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)

Hepatitis G virus(HGV)/GB virus C(GBV-C) is a newly identified virus associated with human hepatitis. The preliminary prevalence studies of HGV infection in Japan were entirely based on the detection of HGV RNA by RT-PCR. However, the selection of the different primer sets in such assay may influence sensitivity of the test because of the extensive genetic heterogeneity of HGV, and influence the estimation of the prevalence of HGV. To address this potential problem, we designed two primer sets from well conserved domains in the 5'NC and NS5 regions of HGV genome, and tested them together with the NS3-derived primer set in RT-PCR for their ability to detect HGV RNA in serial dilution of synthetic viral RNA templates. Subsequently, we used these three primer sets to detect HGV RNA in the sera of 371 Japanese patients with hepatitis B, hepatitis C, and non-A-E hepatitis. The results indicated that the primer set derived from the 5'NC region appeared to be most effective in detecting HGV RNA. The results also showed that only two out of the 126 patients (1.6%) with non-A-E hepatitis were positive for HGV RNA although the RNA were detected more frequently in patients with hepatitis B (2/38; 5.3%) and hepatitis C (17/207; 8.2%), suggesting that HGV is not a common causative agent for non-A-E hepatitis in Japan.
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PMID:Detection of hepatitis G virus RNA in patients with hepatitis B, hepatitis C, and non-A-E hepatitis by RT-PCR using multiple primer sets. 926 Jun 85

Nine sets of nested PCR primers from a 2.6-kb region of the hepatitis G virus (HGV) genome at nucleotide positions 5829 to 8421 were designed and used to analyze serum specimens obtained from patients with community-acquired non-A, non-B hepatitis who were HGV RNA positive. One set of primers was found to be most efficient in detecting HGV and was subsequently used to test 162 HCV-positive and 11 HCV-negative plasma units obtained from individual paid donors. HGV RNA was detected in 30 (17.3%) plasma units, 2 of which were found among the 11 HCV-negative specimens. A complete set of nine PCR fragments was obtained from two patients with community-acquired acute non-A, non-B hepatitis and from four paid donors. All PCR fragments were sequenced and were shown to have a nucleotide similarity of 85.9 to 92.3% and a derived amino acid similarity of 96.0 to 99.0%. The majority of nucleotide changes occurred in the third position of codons. The HGV nucleotide and protein sequences obtained in this study were compared with HCV sequences. Based on this analysis the 2.6-kb fragment was predicted to encode the C-terminal part of the putative NS4b, the entire NS5a, and almost the complete NS5b proteins. Putative protease cleavage sites separating these proteins were also predicted. In serial specimens obtained from the two HGV-infected patients, no significant variations were found in the HGV nucleotide and derived amino acid sequences over time. The HGV sequences obtained from one patient showed no changes over 6 months, whereas more than 99.0% homology was observed for sequences from the second patient over 2.5 years. Heterogeneity analysis performed on 10 sequences obtained in this study and corresponding regions from 6 known full-size sequences of the HGV genomes demonstrated notable discrete heterogeneity consistent with the existence of HGV genetic groups or types.
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PMID:Sequence variation within a nonstructural region of the hepatitis G virus genome. 926 13

Hepatitis G virus (HGV) and GB virus C (GBV-C) are two newly discovered viral agents, different isolates of a positive-sense RNA virus that represents a new genus of Flaviviridae. The purpose of this review is to analyze new data that have recently been published on the epidemiology and associations between HGV and liver diseases such as posttransfusion hepatitis, acute and chronic non-A-E hepatitis, fulminant hepatitis, cryptogenic cirrhosis, and hepatocellular carcinoma. The role of HGV in coinfection with other hepatitis viruses, the response to antiviral therapy, and the impact of HGV on liver transplantation are also discussed. HGV is a transmissible blood-borne viral agent that frequently occurs as a coinfection with other hepatitis viruses due to common modes of transmission. The prevalence of HGV ranges from 0.9 to 10% among blood donors throughout the world and is found in 1.7% of volunteer blood donors in the United States. The majority of patients infected with HGV by blood transfusion do not develop chronic hepatitis, but hepatitis G viremia frequently persists without biochemical evidence of hepatitis. Serum HGV RNA has been found in 0 to 50% of patients with fulminant hepatitis of unknown etiology and 14 to 36% of patients with cryptogenic cirrhosis. The association between HGV and chronic non-A-E hepatitis remains unclear. Although HGV appears to be a hepatotrophic virus, its role in independently causing acute and chronic liver diseases remains uncertain.
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PMID:Hepatitis G virus: is it a hepatitis virus? 926 69

