Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoassays were developed to determine the seroprevalence of antibody against human GB virus C (GBV-C). The antigenic target in each assay was a 44.6-kDa glycosylated protein representing the first 315 amino acids encoded by the GBV-C E2 gene. Sera or plasma were assayed for E2 antibody using an anti-human EIA format in which antigen-coated polystyrene beads were reacted with sample, and bound antibody was detected by addition of enzyme labelled goat anti-human IgG. The presence of anti-E2 antibody was confirmed using a sandwich EIA format in which samples were reacted with antigen coated polystyrene beads, followed by addition of solution phase biotinylated antigen. Detection of antibody captured biotinylated E2 was accomplished by addition of enzyme-conjugated anti-biotin antibody. Antibody against the E2 antigen was detected in 7.4 and 7.8% of 500 sera and 500 plasma, respectively, from US volunteers donating to a Wisconsin blood center, and in approximately 10.7% of hepatitis and retrovirus marker-negative volunteer blood donors from a Missouri blood center. The rate in 1018 sera from US commercial donors at multiple US blood centers was 36.7%. These results indicated a relatively high prevalence of GBV-C exposure in US volunteer donors, and particularly in commercial donors. The clinical implication of the high exposure rate is unclear. These immunoassays are being combined with nucleic acid detection to assess prevalence of GBV-C world wide and to determine if GBV-C plays a role as an etiologic agent.
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PMID:Immunoassays to study prevalence of antibody against GB virus C in blood donors. 939 39

Sera from 77 patients with common variable immunodeficiency (CVID) were tested for GB virus C (GBV-C) RNA, because they are prone to unexplained chronic hepatitis, and from 28 patients with X-linked agammaglobulinemia (XLA) who have a similar primary antibody deficiency but are not prone to hepatitis. Eight CVID and 8 XLA patients were positive; 6 positive CVID and 3 XLA patients had abnormal liver enzymes, explained in 3 by either hepatitis B or C virus infection. Most patients tested had antibodies to the E2 antigen of GBV-C, apparently passively acquired from their immunoglobulin therapy. The high prevalence of GBV-C viremia in CVID and XLA patients is probably explained by their long-term exposure to blood products. Our data indicate that GBV-C does not cause chronic hepatitis in immunocompromised XLA patients and is not the cause of chronic non-B or -C hepatitis in the majority of CVID patients.
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PMID:GB virus C infection in patients with primary antibody deficiency. 960 56

Although it seems to be rather unlikely, it still remains unclear whether hepatitis G virus (HGV) is involved in post-transfusion hepatitis. Prevalence of HGV viremia and persistence in blood donors was determined. ALT and AST values of viremic and non-viremic donations of the donors were compared. 25,006 blood donations were tested for the presence of HGV RNA by reverse transcriptase polymerase chain reaction. ALT and AST were determined for every donation. Sequential serum samples of 105 HGV RNA-positive donors were tested for both HGV RNA and antibodies to the HGV-E2 antigen (anti-E2) by enzyme-linked immunosorbent assay. Stored serum samples of 66 patients from before and after transfusion of HGV RNA-positive units were also tested. 1.6% of the 25,006 blood donations were HGV RNA-positive. One of 105 HGV RNA-positive blood donors showed viremia for more than 6 years. Three donors showed viremia and HGV antibody at the same time. There is no significant difference in ALT and AST activity in HGV RNA-positive donors compared to a control group of healthy donors and also before and after seroconversion to HGV RNA-negative (p > 0.05). Transmission of HGV by blood components has been shown in transfused patients. The prevalence of HGV infection in patients (n = 66) is 17%. Transmission of HGV by blood components does occur. Patients have a significantly higher prevalence of HGV viremia compared to blood donors. In blood donors no liver affection by means of ALT or AST elevation can be seen. Long persistence of HGV viremia is common and the presence of anti-E2 does not exclude viremia.
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PMID:Prevalence, persistence and liver enzyme levels of HGV RNA-positive blood donors determined by large-scale screening and transmission by blood components. 1500 Feb 18

It has been previously demonstrated that platelets (PLTs) can bind and transport HIV-1 infectious virions. Hepatitis C virus (HCV)-HIV-1 co-infection occurs frequently among users of illicit intravenous drugs, thereby increasing the severity of HIV disease and the evolution towards chronic active hepatitis and hepatocellular carcinoma of HCV-related hepatitis. In the present study we investigated whether or not PLTs can carry HCV, and studied the binding mechanisms. Purified PLTs, obtained from healthy donors, HCV negative and HIV negative, were adsorbed with HCV-containing serum and then employed to infect a THP-1 monocytoid cell line. Replication of HCV was observed as shown by positivity for the E2 antigen within THP-1 cells, by indirect immunofluorescence; moreover, HCV-RNA was detected in supernatants of THP-1 cells at day 7 post-incubation with HCV-adsorbed PLTs. The binding of HCV to PLTs seems to involve fibronectin (FN), as already shown in the case of HIV-1. Indeed, treatment with RGD (Gly-Arg-Gly-Asp-Ser), the key oligopeptide of FN binding, inhibits the ability of HCV to be carried by PLTs in infective forms; the same phenomenon occurs with Mabs to FN. Moreover the infection of THP-1 cells seems to increase FN surface expression, as demonstrated by immunofluorescence tests.
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PMID:HCV infective virions can be carried by human platelets. 1538 45