Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two novel potentially hepatotropic flavi-like viruses were recently identified in patients with acute or chronic hepatitis and were provisionally called GBV-C and hepatitis G virus (HGV). The sequence identity analysis of these two viruses clearly indicated that GBV-C and HGV are two isolates of the same virus. In addition, the phylogenic analysis of the aligned viral polyprotein sequences showed that the GBV-C and HGV isolates are closely related to two Flaviviruses (GBV-A and GBV-B) that cause hepatitis in tamarins, and are distantly related to hepatitis C virus (HCV). Taken together, these results demonstrate that GBV-C/HGV belongs to the Flaviviridae family. GBV-C/HGV genomic RNA is detectable in both acute and chronic non-A, nonE hepatitis as well as in a minor proportion of patients with fulminant hepatic failure, hepatocellular carcinoma and in blood donors with or without abnormal alanine aminotransferase. However, the majority of patients with prospectively followed HGV infections have no evidence of liver damage. The high frequency of GBV-C/HGV infections in patients who are coinfected with HBV and/or HCV suggests that these viruses can share a common mode of transmission.
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PMID:GBV-C/HGV: a new human hepatitis-related virus. 910 11

Prevalence of hepatitis G virus (HGV) was determined in a cohort of Chinese blood donors and hepatitis patients by the detection of viral RNA via reverse transcription-polymerase chain reaction. While HGV RNA was detected in only 1 of 150 healthy volunteers, the detection rate among professional blood donors was surprisingly high (21/265, 7.9%), and plasmapheresis was identified as a significant risk factor in this population. It was also shown that an elevated serum alanine aminotransferase level is not a reliable marker for HGV infection. Prevalences of HGV in patients with hepatitis C, with non-A-E hepatitis, and with hepatocellular carcinoma were relatively low (8.2%, 16.7%, and 6.1%, respectively). Striking sequence homology (>90%) shared by 5 HGV cDNA clones implicated that they belonged to the same genotype. Phylogenetic analysis of a 446-bp NS3 cDNA confirmed that this genotype was closely related to the prototype viruses.
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PMID:Prevalence and genotype of hepatitis G virus in Chinese professional blood donors and hepatitis patients. 912 92

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 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 new hepatitis-associated RNA virus of the Flaviviridae family has been identified and named GB virus C/ hepatitis G virus (HGV). We carried out a case-control study to evaluate the association of HGV infection with hepatocellular carcinoma (HCC). We recruited 170 patients hospitalized for HCC (143 male and 27 female, mean age 64 years) and 306 patients hospitalized for nonliver diseases (controls) in Brescia, Italy. HGV RNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and antibodies against HGV E2 protein (anti-E2) by an immunoassay test. HGV RNA was found in 8 cases (4.7%) and 4 controls (1.3%). The relative risk (RR) for HGV RNA positivity adjusted for demographic variables and hepatitis B surface antigen (HBsAg), hepatitis C virus (HCV) RNA, and alcohol was 7.3 (95% confidence interval, 1.7-30.6; P = .009). No HGV RNA-positive subject was also positive for anti-E2. Anti-E2 prevalence did not differ significantly between cases (20%) and controls (15.3%), and no RR increase was found by this marker. Among subjects with HGV exposure (HGV RNA plus anti-E2 positive), a greater proportion of cases (40%) than controls (14%) had transfusion history. The possible role of HGV in HCC etiology seems modest because the population-attributable risk is lower (4%) than those for HBsAg (22%), HCV RNA (36%), and heavy alcohol intake (52%). This study supports the hypothesis of an association between HGV infection and HCC, although at present there are insufficient data on the causality of the association.
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PMID:A case-control study on GB virus C/hepatitis G virus infection and hepatocellular carcinoma. Brescia HCC Study. 939 12

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are known to be associated with hepatocellular carcinoma (HCC). In this study, we investigated the prevalence of the newly described hepatitis G virus (HGV) in patients with HCC. The sera of 85 patients (66 male, 19 female, 61 +/- 11 years) with HCC were studied for the presence of HGV RNA by reverse transcriptase-polymerase chain reaction. Seventeen (20%) of 85 patients with HCC, 10 (16%) of 61 patients with chronic hepatitis B without HCC and 14 (20%) of 68 patients with chronic hepatitis C without HCC were infected with HGV, a significantly higher proportion when compared with two (2%) of 85 healthy controls (P < 0.01). When grouped according to the underlying cause of liver disease, HCC patients with HBV infection (33%), HCV infection (21%), alcoholic liver disease (17%), or cryptogenic cirrhosis (15%) had similar serum levels of HGV RNA. Four of the 17 (24%) HGV-positive patients with HCC were coinfected with HBV and six (35%) with HCV; thus, 59% of HGV-positive patients with HCC were coinfected with other hepatotropic viruses. Seven (41%) HGV-positive patients were infected with HGV only. Patients with HGV infection were more likely to have a history of blood transfusion than patients without HGV infection (P = 0.024). Hence, the prevalence of HGV is significantly higher in patients with HCC in comparison with the healthy population.
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PMID:Prevalence of hepatitis G virus in patients with hepatocellular carcinoma. 943 Mar 61

