Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of hepatitis G virus (HGV) infection on disease activity in hepatitis C related and unrelated liver disease was investigated in 254 individuals using an EIA polymerase chain reaction assay for HGV. One hundred patients had chronic hepatitis C, 26 primary biliary cirrhosis, and 30 alcoholic liver cirrhosis. In addition, 51 hepatitis B surface antigen (HBsAg)-positive and 47 anti-hepatitis C virus (HCV)-positive blood donors were screened. Hepatitis G virus was detected in 18% of patients with chronic hepatitis C, 13% of patients with alcoholic liver cirrhosis, 11% of patients with primary biliary cirrhosis, 10% of anti-HCV-positive blood donors, and 2% of HBsAg-positive blood donors. Virus load and alanine aminotransferase (ALT) levels did not differ significantly in patients with HCV alone versus patients coinfected with HCV and HGV. However, mild liver fibrosis correlated with HGV coinfection. Hepatitis G virus did not influence ALT levels or liver damage in liver disease unrelated to viral infection.
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PMID:Influence of hepatitis G virus infection on liver disease. 949 73

Evidence indicates that the GBV-C or hepatitis G virus can cause persistent infection in humans, but little is known on the importance of vertical transmission. To assess the risk of mother-to-infant transmission and the clinical outcome of infected babies, we investigated 175 anti-HCV positive mothers and followed-up their children for 3-33 months. GBV-C RNA was detected by RT-PCR and anti-E2 antibody was assayed by EIA. Thirty-four (19.4%) women were GBV-C RNA positive and transmission occurred to 21 (61.8%) babies; 20 (95.2%) acquired GBV-C alone, and one (4.8%) GBV-C and HCV. Maternal factors such as intravenous drug use, HIV coinfection, HCV-RNA positivity, and type of feeding were not correlated with GBV-C transmission. GBV-C RNA remained persistently positive in all infected babies but one baby who seroconverted to anti-E2. Seven (35%) babies with GBV-C alone developed marginally elevated ALT; the baby with HCV and GBV-C co-infection had the highest ALT peak value (664 IU/l). Seven of the 141 (5%) babies born to the GBV-C RNA negative mothers acquired HCV and six (85.7%) had abnormal ALT. The mean ALT peak value was significantly higher (P < 0.05) for babies with HCV than for those with GBV-C. None of the children with GBV-C or with HCV became icteric. GBV-C is frequently present in anti-HCV positive women. The infection is transmitted efficiently from mother to baby and rate of transmission is much higher than that for HCV. GBV-C can cause persistent infection in babies but usually without clear evidence of liver disease.
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PMID:Multicenter trial on mother-to-infant transmission of GBV-C virus. The Lombardy Study Group on Vertical/Perinatal Hepatitis Viruses Transmission. 949 68

A recently discovered non-A non-B hepatitis virus has been designated hepatitis G virus (HGV). Blood contamination has been proposed as its mode of transmission. We studied the genoprevalence of HGV in Japanese people at high risk. HGV was identified in serum by a reverse-transcription polymerase chain reaction. HGV was detected in 16.0% of intravenous drug users (IDUs) (n = 25), 16.2% of those with tattoos (n = 37), 10.9% of IDUs with tattoos (n = 55), 5.7% of chronic hepatitis (CH)-C patients (n = 87), and in none of the CH-B (n = 50) or CH non-B non-C (n = 46) patients. Serum alanine aminotransferase (ALT) levels of those infected with HGV alone (n = 3) were all within normal range. In the patients with CH-C, serum ALT levels of those coinfected with HGV were similar to serum ALT levels of those without HGV infection. A phylogenetic tree of isolated HGV clones showed that the HGVs of these subjects bore only a distant-resemblance to clones reported from Africa and North America, and that variation in the phylogenetic index of HGV clones was small. These results suggest that HGV clones from different areas have genetic heterogeneity and that HGV causes no or mild hepatitis.
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PMID:Genoepidemiology and pathogenicity of hepatitis G virus in Japan. 952 1

