Label-free ultra-sensitive colorimetric detection of hepatitis E virus based on oxidase-like activity of MnO2 nanosheets.

Hepatitis E virus (HEV) is an evolving infectious entity that causes viral hepatitis infections worldwide. Current routine methods of identifying and diagnosing HEV are someway laborious and costly. Based on the biomimicking oxidase-like activity of MnO2 nanosheets, we designed a label-free, highly sensitive colorimetric sensing technique for HEV detection. The prepared MnO2 catalyst displays intrinsic biomimicking oxidase-like catalytic activity and efficiently oxidizes the 3,3',5,5'-tetramethylbenzidine (TMB) substrate from colorless to blue colored oxidized TMB (oxTMB) product which can be measured at 652 nm by UV-visible spectrum. When the HEV-DNA was added, DNA adsorbed easily on MnO2 surface through physical adsorption and electrostatic interaction which hinders the oxidase-like catalytic activity of MnO2. Upon the introduction of target, the HEV target DNA binds with its complementary ssDNA on the surface of MnO2, the hybridized DNA releases from the surface of MnO2, which leads to recovery of oxidase-like catalytic activity of MnO2. This strategy was applied to construct a colorimetric technique for HEV detection. The approach works in the linear range of 1 fM-100 nM DNA concentration with the limit of detection (LOD) of 3.26 fM (S/N = 3) and quantitative limit (LOQ) of 36.08 fM. The TMB-MnO2 platform was highly selective for HEV target DNA detection when compared with potential interferences. Result of serum sample analysis demonstrates that this sensing system can be used for clinical diagnostic applications.

Treatment of Hepatitis E.

Hepatitis E virus (HEV) infections are the most common cause of acute hepatitis, but they can also take a chronic course. There is no specific therapy for acute hepatitis, and current treatment is supportive. Choosing ribavirin as the first-line therapy for chronic HEV is advisable, especially in solid organ transplant patients. Pegylated interferon-α has been used successfully for treatment of hepatitis E but is associated with major side effects. Cholestasis is one of the most common, but devastating, manifestations in hepatitis E. Current therapy for HEV aims to treat symptoms. Therapy generally involves several measures, such as vitamins for adequate nutrition, albumin and plasma for supporting treatment, symptomatic treatment for cutaneous pruritus, and ursodeoxycholic acid and S-adenosylmethionine, and Traditional Chinese medicine for removing jaundice. Patients with underlying liver disease may develop liver failure. For these patients, supportive treatment is the foundation. Ribavirin has successfully been used to prevent liver transplantation. Prevention and treatment of complications are important for treatment of liver failure. Liver support devices are intended to support liver function until such time as native liver function recovers or until liver transplantation. Liver transplantation is widely considered as irreplaceable and definitive treatment for acute-on-chronic liver failure, particularly for patients who do not improve with supportive measures to sustain life.

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.

Hepatitis E probably contracted via a Chinese herbal medicine, demonstrated by nucleotide sequencing.

Hepatitis E is endemic in developing countries and may occur as imported hepatitis in industrialized countries. A 46-year-old Japanese man developed immunoserologically diagnosed acute hepatitis E in Japan 4 months after he had made a trip to China. He had bought a Chinese herbal medicine there, taking it occasionally until approximately 6 weeks prior to the onset of acute hepatitis. Nucleotide sequencing of the 3' terminal region of the viral cDNA amplified from the patient's serum by polymerase chain reaction revealed a high degree of homology (99.8% of 752 nucleotides) with the Chinese strain. Thus, the results of sequencing suggest that his hepatitis E was caused by infection with the Chinese strain, via the Chinese herbal medicine.