Patients on maintenance hemodialysis are at increased risk for HGBV-C infection. This virus produces persistent infections, which may be transmitted by transfusions but may also be transmitted by other means.

Hepatitis E, the major form of enterically transmitted non-A, non-B hepatitis, is caused by hepatitis E virus (HEV). HEV is transmitted primarily by the fecal-oral route. Waterborne epidemics are characteristic of hepatitis E in developing regions of Africa, the Middle East, and Southeast and Central Asia, where sanitation conditions are suboptimal; one epidemic has also been documented in North America (Mexico) (32). HEV-associated hepatitis also occurs among individuals in industrialized countries with no history of travel to areas where HEV is endemic (6,9,18,25,36,37,39,41,52,54). Recently, accumulating lines of evidence indicate that hepatitis E is a zoonosis, and pigs or other animals may act as reservoirs for HEV infection in humans (9, 15, 20-24, 27, 39, 42, 45, 56). A significant proportion of healthy individuals in industrialized countries where hepatitis E is not endemic are seropositive for HEV antibodies (8,19,46). Therefore, several epidemiological questions remain unanswered. The success of future studies on clinical and subclinical HEV infection not only in developing countries but also in industrialized countries will greatly depend on the availability of assays that are sensitive and specific.HEV was recently classified as the sole member of the genus Hepevirus in the family Hepeviridae. The genome of HEV is a 7.2-kb, positive-sense, single-stranded RNA. It contains a short 5Ј untranslated region, three open reading frames (ORFs; ORF1, ORF2 and ORF3), and a short 3Ј untranslated region terminated by a poly(A) tract (12,34,44,53). ORF1 encodes nonstructural proteins, ORF2 encodes the capsid protein, and ORF3 encodes a cytoskeleton-associated phosphoprotein. Extensive diversity has been noted among HEV isolates, and HEV sequences have been classified into four major genotypes (genotypes 1 to 4) (37). In Japan, polyphyletic HEV strains of genotype 3 or 4 or both have been isolated from patients with sporadic acute or fulminant hepatitis E who had no history of travel to countries where this virus is endemic (1,25,30,40,41,56).The immunoglobulin M (IgM) class of antibody against HEV (anti-HEV IgM) is used as a reliable and sensitive marker of recent HEV infection (2-4, 38). However, the specificity of the solid-phase assay for anti-HEV IgM has been questioned in some cases, particularly in patients with IgMrheumatoid factors in the serum, which have activity against the Fc portion of IgG directed to HEV antigen and may elicit

To investigate the prevalence of hepatitis E virus (HEV) infection among patients on maintenance hemodialysis, serum samples collected in January 2003 from 416 patients who had been undergoing hemodialysis for 7.6 +/- 6.3 (mean +/- standard deviation) (range, 0.3-26.0) years in a dialysis unit in Japan and serum samples that had been collected from these patients at the start of hemodialysis were tested for IgG antibodies to HEV (anti-HEV IgG) by an "in-house" enzyme-linked immunosorbent assay (ELISA). Overall, 39 patients (9.4%) had anti-HEV IgG in January 2003, and included 35 patients (8.4%) who had already been positive for anti-HEV IgG at the start of hemodialysis and 4 patients (1%) who seroconverted after initiation of hemodialysis. Periodic serum samples that had been collected from the four seroconverted patients were tested for HEV antibodies and HEV RNA. The four patients became positive for anti-HEV IgG in 1979, 1980, 1988, or 2003, and continued to be seropositive until the end of the observation period. Although anti-HEV IgM was not detectable in the four patients, three were infected transiently with apparently Japanese indigenous HEV strains of genotype 3. The patient who contracted HEV infection in 1979 had been transfused with 2 U of blood 21 days before the transient viremia: one of the two stored pilot serum samples had detectable HEV RNA with 100% identity to that recovered from the patient. Our study provides evidence of transfusion-transmitted HEV infection in Japan in 1979, and that the prevalence of de novo HEV infection during hemodialysis was low (1.1% or 4/374).

These data suggest that multiple epigenetic silencing mechanisms are inappropriately active in HCC cells.

Hepatitis C virus infections in medical personnel after needlestick accidents have been documented generally by detection of seroconversion to a hepatitis C virus nonstructural region antigen, c100-3 (a marker of infection). We tested for hepatitis C virus core-derived antibodies and genomic RNA in addition to c100-3 antibody in 159 cases of needlestick exposure that did not involve patients positive for HBsAg. Of these we found 68 cases with index patients positive for both hepatitis C virus RNA and antibodies and members negative for antibodies to HCV core or c100-3 before the needlestick accidents. Seven of these medical personnel became infected with hepatitis C virus after the accidents. Their hepatitis was generally subclinical or self-limited and transient, except for one patient in whom liver enzyme elevation persisted along with the antibodies. In our study, the risk of hepatitis C virus transmission from a single needlestick accident with hepatitis C virus RNA-positive blood was 10%, considerably higher than the 4% estimated in a previous study. We found that donor blood with antibody to an hepatitis C virus core-derived peptide with enzyme-linked immunosorbent assay optical densities greater than 2.0 carried a significant risk of transmitting hepatitis C virus to needlestick victims. No hepatitis C virus seroconversions occurred in medical personnel exposed to hepatitis C virus antibody-negative or hepatitis C virus RNA-negative blood; however, one such exposure resulted in a very mild non-A, non-B, non-C hepatitis.