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)

Recently, a new virus related to flaviviruses, the hepatitis G virus (HGV), or GBV-C virus, was discovered as a putative blood-borne human pathogen. HGV RNA (NS5 region) was amplified by reverse transcription-nested PCR in the sera of 6 of 64 (9%) hemodialysis patients; 2 of 80 (2.5%) West Yukpa Amerindians, a population with a high rate of HBV infection but negative for HCV infection; and 1 patient with an acute episode of non-A, non-B, non-C hepatitis (NABCH). The patterns of single-strand conformation polymorphism of the amplified products were unique among different specimens and similar on follow-up for hemodialysis patients. All patients tested remained HGV RNA positive 1 and 2 years later, without major sequence variation, except for the NABCH patient, for whom a double infection and an apparent clearance of the original dominant variant was observed after 2 years. The sequences of the NS5 amplified products demonstrated 85 to 90% identity with other reported HGV sequences.
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PMID:Hepatitis G virus infection in Amerindians and other Venezuelan high-risk groups. 946 61

A recently discovered non-A-E hepatitis virus has been designated as hepatitis G virus (HGV) and identified as a new member of the Flaviviridae family. Infection by this virus is thought to be associated with blood-borne hepatitis and usually in the presence of hepatitis C or hepatitis B virus (HBV) infection. In this study, the presence of HGV-RNA in serum or plasma and the prevalence of antibodies against an HGV envelope protein (E2) were investigated in patients undergoing chronic hemodialysis using a sensitive reverse-transcriptase polymerase chain reaction and an enzyme-linked immunosorbent assay, respectively. HGV-RNA was detected in 19 of 112 patients investigated (17%) and anti-E2 antibodies were detected in 15 of 106 patients studied (14.2%). With the exception of two patients, the appearance of anti-E2 is associated with the clearance of serum HGV-RNA. The total prevalence of current (HGV-RNA positivity) and/or past (anti-E2 positivity) HGV infection in this patient population is thus 28.6% (32 of 112 patients were positive for serum HGV-RNA and/or anti-E2 antibodies). In apparently healthy blood donors, serum HGV-RNA was detected in four of 358 individuals (1.12%) and anti-E2 was not detected in 50 individuals investigated. From the 19 patients with serum HGV-RNA positivity, nine were coinfected with other hepatitis viruses (seven with HBV; one with HBV, hepatitis C virus [HCV], and hepatitis D virus; and one with HBV and cytomegalovirus). Thirteen of 15 patients with anti-E2 positivity (10 were positive for only anti-E2 and three were also positive for anti-HBc) had no detectable HGV-RNA. In two patients, both HGV-RNA and anti-E2 antibodies were concomitantly present (both patients were coinfected with HCV or HBV). Of the HGV-infected patients, only three who were coinfected with HBV showed elevated serum alanine aminotransferase levels. The serum HCV-RNA and/or anti-HCV were detected in five (4.5%) of 112 patients. From these findings, we conclude that there is a high prevalence of HGV infection (28.6%) compared with HCV (4.5%) in patients undergoing hemodialysis in our hospital. However, approximately 50% of patients had spontaneously lost the viremia and developed anti-HGV-E2 antibodies. We confirm that HGV infection alone is not associated with elevated serum transaminases, and the appearance of anti-HGV-E2 is usually accompanied with clearance of serum HGV-RNA. In contrast to the results of our previous study, the majority of patients infected with HGV are not coinfected with HCV, indicating that HGV is capable of independent transmission. It is likely that there is a preferential HGV acquisition in the hemodialysis unit. The clinical significance of long-term infection with HGV remains to be established.
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PMID:High prevalence of hepatitis G virus infection compared with hepatitis C virus infection in patients undergoing chronic hemodialysis. 946 14

A review of the discovery of the GB viruses (GB virus-A, GB virus-B and GB virus-C) is presented, and the relationship between the GB virus-C and the hepatitis G virus (HGV) is mentioned. The GB virus-A and GB virus-B apparently do not cause liver disease in human. The GB virus C, HGV or GBV-C/HGV is transmitted parenterally, usually through blood transfusions or contaminated needles causing chronical infection. The prevalence of GBV-C/HGV infection among volunteer blood donors is less than 1%, and in patients with C or B hepatitis is more than 10%; the pathogenicity of this agent is not well defined.
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PMID:[Hepatotropic GB and G viruses]. 947 65

