuses were hydropic. Histopathologic examination of the placentas revealed only minor abnormalities. Serology on maternal samples at birth revealed delayed or absent B19 IgG responses in five of seven cases. Two women were B19 IgG seropositive at the time of delivery but had unusual infection patterns; persistent viraemia for at least five months before birth in one case and likely persistence or re-infection by B19 in the other., Conclusion: In our study, 7.5% of IUFDs in the third trimester may have been caused by parvovirus B19 infection, without signs of fetal hydrops. This finding indicates that B19 PCR should be included in the routine investigation of IUFD.