Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some 20% of cases of posttransfusion and sporadic hepatitis non-A, non-B are anti-HCV negative. In 1995 it proved possible in collaboration of Genelabs with Boehringer Co. Mannheim to identify a new RNA virus which causes acute and chronic hepatitis in humans and tamarins. The genome of the virus contains some 2900 amino acids, and as to its structure, it resembles flaviviruses. It was described as hepatitis G virus (HGV). It differs from the hepatitis C, virus as it has only a 26% homology of amino acids. It is transmitted through blood during transfusion along with other parenteral routes of infection. Risk groups comprise i.v. drug addicts, blood donors and patients with thalassaemia and repeated blood transfusions. HGV can infect the liver as an independent virus or along with the virus of hepatitis B or C (dual infection). As to clinical aspects, hepatitis G is very mild and not associated with jaundice. Some patients develop chronic hepatitis. About half the patients infected with HGV have only a slightly raised transaminase activity, the remainder have normal liver enzymes. As compared with hepatitis C, the mean transaminase activity is one half. It can be diagnosed by assessment of HGV RNA by means of PCR. In the USA the prevalence of HGV RNA in blood donors with normal ALT activity is 1.7% and in donors with increased ALT activity 1.5%. The virus is sensitive to interferon, after treatment the serum concentration of HGV RNA declines rapidly but after withdrawal of treatment the values return to pre-treatment levels. This is the first report on the newly discovered hepatitis G virus.
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PMID:[The discovery of hepatitis G virus]. 862 84

To study the incidence and outcome of GB virus C (GBV-C) infection in blood recipients. Serum samples collected in a prospective study were examined for GBV-C RNA by a nested polymerase chain reaction assay. Among the 400 adults who underwent cardiac surgery, 40 were positive for GBV-C RNA, including six whose pretransfusion sera were already positive and seven coinfected with hepatitis C virus (HCV) during transfusion. The risk of transmission was estimated to be approximately 0.46% per donor. GBV-C viremia was detectable 1 week after transfusion and could persist for 8 years. However, no evident symptoms or signs were noted in the 25 patients infected by GBV-C alone, and the average peak serum alanine aminotransferase activity was 31 IU/L only (range, 12 to 123), with persistently normal levels in 20 patients. In the seven patients coinfected with HCV, the clinical courses of posttransfusion hepatitis were similar to those infected by HCV alone. In eight patients with posttransfusion non-A approximately E hepatitis, only one was positive for GBV-C RNA. Sixty samples were chosen to test hepatitis G virus (HGV) sequences, 26 of the 30 GBV-C positives were positive for HGV RNA in contrast to none of the 30 GBV-C negative samples. In conclusion, GBV-C can be transmitted by transfusion in approximately 9% of patients who underwent cardiac surgery. Nevertheless, this virus does not seem to cause classic hepatitis in most instances.
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PMID:A prospective study of transfusion-transmitted GB virus C infection: similar frequency but different clinical presentation compared with hepatitis C virus. 878 48

A new member of the Flaviviridae family has recently been cloned and completely sequenced. The new virus, tentatively named hepatitis G virus (HGV) and known to be closely related to GB virus C (GBV-C), is transmitted by blood and blood products, intravenous drug use and other behaviour associated with a high risk of parenteral exposure to blood. The association of the virus with hepatitis is demonstrated by the presence of raised liver transaminase (alanine aminotransferase, ALT) levels in patients infected with HGV in the absence of other identifiable causes of hepatitis. No patient sera from groups exposed to blood and blood products were found to be positive when tested for the presence of GBV-A or GBV-B sequences, two other recently described flaviviruses. Forty-five per cent of the HGV-infected patients investigated had normal ALT suggesting the existence of a normal carrier state. Persistent infection of up to 13 years duration was observed. Co-infection with hepatitis B or hepatitis C viruses (HBV and HCV) was commonly seen presumably because of shared risk factors. None of five patients with fulminant hepatic failure was positive for HGV infection. The virus is sensitive to interferon-alpha, but sustained responses were not seen with the treatment regimens used for HBV and HCV. Viral titres increased during immunosuppression following liver transplantation and the higher levels of viraemia were in one case accompanied by elavated ALT. Whether HGV (GBV-C) replicates in the liver in some or all cases remains to be established. Preliminary data suggest that it is present within peripheral blood lymphocytes.
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PMID:Hepatitis G virus infection: clinical characteristics and response to interferon. 903 Oct 63