Regarding the newly discovered hepatitis G virus (HGV), little is known about its relation to the cause and clinical significance of acute and chronic liver disease and hepatocellular carcinoma. Lacking a reliable serum immunoassay, the only method available for detecting the viral RNA in patients consists of the rather costly and time consuming RT-PCR. HGV has a worldwide distribution with up to 5% voluntary and 12.9% commercial blood donors infected, yet it appears to be asymptomatic. Moreover, HGV is frequently found as a coinfection with HCV or, to a lesser extent, HBV with symptoms tending to follow the patterns known for HCV or HBV infection, respectively. Being a blood-borne virus, it is most prevalent among members of high risk groups, such as IVDUs, patients on hemodialysis, recipients of blood and blood products and patients infected with HCV, HBV, or HIV, HGV can be parenterally, vertically, or sexually transmitted and after prolonged exposure, the virus may be eliminated by the patient's immune response. As yet, no unambiguous evidence exists regarding HGV's role in causing acute or chronic liver disease and, apart from a few isolated reports to the contrary, the infections appear rather mild. Therefore, more studies are required before a decision can be made whether to routinely screen blood donors for the presence of HGV RNA.
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PMID:Does hepatitis G virus cause significant clinical liver disease? 965 85

Hepatitis G virus (HGV) is a flavivirus that can cause acute hepatitis and persistent infection but its role in chronic liver disease or primary liver cancer is unproven. In this study we have examined the prevalence of HGV RNA in the serum of patients with hepatitis C virus (HCV) infection and in patients with cryptogenic chronic liver disease, including non-alcoholic steatohepatitis (NASH), and in patients with HCV-related hepatocellular carcinoma (HCC) and HCC arising in patients with cryptogenic liver disease. One-hundred and thirty patients who were positive for antibody to HCV (anti-HCV), 54 patients with cryptogenic chronic liver disease (including 17 patients with NASH) and 46 patients with hepatitis C-related (n = 27) or cryptogenic liver disease-related HCC (n = 19) were studied. HGV RNA was detected using nested reverse transcriptase-polymerase chain reaction (RT-PCR) and was found in 16.1% of patients with HCV infection. HGV RNA was not detected in any patient with cryptogenic liver disease. In patients with HCC, 7/34 samples were positive for HGV RNA and six out of seven HGV-positive subjects also had HCV infection. Only one patient with HCC in cryptogenic liver disease was positive for HGV RNA. Hence, cryptogenic liver disease in the UK is not caused by HGV/GBVc infection. It seems unlikely that HGV plays a significant role in hepatocarcinogenesis.
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PMID:Hepatitis G infection: role in cryptogenic chronic liver disease and primary liver cell cancer in the UK. Trent Hepatitis C virus Study Group. 965 69

By using reverse transcription and PCR for NS3 and 5'-untranslated regions (5'UTR) of the viral genome, prevalence of GB virus C/hepatitis G virus (GBV-C/HGV) infection in Chiang Mai, Thailand, was studied. High prevalence of GBV-C/HGV infection was observed among intravenous drug users (32%) and hemodialyzed patients (25%). The prevalence was also considerably high among patients with chronic liver disease, such as chronic hepatitis (9%), liver cirrhosis (12%) and hepatocellular carcinoma (10%). On the other hand, the prevalence among healthy blood donors (1%) was significantly lower than that of the above high-risk groups. GBV-C/HGV RNA positivity was significantly higher in individuals with antibodies against hepatitis C virus (24%) than in those without (5%). Phylogenetic analysis of the 5'UTR sequences classified Thai GBV-C/HGV isolates into three groups; (i) a group of isolates that are commonly found in the United States and Europe, (ii) a group of isolates that are commonly found in Asia, and (iii) a group of novel sequence variants.
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PMID:GB virus C/hepatitis G virus (GBV-C/HGV) infection in Chiang Mai, Thailand, and identification of variants on the basis of 5'-untranslated region sequences. 967 5

We performed a retrospective study to determine the prevalence of hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis G virus (HGV) genomes in formalin-fixed, paraffin-embedded liver tissues from hepatocellular carcinoma (HCC) patients in various geographic areas. The prevalence of each hepatitis virus in the liver tissues that have both carcinoma and noncarcinoma regions was different among the countries. HCV was the most prevalent in Japan (75 of 122 [61.5%]), Spain (9 of 15 [60%]), and the United States (27 of 65 [41.5%]); HBV was the most prevalent in Korea (45 of 55 [82%]) and among Japanese Americans in Hawaii (4 of 8 [50%]). Genotype II/1b was the most common genotype of HCV encountered in HCCs in these countries. In contrast, HGV RNA was undetectable in all tested HCCs. "Cryptogenic HCC," defined as HCC of unknown etiology, was seen 4 (3%) and 4 (6.2%) of Japanese and American patients, respectively, but this was not found in other countries. Interestingly, patients with HCC related to primary biliary cirrhosis (4.6%), who were excluded from analysis as hepatitis virus infections, were present only in the United States, but not in other countries. This study suggests that HCV, particularly genotype II/1b, and HBV may play an important role in hepatocarcinogenesis in these countries. There was no evidence of any relation between HGV infection and development of HCC.
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PMID:In situ detection of hepatitis B, C, and G virus nucleic acids in human hepatocellular carcinoma tissues from different geographic regions. 969 26


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