Arsenic exposure and hepatitis E virus infection during pregnancy.

BACKGROUND: Arsenic has immunomodulatory properties and may have the potential to alter susceptibility to infection in humans. OBJECTIVES: We aimed to assess the relation of arsenic exposure during pregnancy with immune function and hepatitis E virus (HEV) infection, defined as seroconversion during pregnancy and postpartum. METHODS: We assessed IgG seroconversion to HEV between 1st and 3rd trimester (TM) and 3 months postpartum (PP) among 1100 pregnancies in a multiple micronutrient supplementation trial in rural Bangladesh. Forty women seroconverted to HEV and were matched with 40 non-seroconverting women (controls) by age, parity and intervention. We assessed urinary inorganic arsenic plus methylated species (∑As) (µg/L) at 1st and 3rd TM and plasma cytokines (pg/mL) at 1st and 3rd TM and 3 months PP. RESULTS: HEV seroconverters' urinary ∑As was elevated throughout pregnancy. Non-seroconverters' urinary ∑As was similar to HEV seroconverters at 1st TM but declined at 3rd TM. The adjusted odds ratio (95% confidence interval) of HEV seroconversion was 2.17 (1.07, 4.39) per interquartile range (IQR) increase in average-pregnancy urinary ∑As. Increased urinary ∑As was associated with increased concentrations of IL-2 during the 1st and 3rd TM and 3 months PP among HEV seroconverters but not non-seroconverters. CONCLUSIONS: The relation of urinary arsenic during pregnancy with incident HEV seroconversion and with IL-2 levels among HEV-seroconverting pregnant women suggests arsenic exposure during pregnancy may enhance susceptibility to HEV infection.

Infection dynamics of hepatitis E virus in naturally infected pigs in a Chinese farrow-to-finish farm.

To analyze the changes that occur in pigs during hepatitis E virus (HEV) infection, 256 serial serum samples were obtained from 32 pigs from one pig farm at ages 0 (cord blood), 15, 30, 60, 75, 90, 120, and 150 days. All HEV markers were assayed in these samples and showed that total anti-HEV antibodies and IgG formed two peaks. The first peak occurred at 0-60 days and the second after 75 days. No markers of infection, such as HEV RNA, antigen and anti-HEV IgM, were detectable during the first peak. Most newborn piglets (< 24 h of age) were negative for total anti-HEV and IgG. However, colostrum from all of the sows had evidence of these antibodies. Thus, the anti-HEV in the first peak was assumed to be acquired from maternal milk. Some infectious markers were positive at the beginning of second peak. PCR products were cloned and sequenced and the results indicated those sequences belonged to HEV genotype 4. The antibody present during the second peak may be induced by natural infection with HEV. In conclusion, pigs are susceptible to HEV infection and may remain infectious after the first peak of anti-HEV antibody.

Should HEV infected mothers breast feed?

OBJECTIVE: The aim of this study was to determine by a prospective study: the presence of anti-hepatitis E virus (HEV) and or HEV RNA in the colostrum of HEV infected mothers; transmission of HEV to infants from their mothers by breast-feeding. METHOD: Ninety-three infected pregnant mothers in the third trimester of pregnancy of which 36 were positive for anti-HEV antibodies and 57 for HEV RNA (index patients) and 90 healthy pregnant mothers (control subjects) were studied. Maternal blood was taken at 7th and 9th of gestation and also within 5 days post-partum, along with colostrum and tested for anti-HEV and HEV RNA. Blood samples were collected from all infants at birth (cord blood) and at 1, 3, and 6 and 9 months of age. RESULTS: There were 12 cesarean sections and eighty full term vaginal deliveries. Anti-HEV antibody and HEV-RNA was present in the colostral samples but in significantly lower levels ( p<0.001) as compared to corresponding maternal levels. Within 2 weeks post-partum, 6 of these 93 index patients, whose infants were anti-HEV antibody and HEV RNA negative at birth, developed acute hepatic disease. These mothers, four of whom delivered by cesarean section, had anti-HEV titers ranging from 1:10,000 to 1:60,000 and HEV RNA ranging from 1.5x10(6) to 2.5x10(4) copies/ml. Due to acute maternal disease their six respective infants were formula fed. Four of these infants were in close maternal contact, frequently kissed and cuddled, and developed symptomatic liver disease by 6-8 weeks of age. Apart from these 6 infants the remaining were exclusively breast-fed for 3.6+/-0.32 months. There was no evidence of HEV infection in the remaining babies. All mother-infant pairs from the control group remained anti-HEV negative throughout this study. CONCLUSION: Although anti-HEV antibody and HEV-RNA are present in the colostrum of HEV infected mothers, breast-feeding appears to be safe for these infants. However this report must be confirmed by others. Transmission of infection may occur postpartum, through close contact of mother-infant pairs, especially in the presence of acute maternal disease.