AIM The aim of this study was to assess the cognitive and behavioural development of children with healthy birth outcomes whose mothers were exposed to prenatal stress but did not experience pregnancy complications. METHOD In this prospective study, self-reported data, including the Prenatal Life EventsChecklist about stressful life events (SLEs) during different stages of pregnancy, were collected at 32 to 34 weeks' gestation. Thirty-eight healthy females (mean age 27y 8mo, SD 2y 4mo) who were exposed to severe SLEs in the first trimester were defined as the exposed infant group, and 114 matched comparison participants were defined as the unexposed infant group (1:3). Maternal postnatal depressive symptoms were assessed with the Edinburgh Postnatal Depression Scale. The Bayley Scales of Infant Development and the Toddler Temperament Scale were used to evaluate the cognitive development and temperament characteristics of the infants with healthy birth outcomes when they were 16 to 18 months old.RESULTS A randomized block multivariate analysis of covariance showed that the mental development index scores of the infants of mothers with prenatal exposure to SLEs in the first trimester averaged seven points (95% confidence interval 3.23-10.73 points) lower than those of the unexposed infants. Moreover, the infants in the exposed group achieved higher scores for regularity (adjusted mean [SD] INTERPRETATION This study provides evidence that lower cognitive ability and less optimal worse behavioural response in infants might independently result from prenatal maternal stress.Studies carried out using animal-based models present evidence that exposure to prenatal stress may increase vulnerability to atypical cognitive and neurobehavioral development, altering the development of several brain areas (including the prefrontal cortex, hippocampus, and amygdala) and the programming of the hypothalamicpituitary-adrenal axis.1,2 A certain amount of life stress is unavoidable for humans. A substantial body of evidence, however, has linked maternal exposure to stressful life events (SLEs) during pregnancy with cognitive and behavioural development in the offspring. The early stages of pregnancy in humans, from 8 to 24 weeks' gestational age, are particularly important for development. During this period, major neurodevelopmental events occur, including the proliferation, differentiation, and migration of neurons. Several brain areas, such as the hippocampus and amygdala, are already differentiated during this period.3,4 Our previous study, and others 5,6 have shown that maternal exposure to SLEs in the first trimester is associated with adverse birth outcomes and lower general intellectual ability. It is rational to postulate that stress during the first trimester might interfere with neurodevelopmental processes, resulting in atypical cognitive and behavioural development.Ecological investigations have found that prenatal exposure to a natural disaster is associated with lower cognitive and language abilities.6 Population-ba...

We examined the relationship between maternal depressive symptoms in late pregnancy and Epstein-Barr virus reactivation before delivery. In this prospective observational study, prevalence of Epstein-Barr virus reactivation within one week before delivery was compared between 163 pregnant women with depressive symptoms at 33 to 34 weeks of gestation and a computer-generated control group of 163 pregnant healthy women without depressive symptoms. Depressive symptoms at 33 to 34 weeks of gestation were significantly related to the prevalence of Epstein-Barr virus reactivation before delivery after adjustment for potential confounders (adjusted OR52.74, 95%CI: 1.23-6.08). Compared to that in the control group, the prevalence of Epstein-Barr virus reactivation was higher in women with depressive symptoms accompanied by higher negative coping (24.2% compared with 7.9%; adjusted OR53.67, 95%CI: 1.47-9.16). Maternal depressive symptoms in late pregnancy are associated with Epstein-Barr virus reactivation, and this association could be moderated by maternal coping style.E pstein-Barr virus (EBV) is a member of the herpesvirus family, and about 90% of women have serologic evidence of previous infection 1 . Like other herpes viruses, EBV has the ability to remain latent in the body and becomes reactivated at a later time. It has been reported that maternal EBV reactivation in pregnancy is related to the adverse offspring development including severe symmetrical fetal growth restriction, lower birthweight, and leukemia 2-4 .Maternal depression is a mood disorder that begins before or immediately after childbirth. Between 12.7% and 23% of pregnant women will experience a depressive disorder 5,6 . Epidemiological evidence demonstrates that elevated levels of depressive symptoms in mothers are related to the adverse offspring development, such as lower birth weight, small for gestational age and child maladjustment 7-9 . However, the possible mechanisms underlying the association between maternal depression and adverse offspring development remain unclear. Results from animal studies suggested that maternal stress might negatively influence offspring outcomes through a process known as fetal programming 10 . Prenatal stress can lead to increased fetal exposure to glucocorticoids, which could permanently alter the HPA function of the offspring 11,12 . But the evidence from human studies about fetal programming is limited and inconsistent yet [13][14][15][16][17] .Recently, Haeri et al found that women with depression had higher prevalence of EBV reactivation 18 . Their research seems to suggest a potential novel viral model which may elucidate biological pathways underlying how maternal psychosocial stress impacts fetal development. However, this result hasn't been repeated in heterogeneous pregnant women populations. Thus, it would be helpful to support this hypothesis by adding evidence about the relationship between prenatal psychosocial stress and EBV reactivation in pregnant women during different stages of gestation from...