Brief Report: No Evidence for Parvovirus B19 or Hepatitis E Virus as a Cause of Acute Liver Failure

Digestive Diseases and Sciences (Impact Factor: 2.61). 09/2006; 51(10):1712-1715. DOI: 10.1007/s10620-005-9061-5
Source: PubMed


Viral hepatitis A and B are known to cause acute liver failure. While nearly 20% of acute liver failure cases are of indeterminate
etiology, screening for other viruses has not been uniformly performed. We looked for evidence for parvovirus B19 and hepatitis
E virus in sera from U.S. acute liver failure patients. For B19, 78 patients’ sera, including 34 with indeterminate etiology,
were evaluated by DNA dot-blot hybridization, reverse transcription polymerase chain reaction, and enzyme-linked immunosorbent
assay for immunoglobin G and M antibodies; none showed evidence for infection. In like manner, 126 patients’ sera were analyzed
for hepatitis E virus RNA by reverse transcription polymerase chain reaction and for hepatitis E virus immunoglobin G and
M antibodies by enzyme-linked immunosorbent assay; no acute hepatitis E virus cases were identified. If a unique acute liver
failure virus exists, it is neither of these candidate agents.

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    • "Although HEV generally causes a self-limited acute infection and mortality rates are generally lower, acute severe liver disease and fulminant hepatitis can occur, resulting in an overall fatality rate of 0.5 to 3 percent and as high as 20% in pregnant women (8-10). There are many studies about epidemiology of HEV in general population, but the data among patients with end stage renal disease (ESRD) are few and give conflicting results (11-15); therefore further studies are needed. "
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    ABSTRACT: Background:Many studies have been done on the epidemiology of Hepatitis E on general population, but the data among patients with end stage renal disease (ESRD) are few and give conflicting results.Objectives:The aim of this study was to investigate the prevalence of hepatitis E virus (HEV) infection and its relationship in ESRD patients undergoing maintenance hemodialysis (HD).Patients and Methods:This cross-sectional study was carried out on ESRD patients treated with HD in Imam Khomeini Hospital, Ahvaz city, Southwest of Iran. Blood sampling of patients was collected immediately before the dialysis session and the serum were evaluated for anti-HEV IgG titers by enzyme-linked immunosorbent assays. The statistical package for social sciences (SPSS) version 15 software was used for data analysis.Results:Out of 47 ESRD patients, 27 were male (57.4%) and 20 were female (42.6%), with mean age of 55.27 ± 8.1 years. The prevalence of anti-HEV antibody was 10.6 % (five patients, four male and one female). The mean age of HEV positive and negative patients were 58 ± 5.52 and 53.82 ± 15.55 years, respectively without any significant difference (P = 0.058). There also was no significant association between HEV and gender (P = 0.28). The mean time of HD in HEV positive and negative patients were 1224.2 and 1168.5 days, respectively with no significant association (P = 0.88). In addition, there also was no association between HEV and HCV (P = 0.61).Conclusions:According to the present study, the prevalence of anti-HEV IgG antibody was 10.63 % among chronic HD patients and there was no association between HEV, age, gender, duration of HD and HCV antibody titer.
    Jundishapur Journal of Microbiology 05/2014; 7(5):e6993. DOI:10.5812/jjm.6993 · 0.39 Impact Factor
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    • "Wong et al. 16 reported no association with fulminant hepatitis or hepatitis-associated aplastic anemia. Lee et al. 19 reported no evidence for hepatitis E or parvovirus B19 infection in patients with acute liver failure. "
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    ABSTRACT: Fulminant hepatitis and biliary atresia are serious problems and their causes have not been explained well. We investigated whether or not erythrovirus B19 is a candidate etiologic agent in such liver disease patients who had undergone liver transplantation. Liver tissues from 47 patients consisted of 28 fulminant hepatitis and 19 biliary atresia were examined to detect B19 genes by PCR and further analyzed their genomic characterization. B19 DNA was detected by nested PCR in 10 of 28 cases (35.7%) livers in the fulminant hepatitis group and 7 of 19 (36.8%) livers in the biliary atresia group, respectively (statistically not significant). Importantly, among the 8 hepatic B19 DNA-positive patients who had paired samples of liver and serum, the serum B19 genome was detectable in only one case. B19 mRNA was identified in all of 10 fulminant hepatitis cases with hepatic B19 DNA, but only 1 out of 7 (14.3%) cases in biliary atresia tested. Furthermore, we obtained ten isolates having the B19 genome with nearly full-length sequences. Interestingly, phylogenetic analysis based on the NS1 gene revealed three different clusters: two for isolates from fulminant hepatitis and the other for isolates from biliary atresia. Our results presented here suggested that B19 may be an etiologic agent of fulminant hepatitis.
    International journal of medical sciences 02/2007; 4(2):105-9. · 2.00 Impact Factor
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