Genotype 4 Hepatitis E virus replicates in the placenta, causes severe histopathological damage, and vertically transmits to fetuses.

BACKGROUND: Hepatitis E virus (HEV) infection in pregnant women causes adverse pregnancy outcomes, including maternal death, premature delivery, stillbirth, and fetal infection. However, the pathogenesis of maternal and fetal HEV infection is unclear. METHODS: Placenta and placental appendixes were collected from HEV-4 infected pregnant women to explore the vertical transmission of HEV from mothers to fetuses. RESULTS: HEV-4 replicated in the placenta, placental membrane, and umbilical cord and was vertically transmitted from mothers to fetuses. HEV-4 placental infection resulted in serious histopathological damage, such as fibrosis and calcification, and severe inflammatory responses. Adverse maternal outcomes were observed in 38.5% of HEV-4 infected pregnant women. The distinct cytokine/chemokine expression patterns of HEV-infected pregnant women and nonpregnant women may contribute to the adverse pregnancy outcomes. Furthermore, the impaired maternal and fetal innate immune responses against HEV-4 facilitated viral replication during pregnancy. CONCLUSION: HEV-4 replicates in the placenta and is vertically transmitted from mothers to fetuses, causing severe histopathological damage.

Suppression and recovery of reproductive behavior induced by early life exposure to mercury in zebrafish.

While mercury (Hg)-induced reproductive impairments have been demonstrated in fishes, the effects of exposure to Hg2+ during early life stages on the reproductive behavior in adulthood and the persistency of these effects in the next generation remain largely unknown. In this study, zebrafish embryos were exposed to 0.6, 3, or 15 µg·L-1 Hg2+ for 5 days and then reared for an additional 115 days in clean water, from which embryos were obtained and cultured in clean water for 120 days as the F1 generation. Increased Hg levels in brains and decreased survival and growth were observed in individuals exposed to Hg2+ during early life stages. Early life exposure to Hg2+ reduced the frequency of touching in males as well as the frequency and duration of visits to the spawning area by females, males, or both sexes simultaneously, and resulted in lesser spawning and fertilization. Moreover, early life exposure to Hg2+ interfered with the transcription of genes encoding neuropeptides and hormones related to reproduction, which could be responsible for diminished sexual behavior and reduced reproductive outcomes. In the F1 generation, such alterations were not observed in either females or males, indicating that the disruption of normal patterns of reproductive behavior caused by early life exposure to Hg2+ did not persist and was recovered. Overall, this study demonstrated that exposure to Hg2+ during early life stages suppressed the reproductive behavior of adult fish but this disruption could be recovered in the F1 generation.

Exposure of zebrafish to environmentally relevant concentrations of mercury during early life stages impairs subsequent reproduction in adults but can be recovered in offspring.

Mercury (Hg) is a global pollutant that poses potential threats to health of fishes. Although effects of Hg on reproduction of fishes have been documented, little is known about effects of exposure to Hg2+ during early life stages on subsequent reproductive fitness of adults or whether these effects can be transferred to offspring. In this study, zebrafish embryos were exposed to environmentally relevant concentrations of Hg2+ (0.6, 3 or 15 µg/L) for 5 days and then depurated in clean water for another 115 days. Exposure to Hg2+ during early life stages disturbed the balance of sex hormones and gametogenesis by altering expression of mRNA for genes involved in the hypothalamic-pituitary-gonadal axis, which resulted in delayed gonadal development and lesser gonado-somatic index, thereby resulting in lesser fecundity. A similar, but less pronounced effect was observed in F1 females that were not exposed directly to Hg, whereas such damage was neither observed in F1 males nor either sex during the F2 generation. Exposure to Hg2+ during early life can impair subsequent reproduction in adults and has intergenerational effects on F1 females, but this reproductive damage can be recovered in F1 males and in F2 females.