The aim of this study was to determine the prevalence of infection with the newly described hepatitis G virus (HGV) in a liver transplant cohort, and to establish the frequency and nature of hepatitis in those with and without HGV infection. A reverse transcriptase-polymerase chain reaction technique was employed to determine viraemia in the patients, and liver biopsies taken at different times after transplantation were assessed histologically. Hepatitis G virus RNA was detected in 47% of the liver transplant recipients investigated. Those positive for HGV had received significantly more blood or blood products than the HGV-negative patients. The frequency of abnormal liver function tests was similar in HGV-positive and HGV-negative recipients. Bile duct epithelial cell damage was more frequently seen in those with HGV viraemia. This study indicates that almost half of the liver transplant recipients in Northern England are positive for HGV, and that infection is associated with exposure to blood and blood products. It appears that, in the immunosuppressed patient, HGV does not cause clinically significant liver disease, at least up to 2 years after transplantation. If HGV infection is associated with hepatitis outside this clinical setting, it is likely that the liver damage is immunopathologically mediated rather than as a result of direct viral cytotoxicity.
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PMID:Hepatitis G virus does not cause significant liver disease after liver transplantation. 949 15

The development of molecular biology techniques has enabled us to clone the genetic sequence of three new hepatitis viruses, namely, hepatitis C virus, hepatitis E virus and hepatitis G, or GBV-C virus in the last decade. Hepatitis C virus (HCV) is now known to account for the majority of the parenterally transmitted non-A, non-B hepatitis and hepatitis E virus (HEV) is the major cause of the epidemics of enterally transmitted non-A, non-B hepatitis in the less developed countries, mainly through contaminated water supplies. While 80% of those who were infected with HCV will become chronic carriers, there is no known chronic carrier state for HEV. To date, 6 major genotypes of HCV were identified, with various variants of genotype 6 described in Southeast Asia. In Singapore, the majority of our chronic hepatitis C patients are infected with genotype 1. The seroprevalence rate of HEV is 10% to 14% in Singapore. This probably reflects our suboptimal sanitary condition in the past rather than a reflection of a currently high HEV infection rate in our population. However, local cases of acute hepatitis E have been reported. As for the most recently cloned hepatitis G virus, its aetiologic role in the remaining cases of non-A, non-B hepatitis is still unclear. Some preliminary evidence suggests that it may be just an innocent bystander with limited pathogenicity and it certainly cannot account for all the remaining cases of non A-E hepatitis. Hence, the search for yet another hepatitis virus continues.
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PMID:Hepatitis C, E and G virus--three new viruses identified by molecular biology technique in the last decade. 949 78

Sera from 62 hepatitis C virus (HCV)-infected Swedish blood donors were tested by a nested polymerase chain reaction using primers targeting the 5'-noncoding region of the GB virus-C/hepatitis G (GBV-C/HGV) genome and an enzyme-linked immunosorbent assay that detects antibodies to the envelope protein E2 of GBV-C/HGV (anti-E2). Fourteen (22%) and 21 (34%) of the 62 blood donors were found to be GBV-C/HGV RNA and anti-E2 positive, respectively. None of the blood donors was positive for both GBV-C/HGV RNA and anti-E2. Thus, 35 of 62 (56%) HCV-infected donors had been exposed to GBV-C/HGV infection. At sequencing of the 14 GBV-C/HGV isolates, 12 were identified as subtype 2a and 2 as subtype 2b. One of 7 (14%) donors with mild liver disease such as steatosis and nonspecific reactive hepatitis had been exposed to GBV-C/HGV vs. 34 of 55 (62%) with chronic hepatitis with or without cirrhosis (P = 0.04). All other differences in histology were small between HCV and dual HCV GBV-C/HGV-infected donors. In conclusion, more than half of HCV-infected Swedish blood donors in this study were positive for either GBV-C/HGV RNA or anti-E2. GBV-C/HGV viremia and seropositivity were mutually exclusive.
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PMID:GBV-C/HGV infection in hepatitis C virus-infected deferred Swedish blood donors. 949 62