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) is a newly described RNA virus that is parenterally transmitted and has been found frequently in patients with chronic hepatitis C infection. To determine the impact of hepatitis G virus co-infection on morbidity and mortality following liver transplantation, we measured HGV RNA by polymerase chain reaction in pre and posttransplantation sera from a cohort of patients transplanted for chronic hepatitis C and a control group of patients transplanted for nonviral causes who were negative for hepatitis C virus (HCV) RNA in serum. The overall prevalence rate of HGV RNA in transplanted patients with chronic hepatitis C was 20.7%. HGV infection was present before transplantation in 13% while it appeared to have been acquired at the time of transplantation in 7.4%. Mean serum alanine aminotransferase activity, hepatic histological activity, and patient and graft survival were similar between HGV-positive and HGV-negative patients. The prevalence rate of HGV RNA in transplanted controls was 64% (P < .01) with a significantly higher rate of acquisition of HGV infection following transplantation (53%, P < .001) when compared with patients with chronic hepatitis C. Mean serum alanine aminotransferase activity was significantly lower in the control patients with HGV infection alone following transplantation than in patients co-infected with hepatitis C (37 +/- 9 vs. 70 +/- 33 U/L, P < .01). Thus, HGV is frequently found in transplantation patients co-infected with hepatitis C although it appears to have minimal clinical impact. In patients transplanted for nonviral causes of end-stage liver disease, a high rate of hepatitis G acquisition at the time of transplantation may occur but does not appear to predispose to chronic hepatitis.
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PMID:Hepatitis G virus co-infection in liver transplantation recipients with chronic hepatitis C and nonviral chronic liver disease. 914 51

There is limited information about the long-term efficacy of prolonged therapy (more than 6 months) with interferon alpha in hemophilic patients with chronic hepatitis C who are not coinfected with the human immunodeficiency virus (HIV-1). One hundred and seven hemophiliacs were randomly assigned to 3 million U of interferon alpha2b three times weekly for 12 months or no therapy. The patients were followed up for at least 12 months posttreatment. Response was assessed by both serial alanine aminotransferase (ALT) levels and hepatitis C virus (HCV)-RNA measured by reverse transcribed polymerase chain reaction (RT-PCR) method. Before treatment, serum levels of HCV-RNA were measured quantitatively by second-generation branched-DNA assay and the HCV genotype was determined by RT-PCR. Serum HGV-RNA, a marker of infection with the hepatitis G virus, was also measured by RT-PCR. Normalization of ALT was sustained and serum HCV-RNA was cleared in 6 of 45 treated patients, compared with none of the 50 untreated controls (13% v 0% P < .01). Low pretreatment viremia was the only feature that was associated with an increased likelihood of sustained response (P < .01). This study shows that multitransfused hemophiliacs with chronic hepatitis C not coinfected with HIV-1 respond at low rates to prolonged interferon therapy.
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PMID:A multicenter controlled, randomized, open trial of interferon alpha2b treatment of anti-human immunodeficiency virus-negative hemophilic patients with chronic hepatitis C. Hepatitis Study Group of the Association of Italian Hemophilia Centers. 942 35