The prevalence of hepatitis B virus (HBV), hepatitis C virus (HCV), and GB virus C or hepatitis G virus (GBV-C/HGV) infections was determined in 289 patients with liver disease in Ho Chi Minh City and 890 healthy inhabitants of its rural area, Dalat City, Vietnam, respectively. Serum HCV RNA and GBV-C/HGV RNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). HBsAg, HCV antibodies, and GBV-C/HGV RNA were detected in 139 (47%), 69 (23%), and ten (3%) subjects, respectively, often accompanied by elevated serum levels of alanine aminotransferase. HBsAg and HCV antibodies or HCV antibodies and GBV-C/HGV RNA were detectable simultaneously in 8% and 2% of the patients, respectively. In the inhabitants, HBsAg, HCV antibodies, and GBV-C/HGV RNA were found in 51 (5.7%), nine (1.0%), and 11 (1.2%) subjects, respectively. Thus, the prevalence of HBsAg, HCV antibodies, and GBV-C/HGV RNA was significantly higher in liver disease patients than those in the general population. In the samples from 69 patients and nine inhabitants who were seropositive for HCV antibodies, HCV RNA was detectable in 42 (61%) and 4 (44%), respectively. In patients with liver disease, ten belonged to HCV genotype 1a, ten to HCV 1b, three to HCV 2a, four to HCV 2b, and two to HCV 3a by PCR with genotype-specific primers. Nine patients had mixed genotypes, and the remaining four were not classified. Of the GBV-C/HGV RNA-positive individuals, two patients and two inhabitants were positive for HBsAg, while none of the residents had HCV antibodies, although six HCV antibodies (60%) and four HCV RNA (40%) were found in patients. When a phylogenetic tree of GBV-C/HGV was constructed based on the nucleotide sequences, the 21 isolates were classified into at least two genotypes; four isolates belonged to G2, and 17 to G3. The results indicate that in Ho Chi Minh HCV infection prevails with broad distribution of genotypes together with HBV infection among patients with liver disease. This study suggests that GBV-C/HGV infection occurs independently in the two different districts in association with HCV infection.
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PMID:Prevalence of hepatitis B, hepatitis C, and GB virus C/hepatitis G virus infections in liver disease patients and inhabitants in Ho Chi Minh, Vietnam. 955 89

This study evaluated the epidemiology and impact of hepatitis G virus (HGV) infection in patients with chronic hepatitis B and C. Serum samples were obtained from 128 consecutive untreated patients with chronic hepatitis B (72 cases) or C (56 cases). The presence of HGV RNA was determined by PCR amplification of the 5'untranslated region; the sensitivity of the assays was ten template copy equivalents. The prevalence of HGV RNA in hepatitis B and C was found to be 25% and 34%, respectively. HGV-positive and HGV-negative patients did not differ with respect to risk factors for infection, age, sex, or alanine aminotransferase activity. Similarly, there was no difference in the severity of liver disease, as assessed with HAI score. In conclusion, we found a very high prevalence of HGV infection in chronic hepatitis B and C patients in Poland. Nevertheless, no evidence was found that HGV coinfection has any impact on the severity of the underlying disease.
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PMID:Hepatitis G virus coinfection in chronic hepatitis B and C patients in Poland. 956 82

The prevalence of hepatitis G virus (HGV) RNA was compared in a cohort of 89 thalassemic children (age range, 1-16 years) with a history of multiple blood transfusions, recruited from the hematology outpatient clinic at Thailand's Chulalongkorn Hospital and in specimens from 200 blood donors at the Red Cross in Bangkok. 29 specimens (32.6%) from thalassemic children, compared with 10 (5%) from blood donors, demonstrated detectable HGV RNA by reverse transcriptase analysis. 48% of the HGV-RNA-positive thalassemic children had elevated alanine aminotransferase levels, compared with 51.9% of the cohort without detectable HGV RNA; a finding that supports the assumption HGV infection does not cause detectable hepatitis. HGV RNA prevalence was 11.8% among children with 2-10 transfusions, 48.8% with 11-50 transfusions, 21.7% in those with 51-100 transfusions, and 16.7% among those with over 100 transfusions. This pattern suggests that at least some of the children recovered from HGV infection and may have developed immunity to reinfection. The clinical significance of HGV, as well as the apparent immunity acquired against reinfection, merit further investigation.
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PMID:High prevalence of hepatitis G virus infection in multiply transfused children with thalassaemia. 957 Feb 37

Homologies were sought between the putative amino acid sequences of GB virus C/hepatitis G virus (GBV-C/HGV) and the GOR epitope or the liver/kidney microsome-1 (LKM-1) epitope, which share partial sequence identity with the hepatitis C virus (HCV) polyprotein. Anti-GOR antibody (anti-GOR) was assayed among 100 subjects with GBV-C/HGV RNA. Twenty-one and 25 subjects were coinfected with hepatitis B virus (HBV) or HCV, respectively. Homologies were found between the NS5 or E2 polyproteins of GBV-C/HGV and the GOR epitope or the LKM-1 epitope, respectively. These segments of GBV-C/HGV polyproteins sharing identity with the GOR or the LKM-1 epitope were well conserved among three genotypes of GBV-C/HGV. However, only 1 of 55 subjects (1.8%) with GBV-C/HGV RNA, but not with HBV or HCV, was positive for anti-GOR. The positivity for anti-GOR among the group with GBV-C/HGV RNA alone was significantly lower than that among the groups with HCV RNA (P < 0.01 and P < 0.05, respectively). Only 2 of 55 subjects (3.6%) with GBV-C/HGV RNA alone exhibited elevation of alanine aminotransferase. The incidence of liver dysfunction among the group with GBV-C/HGV RNA alone was significantly lower than the incidence among the groups with GBV-C/HGV RNA and hepatitis B surface antigen (HBsAg) or HCV RNA (P< 0.01 and P< 0.01, respectively). These data indicate that 1) there is no association between GBV-C/HGV infection and the presence of anti-GOR, and 2) GBV-C/HGV infection is not related to chronic liver dysfunction.
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PMID:Lack of anti-GOR antibody among subjects with GB virus C/hepatitis G virus RNA. 959 33