Patients on maintenance hemodialysis are frequently infected with hepatitis C virus (HCV). The long-term effect of alpha interferon therapy has not yet been assessed, or the influence of co-infection with the newly discovered hepatitis G/hepatitis GB virus-C (HGV/HGBV-C) upon therapy outcome. Eleven anti-HCV and HCV RNA-positive hemodialysis patients, 3 of whom had HGV/HGBV-C infection were given 3 mega-units of alpha 2b recombinant interferon subcutaneously 3 times weekly for six months. The mean follow-up after cessation of therapy was 24 +/- 8 months (range: 18-30 months). Sustained serum HCV RNA clearance, as assessed by PCR analysis, occurred in 5/11 patients (45.5%). Two had received a cadaveric kidney transplant at 16 and 18 months post-treatment and were treated by immunosuppressive therapy; HCV RNA remained undetectable in both serum and a liver biopsy. HCV was eradicated in 3 of the 6 patients infected with HCV genotype 1b, which is less sensitive to alpha-interferon than other HCV genotypes. Among the 3 patients infected with both HCV and HGV/HGBV-C, alpha-interferon cleared the HCV RNA from one patient, but not the HGV/HGBV-C RNA. In view of the high rate of HCV eradication after alpha-interferon therapy and its fair tolerance, we suggest that HCV RNA-positive dialysis patients should be treated before transplantation, regardless of their aminotransferase levels or liver histological score, since alpha interferon therapy after renal allografting is associated with an unacceptable rate of renal failure. Our preliminary data indicate that HGV/HGBV-C does not interfere with sustained HCV RNA clearance.
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PMID:[HCV RNA clearance after treatment with interferon-alpha in chronic hemodialysis patients with or without coinfection by HGV/HGBV-C]. 949 68

To investigate the prevalence of hepatitis G virus (HGV/GBV-C) in patients with liver disease and to confirm its hypothesized ability to cause liver damage, we studied 130 subjects; 61 had chronic hepatitis C virus infection and 69 had acute hepatitis of either defined etiology (n = 57) or of unknown origin (n = 12). Positivity for HGV/GBV-C RNA was detected in 10 of the 61 subjects with chronic hepatitis C (16.3%) and in 11 of the 57 subjects with acute hepatitis of defined etiology (19%), whereas we failed to detect HGV/ GBV-C viremia in subjects with hepatitis of nonestablished etiology. Patients exhibiting positivity for HGV/GBV-C RNA were found to be comparable to those exhibiting negativity for HGV/GBV-C RNA in terms of both liver function tests and Knodell's score (in liver biopsies); the affect of HGV/GBV-C infection on the biohumoral and histological activity in patients with chronic hepatitis C therefore appears to be minimal or absent. Similar clinical features were observed in patients with acute hepatitis of known etiology whether they were positive or negative for HGV/GBV-C RNA. However, long-term clinical studies are still required to clarify the actual impact of HGV/GBV-C co-infection. In our geographic, i.e., a region or north-east Italy, HGV/GBV-C infection appears to be strictly related to intravenous drug use, and this agent does not seem to be responsible for acute hepatitis of unknown etiology; other etiological agents are probably involved.
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PMID:HGV/GBV-C infection in patients with acute hepatitis of different etiology and in patients with chronic hepatitis C. 949 23

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

Hepatitis G virus (HGV) was transmitted to 2 chimpanzees by inoculation with human plasma containing approximately 10(8) genome equivalents (GE) of HGV. The infection was characterized by the late appearance (weeks 10 and 11 after inoculation [pi]) of viremia that persisted throughout the 120-week follow-up. Serum HGV titer increased steadily until it plateaued at 10(6)-10(7) GE/mL. However, despite this relatively high titer, neither of the chimpanzees developed hepatitis. The sequence of the viral genome, recovered from each chimpanzee at week 77 pi, differed from that of the inoculum by 5 nt (2 aa) and 27 nt (2 aa). Two more chimpanzees were inoculated with a first-passage plasma pool. The chimpanzee inoculated with approximately 10(6.7) GE of HGV had viremia at week 1 pi. However, the viral titer increased with the same kinetics as observed in the first passage. The second chimpanzee inoculated with approximately 10(4.7) GE of HGV had late appearance (week 7 pi) of viremia.
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PMID:Experimental infection of chimpanzees with hepatitis G virus and genetic analysis of the virus. 953 56


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