COVID-19 in pregnancy: What we know from the first year of the pandemic.

The COVID-19 pandemic has infected nearly 178 million people and claimed the lives of over 3.8 million in less than 15 months. This has prompted a flurry of research studies into the mechanisms and effects of SARS-CoV-2 viral infection in humans. However, studies examining the effects of COVID-19 in pregnant women, their placentae and their babies remain limited. Furthermore, reports of safety and efficacy of vaccines for SARS-CoV-2 in pregnancy are limited. This review concisely summarises the case studies and research on COVID-19 in pregnancy, to date. It also reviews the mechanism of infection with SARS-CoV-2, and its reliance and effects upon the renin-angiotensin-aldosterone system. Overall, the data suggest that infection during pregnancy can be dangerous at any time, but this risk to both the mother and fetus, as well as placental damage, increases during the third trimester. The possibility of vertical transmission, which is explored in this review, remains contentious. However, maternal infection with SARS-CoV-2 can increase risk of miscarriage, preterm birth and stillbirth, which is likely due to damage to the placenta.

Quality control measures for placental sample purity in DNA methylation array analyses.

The purity of tissue samples can affect the accuracy and utility of DNA methylation array analyses. This is particularly important for the placenta which is globally hypomethylated compared to other tissues. Placental villous tissue from early pregnancy terminations can be difficult to separate from non-villous tissue, resulting in potentially inaccurate results. We used several methods to identify mixed placenta samples using DNA methylation array datasets from our laboratory and those contained in the NCBI GEO database, highlighting the importance of determining sample purity during quality control processes.

Sexual Dimorphism in Adverse Pregnancy Outcomes - A Retrospective Australian Population Study 1981-2011.

OBJECTIVES: Sexual inequality starts in utero. The contribution of biological sex to the developmental origins of health and disease is increasingly recognized. The aim of this study was to assess and interpret sexual dimorphisms for three major adverse pregnancy outcomes which affect the health of the neonate, child and potentially adult. METHODS: Retrospective population-based study of 574,358 South Australian singleton live births during 1981-2011. The incidence of three major adverse pregnancy outcomes [preterm birth (PTB), pregnancy induced hypertensive disorders (PIHD) and gestational diabetes mellitus (GDM)] in relation to fetal sex was compared according to traditional and fetus-at-risk (FAR) approaches. RESULTS: The traditional approach showed male predominance for PTB [20-24 weeks: Relative Risk (RR) M/F 1.351, 95%-CI 1.274-1.445], spontaneous PTB [25-29 weeks: RR M/F 1.118, 95%-CI 1.044-1.197%], GDM [RR M/F 1.042, 95%-CI 1.011-1.074], overall PIHD [RR M/F 1.053, 95%-CI 1.034-1.072] and PIHD with term birth [RR M/F 1.074, 95%-CI 1.044-1.105]. The FAR approach showed that males were at increased risk for PTB [20-24 weeks: RR M/F 1.273, 95%-CI 1.087-1.490], for spontaneous PTB [25-29 weeks: RR M/F 1.269, 95%-CI 1.143-1.410] and PIHD with term birth [RR M/F 1.074, 95%-CI 1.044-1.105%]. The traditional approach demonstrated female predominance for iatrogenic PTB [25-29 weeks: RR M/F 0.857, 95%-CI 0.780-0.941] and PIHD associated with PTB [25-29 weeks: RR M/F 0.686, 95%-CI 0.581-0.811]. The FAR approach showed that females were at increased risk for PIHD with PTB [25-29 weeks: RR M/F 0.779, 95%-CI 0.648-0.937]. CONCLUSIONS: This study confirms the presence of sexual dimorphisms and presents a coherent framework based on two analytical approaches to assess and interpret the sexual dimorphisms for major adverse pregnancy outcomes. The mechanisms by which these occur remain elusive, but sex differences in placental gene expression and function are likely to play a key role. Further research on sex differences in placental function and maternal adaptation to pregnancy is required to delineate the causal molecular mechanisms in sex-specific pregnancy outcome. Identifying these mechanisms may inform fetal sex specific tailored antenatal and neonatal care.