To assess the biochemical and histological characteristics of hepatitis G virus (HGV) infection, we examined four patients who were infected with HGV only (HGV group), and compared them with 16 patients infected with both HGV and hepatitis C virus (HCV; HGV + HCV group) and 18 patients infected with HCV only (HCV group). Biochemical examination showed a significantly low level of serum alanine aminotransferase (ALT) in the HGV group, and that the gamma-glutamyl transpeptidase (gamma-GTP)/ALT ratio in the same group was significantly higher than in the other two groups. Although all three patient groups had a similar degree of liver fibrosis, both the degree of periportal inflammation and total histological activity index were significantly lower in the HGV group than in the other two groups. Fibrous enlargement of the portal tract without lymphoid infiltration and thin fibrous septa was characteristically observed in the HGV group. No significant difference was found between the HGV + HCV group and HCV group. Our results suggest that biochemical and histological changes in HGV infection are very mild and quite different from those of HCV infection.
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PMID:Biochemical and histological features of hepatitis G virus infection. 973 67

The clinical impact of GB virus-C (GBV-C)/hepatitis G virus (HGV) infection on various causes of acute hepatitis and fulminant hepatitis is controversial. In this study, serum samples from 164 patients with acute hepatitis of various causes, 34 asymptomatic hepatitis B virus (HBV) carriers, and 34 healthy adults were tested for GBV-C/HGV RNA by reverse transcription-nested polymerase chain reaction using primers based on the 5'-untranslated region. Nucleotide sequences of GBV-C/HGV RNA from various groups were compared. The prevalence of GBV-C/HGV RNA was significantly higher in patients with acute hepatitis D virus (HDV) superinfection than in HBV carriers or healthy controls (10/37 vs. 2/34, P < 0.02; 10/37 vs. 1/34, P < 0.005). GBV-C/HGV RNA was detected in 11.1% of acute hepatitis A patients, 9.5% of acute hepatitis B patients, 15.8% of acute hepatitis C patients, 12.5% of acute hepatitis E patients, 11.8% of chronic hepatitis B patients with acute exacerbation, and 11.1% in patients with non-A to -E hepatitis; each was not significantly higher than that in HBV carriers or healthy adults. There were no significant differences in gender, age, serum albumin, bilirubin, and alanine aminotransferase levels nor in the occurrence of fulminant hepatitis (6/28 vs. 36/136) between patients with or without GBV-C/HGV RNA. All six patients with fulminant hepatitis who had GBV-C/HGV RNA were complicated by infection with hepatitis B, C, or D. The GBV-C/HGV clones from 21 patients with or without fulminant hepatitis belonged to group 3. No particular strain of GBV-C/HGV was associated with fulminant hepatitis.
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PMID:Prevalence, implication, and viral nucleotide sequence analysis of GB virus-C/hepatitis G virus infection in acute fulminant and nonfulminant hepatitis. 974 66

GB virus-C/hepatitis G virus (GBV-C/HGV) is an RNA virus that can be transmitted by transfusion with the diagnosis based on the detection of serum GBV-C/HGV RNA by reverse transcription-polymerase chain reaction. In order to evaluate the role of antibodies to the E2 protein (anti-E2) of GBV-C/HGV in patients with acute posttransfusion hepatitis, anti-E2 was measured in one patient with acute GBV-C/HGV infection, five patients with acute GBV-C/HGV and hepatitis C virus (HCV) coinfection, and four patients with positive pretransfusion GBV-C/HGV RNA who were superinfected with HCV after transfusion. One patient with acute GBV-C/HGV infection remained GBV-C/HGV RNA-positive 18 months after transfusion and did not develop anti-E2. Among five patients with acute GBV-C/HGV and HCV coinfection, one lost GBV-C/HGV RNA 28 months after transfusion and developed anti-E2 independent of serum alanine aminotransferase levels. The other four patients remained GBV-C/HGV RNA-positive and anti-E2-negative at the end of follow-up. Among four patients with positive pretransfusion GBV-C/HGV RNA and super-infected with HCV, one lost GBV-C/HGV RNA 2 months and one 10 months after superinfection and subsequently developed anti-E2. The other two patients remained GBV-C/HGV RNA-positive without anti-E2 at the end of follow-up. Sixty-five samples tested were mutually and exclusively positive for either GBV-C/HGV RNA or anti-E2; only one sample was positive for both GBV-C/HGV RNA and anti-E2. In conclusion, the development of anti-E2 of GBV-C/HGV usually indicates the clearance of serum GBV-C/HGV RNA in patients with acute posttransfusion hepatitis.
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PMID:Detection of antibodies to E2-protein of GB virus-C/hepatitis G virus in patients with acute posttransfusion hepatitis. 989 Apr 27


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