The risk of hepatitis virus transmission from tranfusions has declined dramatically from that of the 1940s when posttransfusion hepatitis (PTH) was first appreciated. Introduction of hepatitis B surface antigen screening and conversion to volunteer donors for whole-blood donations in the late 1960s and early 1970s led to substantial reduction in PTH cases. However, up to 10% of the recipients continued to develop PTH, most cases of which were attributed to an unknown non-A, non-B viral agent. Implementation of surrogate marker testing (i.e., alanine aminotransferase and anti-hepatitis B virus core antigen) for residual non-A, non-B hepatitis in the late 1980s reduced the per unit risk of PTH from 1 in 200 to about 1 in 400. Hepatitis C virus was discovered in 1989 and quickly was established as the causative agent of > 90% of non-A, non-B PTH. Introduction of progressively improved antibody assays in the early 1990s reduced the risk of PTH due to hepatitis C virus to about 1 in 100000. Although additional hepatitis viruses exist (e.g., hepatitis G virus), these appear to be minor contributors to clinical PTH, which has been virtually eradicated.
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PMID:History of posttransfusion hepatitis. 926 99

Hepatitis G virus (HGV), which was recently identified, is a single, plus-stranded RNA virus that is thought to replicate via minus-stranded RNA, but no information is available about the distribution of either plus- (genomic) or minus- (replicative) stranded HGV RNAs in HGV infected patients. We, therefore, tested the serum, liver tissue, and peripheral blood mononuclear cells (PBMCs) of six hepatitis patients with HGV infection for the presence of plus- and minus-stranded HGV RNA. The RT-nested PCR was used with primers derived from 5'-noncoding region of the genome. Before RT-PCR analysis, the 3'-termini of RNA specimens were chemically modified to discriminate between plus- and minus-stranded HGV RNA. Plus-stranded HGV RNA was detected in the serum and liver tissue of all six patients and in the PBMCs of five patients. Minus-stranded RNA was detected in the liver tissue of all six patients, in the serum of two patients, and in the PBMCs of one patient. In summary, the detection of minus-stranded HGV RNA in liver tissue may indicate that HGV replicates in the liver.
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PMID:Plus- and minus-stranded hepatitis G virus RNA in liver tissue and in peripheral blood mononuclear cells. 926 2

The identification of the major agents causing human hepatitis (Hepatitis A, B, C, D and E Viruses) was achieved during the last 30 years. These viruses are responsible for the vast majority of human viral hepatitis cases, but there are still some cases epidemiologically related to infectious agents without any evidence of infection with known virus, designated as hepatitis non A-E. Those cases are considered to be associated with at least three different viruses: 1--Hepatitis B Virus mutants expressing its surface antigen (HBsAg) with altered epitopes or in low quantities; 2--Another virus probably associated with enteral transmitted non A-E hepatitis, called Hepatitis F Virus. Still more studies are necessary to better characterize this agent; 3--Hepatitis G Virus or GB virus C, recently identified throughout the world (including Brazil) as a Flavivirus responsible for about 10% of parenteral transmitted hepatitis non A-E. Probably still other unknown viruses are responsible for human hepatitis cases without evidence of infection by any of these viruses, that could be called as non A-G hepatitis.
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PMID:GB virus C/hepatitis G virus and other putative hepatitis non A-E viruses. 929 92

The newly cloned and characterized hepatitis GB virus-C (HGBV-C), which is the same virus as the independently discovered hepatitis G virus, has a global distribution, is transmitted parenterally, and causes chronic viremia. The pathological consequences of infection with HGBV-C are uncertain, and its hepatocarcinogenic potential is unknown. We used a case-control format to compare the prevalence of HGBV-C infection in 167 southern African blacks with hepatocellular carcinoma (HCC) and 167 race-, age-, and sex-matched hospital-based control subjects, and to test for possible interactive effects between this virus and hepatitis B and C viruses in the development of the tumor. The presence of HGBV-C ribonucleic acid was detected in serum samples by reverse transcription, amplification of the resulting complementary deoxyribonucleic acid by the polymerase chain reaction (PCR), and Southern hybridization using a probe from the NS3/helicase region of the genome. Serum samples were also tested for the presence of hepatitis B virus surface antigen, antibodies to hepatitis C virus, and hepatitis C virus ribonucleic acid. Individuals infected with HGBV-C did not have an increased relative risk of developing HCC (relative risk 0.9; 95% confidence limits 0.5, 1.7). Moreover, co-infection with HGBV-C did not further increase the risk of tumor development in patients who were chronically infected with hepatitis B and/or C viruses. HGBV-C is unrelated to hepatocellular carcinoma development in black Africans.
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PMID:Does hepatitis GB virus-C infection cause hepatocellular carcinoma in black Africans? 930 6

