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
1liver-infiltrating lymphocytes 4 of patients with chronic hepa-A cytotoxic T lymphocyte (CTL) response to the hepatitis C, the role of CTL responses in HCV infection is untitis C virus (HCV) nucleoprotein residues 88-96 that are known. HCV infection frequently persists and is implicated the minimal and optimal epitope for human leukocyte in the development of chronic hepatitis, cirrhosis, and hepatoantigen (HLA) B44-restricted CTLs was assessed in 27 cellular carcinoma. 5 Posttransfusion HCV infection has de-HLA B44-positive patients with chronic HCV infection.creased substantially after introduction of an anti-HCV assay Serum HCV RNA concentration and the amino acid sefor blood screening, but community-acquired HCV infection quence of the residues 81-100 were also determined.still occurs. Interferon therapy is effective in less than 50% Three patients were infected with HCV with uncommon of patients with chronic hepatitis C. 6 Understanding the role amino acid substitutions within the epitope. One was of CTL responses in HCV infection may contribute to the infected with HCV with an amino acid substitution in development of strategies for the prevention of HCV infection the flanking residues of the epitope. To stimulate CTLs and the elimination of HCV from infected individuals. in the peripheral blood, 9-mer peptides that correRecently, we showed the presence of CTLs that recognize sponded to the residues 88-96 of the individual patients endogenously synthesized HCV antigen in the peripheral were synthesized and used. Seven of the 27 patients demblood of some patients with HCV infection by stimulation onstrated a CTL response to the residues 88-96 with of peripheral blood lymphocytes (PBLs) with HCV synthetic specific cytotoxic activities higher than 20%. The CTL peptides.3 activities were significantly higher in patients with a The CTLs recognized an epitope in the HCV nucleoprotein low titer of serum HCV RNA than in those with a high residues 81-100 in association with human leukocyte antigen titer of serum HCV RNA (P Å .0006). Some of the patients (HLA) B44. The minimal and optimal epitope was further dethat demonstrated a CTL response to the residues 88-fined to be the residues 88-96. 7 The 9-mer peptide of the resi-96 also demonstrated a CTL response to a newly identidues 88-96 was recognized by and stimulated the CTLs more fied HLA B44-restricted CTL epitope or a known HLA efficiently than the 20-mer peptide of the residues 81-100. A11-restricted CTL epitope or both. No apparent associa-In a characteristic antiviral CTL response in vivo, immunotion was observed between the CTL response and the dominant CTLs recognize only one or a few multiple immunostage of disease, or between the CTL response and the genic CTL epitopes in the antigen, 8,9 but as many as five grade of necroinflammatory activity. The results suggest different epitopes for HCV-specific CTLs were detected in a that the HLA B44-restricted CTLs together with other single individual. 10 CTL activities to HCV could not be dem-HCV-specific CTLs ...
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A novel coupling reagent, meta-maleimidobenzoyl N-hydroxysuccinimide ester was synthesized. Using this reagent, insulin was conjugated very easily with beta-D-galactosidase [EC 3.2.1.23] in neutral, aqueous solution. No reduction of the enzyme activity was observed during the coupling procedure. The competitive bindings of the conjugate and insulin to anti-insulin serum were tested. The results indicated that the conjugate has enough immune reactivity for use in enzyme coupled immunoassay. Using this assay 20-800 pg of insulin were detectable.
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