The hepatitis G virus (HGV) has recently been identified as a new member of the Flaviviridae family. Infection by this virus is thought to be associated with blood borne hepatitis. In this study, the presence of HCV- and HGV-RNAs in serum or plasma (175 patients) and in peripheral blood mononuclear cells (PBMC) (133 patients) was investigated in patients with clotting disorders using a sensitive reverse transcriptase polymerase chain reaction (RT-PCR). HGV-RNA was detected in serum of 26 patients (14.8%). In apparently healthy blood donors, serum HGV-RNA was detected in 4 of 358 individuals investigated (1.12%). Ninety two percent of the 26 serum HGV-RNA positive patients had coinfection with the hepatitis C virus (HCV), especially with HCV genotype 1b, the most common genotype in Belgium. Of these coinfected patients, 15 (62.5%) showed elevated serum ALT levels. Two patients who were solely infected with HGV had normal serum ALT.HGV-RNA in PBMC was found in 18 patients, of whom 3 were negative for serum HGV-RNA. As in case of HCV, HGV-RNA in PBMC is preferentially sensitive to interferon treatment. Nevertheless, rapid reappearance of HGV-RNA in PBMC was observed after cessation of treatment. In one patient, persistent serum ALT elevation seems to be associated with continued HGV viremia, despite the disappearance of serum HCV-RNA.
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PMID:Hepatitis G viral RNA in serum and in peripheral blood mononuclear cells and its relation to HCV-RNA in patients with clotting disorders. 918 94

A 68-year-old man with moderate liver dysfunction diagnosed with atypical pneumonia showed serum alanine aminotransferase and gamma-glutamyltranspeptidase levels which revealed a sustained abnormality over six months. Hepatitis GB virus type C/hepatitis G virus demonstrated in his serum by reverse transcription-polymerase chain reaction. Liver histology showed steatohepatitis typically observed in alcoholic hepatitis without a remarkable drinking history. This case suggests that hepatitis GB virus type C/hepatitis G virus may induce chronic hepatitis and that there may be cases with chronic hepatitis induced by this virus in patients who have been diagnosed with alcoholic liver disease, even in cases with typical histology of alcoholic hepatitis.
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PMID:Chronic hepatitis infected with hepatitis GB virus type C/hepatitis G virus presenting as non-alcoholic steatohepatitis. 918 58

A new virus named hepatitis G virus (HGV) has been detected recently. Until now, no assays for the detection of antibodies against different HGV proteins have been commercially available. Therefore, a strip immunoblot assay has been established to investigate seroreactivity against recombinant structural (core) and nonstructural proteins (NS3 and NS4) of HGV produced in Escherichia coli. Seropositivity for HGV was evaluated and concordanced with HGV polymerase chain reaction (PCR) results in 709 subjects. These individuals were classified into a nonrisk or a risk group, on the basis of infection with human immunodeficiency virus (HIV) or hepatitis C virus (HCV) or frequent parenteral exposure, including hemophilia, intravenous drug addiction, receipt of blood transfusion, or hemodialysis. The nonrisk group consisted of 257 healthy blood donors with normal alanine transaminase (ALT) levels (ALT < 30 U/L) and 154 patients with suspected non-A-E hepatitis (ALT > 45 U/L). In the group of healthy blood donors, 1.9% (5 of 257) had detectable HGV viremia and 15.9% (41 of 257) showed antibody response to HGV. In the collective of patients with suspected non-A-E hepatitis, results from 1.9% of patients (3 of 154) were positive by HGV PCR, and 15.6% of patients (24 of 154) showed seropositivity against the recombinant HGV proteins. In six groups of patients (n = 298) with different risk factors, the prevalence of both HGV viremia (V) and serological reactivity (SR) was higher compared with that of the nonrisk group: V, 6.80%-35.2%; serological reactivity (SR), 25.4%-52.9%. The following conclusions can be derived from our data. HGV infection is widespread in the general population. The prevalence of antibodies against HGV or detectable HGV viremia is higher in patients with risk factors for parenteral viral transmission than in those without risk factors. The majority of HGV infections (70.2%) is self-limiting and not persistent in our collective of patients. We found no correlation between HGV viremia and clinical or biochemical signs of hepatitis in individuals without risk factors for acquiring parenterally transmitted agents.
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PMID:Distribution of hepatitis G viremia and antibody response to recombinant proteins with special regard to risk factors in 709 patients. 925 64


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