A possible agent for human non-A-E hepatitis has been identified and named hepatitis G virus (HGV). The aim of this study is to evaluate the prevalence of serum HGV-RNA among hemodialysis patients in our country and the possible correlations of serum HGV-RNA with antibody to hepatitis C virus (anti-HCV), chronic liver dysfunction, number of blood transfusions, serum hepatitis B surface antigen (HBs Ag), duration of hemodialysis therapy, history of renal transplantation and patients' age and sex. Seventy-eight hemodialysis patients and 59 healthy controls were included in the study. Twenty-seven of 78 hemodialysis patients (34.6%) and two of the 59 healthy controls were serum HGV-RNA positive (p < 0.01, x2 = 17.8). There was no significant difference between the HGV-RNA positive and HGV-RNA negative groups regarding mean duration of dialysis therapy, anti-HCV, chronic liver dysfunction, number of blood transfusions, serum HBs Ag, duration of hemodialysis therapy, history of renal transplantation and patients' age and sex. In conclusion, hemodialysis patients carry the risk for HGV infection and transmission routes and clinical significance of HGV infection in these patients remain to be defined.
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PMID:Prevalence of serum HGV-RNA among hemodialysis patients in Turkey. 933 67

We have determined the nucleotide sequence of the 5'-terminal region of the hepatitis G virus (HGV) genome in 11 hepatitis patients from three cities in China. Phylogenetic analyses revealed that the Chinese isolates were genetically distinct from previously described West African isolates (type 1) and American, European and East African isolates (type 2), with a mean sequence divergence of approximately 10%. The mean divergence between isolates from Lanzhou, in the northwest of China, and those from Shanghai and Nanjing, on the east coast of China, was 5% (range 3-7%). The isolates from Shanghai and Nanjing were closely related to a common strain in Japan, while some of those from Lanzhou were closely related to a southeast Asian type 3 isolate. Thus, the Chinese isolates belong to the type 3 variant of HGV.
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PMID:Evolutionary analysis of the 5'-terminal region of hepatitis G virus isolated from different regions in China. 934 67

Hepatitis G virus (HGV) and hepatitis GB virus (GBV-C) have been reported as possible causes of non-A-E transfusional hepatitis. To assess the prevalence of hepatitis G virus infection in haemophiliacs we retrospectively investigated the presence of viral RNA in 92 patients with and without HCV infection. HGV/GBV-C RNA was reverse transcribed and amplified with primers from the 5' non-coding region of the genome. RNA was detected in 16/92 patients (17.4%). Restriction enzyme analysis revealed that the 16 patients belonged to the HGV-like genotype. Serology with E2-specific antibodies demonstrated that HGV viraemia underestimates previous infection by HGV. 33 patients were positive for HGV; all but two have cleared HGV RNA. 47/92 patients had a marker of prior infection by HGV. No difference between HGV RNA positive and negative patients was observed concerning age, diagnosis, HIV and HCV status. Previous HBV infection correlated with the frequency of HGV infection. There was no difference in alanine aminotransferase levels between HGV positive and negative patients. All 18 patients exposed to only virally inactivated plasma-derived concentrates were negative for both HGV RNA and anti E2 antibodies. Prior exposure to untreated concentrates correlated with HGV viraemia (P=0.03), HGV seropositivity (P=0.0002), and markers of HGV infection (P<0.0001). In haemophiliacs with a past exposure to non-inactivated concentrates, persistence of HCV RNA (53/74 patients) was more frequent than HGV RNA persistence (16/74 patients) although HGV viraemia is more frequent than HCV viraemia in blood donors. This may be related to a greater ability of individuals to clear HGV infection and suggests that hepatitis G virus infection in multi-transfused patients has a better outcome than infection with other blood-borne viruses.
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PMID:Prevalence of hepatitis G virus RNA in a monocentric population of French haemophiliacs. 935 26


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