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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver transplantation remains a problem for end stage liver disease due to chronic viral hepatitis, in contrast to the success with fulminant hepatitis B, D and C in which recurrence of viraemia is relatively rare. Following transplantation for chronic HCV disease recurrence of hepatitis C is infrequent and does not appear to be an important clinical problem. The complete picture will only be described when a suitable HCV-RNA test becomes routinely available. Patients with cirrhosis due to hepatitis B, with low levels of viraemia, or patients with hepatitis D are less likely to develop reinfection than those with high levels of HBV viraemia. The use of hepatitis B immunoglobulin in high doses for prolonged periods delays rather than prevents recurrence. It is a very expensive ancillary treatment. Patients with chronic hepatitis D related cirrhosis in whom levels of hepatitis B replication are suppressed, have a low recurrence rate even without immunoglobulin prophylaxis although HDAg remains in the liver. Hepatitis only reoccurs with recurrence of HBV infection. Unfortunately transplantation of HBV DNA and HBeAg positive patients has many shortcomings, and reinfection of the engrafted liver and subsequent development of hepatitis B is common. Survival rates are reduced in this latter group. At present there are no firm recommendations that can be given to prevent recurrence: HBIG in large doses and for prolonged periods would appear to be insufficient to prevent reinfection and these patients often die of recurrent disease. A major challenge for transplant groups will be the prevention of viral reinfection particularly in this latter group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver transplantation for chronic viral hepatitis. 174 98

We studied the relations between HBV heterogeneity and different phases of HBV infection and disease in 145 HBsAg-positive carriers followed-up for 28 months (range 24-60 months). Viraemia was characterized for the relative prevalence of wild-type and HBeAg minus HBVs after HBV-DNA amplification by PCR using an oligonucleotide hybridization assay. HBeAg minus HBV was detected in 27% of immunotolerant HBV carriers, in 67% of patients with chronic hepatitis B (immunoelimination phase) and in 17% of HBsAg carriers with latent infection. Serum HBV-DNA and IgM anti-HBc became undetectable and ALT levels normalized, either spontaneously or after interferon therapy in 12 (36.3%) of 33 patients with an exclusive wild-type viraemia, but only in two (5.7%) of 35 patients with homogeneous HBeAg minus HBV (p = 0.005). An HBeAg minus viraemia higher than 20% was associated, in both HBeAg- and anti-HBe-positive patients, with HBV-induced liver disease and an unfavourable outcome of hepatitis. These findings suggest that surgence of HBeAg defective HBV is a virus strategy to survive under peculiar conditions dictated by the interplay between HBV and the host's immune system. The HBeAg/anti-HBe serological status is determined not only by the extent of virus replication and integration of HBV-DNA into cellular DNA but also by heterogeneity of HBV. The study of HBV heterogeneity in baseline sera of patients undergoing antiviral therapy appears to have a predictive value of the outcome of HBV infection in the single patient.
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PMID:'e' antigen defective hepatitis B virus and course of chronic infection. 182 19

Immunosuppression is known to influence the state of chronic hepatitis B virus infection, and is thought to increase the risk of developing chronic infection in newly exposed individuals. Cyclosporin A (CsA), an immunosuppressive agent that inhibits Th cell function, was administered to woodchucks chronically infected with woodchuck hepatitis virus (WHV), and resulted in a decreased severity of chronic hepatitis and an increased viremia during the treatment. Adult woodchucks inoculated with WHV and given CsA for 14 wk had increased viremias, decreased acute phase liver injury, and developed chronic infections at a higher rate compared with immunocompetent woodchucks given virus alone (chronicity in seven of seven WHV + CsA + vs zero of nine WHV + CsA-; p less than 0.001). These results in a relevant animal model of hepatitis B virus infection indicate: 1) that liver injury in acute hepadnavirus infections is immune-mediated and not a direct cytopathic effect of virus replication; 2) that Th cells function in the inflammatory response and in the immunologic control of hepadnavirus infection; and 3) that suppression of Th cell function in acute hepadnavirus infection decreases liver injury but alters the outcome of infection in favor of chronicity. These results also suggest continued challenges in the application of CsA in liver transplantation for hepatitis B virus-induced diseases.
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PMID:Cyclosporin A modulates the course of woodchuck hepatitis virus infection and induces chronicity. 182 6

The pathogenesis of inclusion body hepatitis was studied following the oral administration of a serotype 8 strain of avian adenovirus into 2-day-old specific pathogen free chickens. Viral antigens were detected in tissues at various times post inoculation (pi) by enzyme-linked immunosorbent assay and by immunocytochemistry. Viral antigens were detected in intestinal epithelium from 12h to 13 days pi and in the plasma fraction of blood by 24 h pi. A biphasic, cell-free viremia with peaks at 2 and 7 days pi was recorded. Antigens were first detected in the liver from 2 days and reached peak levels at 6 days pi. The second peak of viral antigens in blood plasma was probably due to release of virus from damaged hepatic cells. Initially, viral antigens in the liver were restricted to cells lining the sinusoids but increasing involvement of hepatocytes occurred with time. Small amounts of viral antigens were detected in other tissues. Following the appearance of neutralizing antibodies in serum from 7 days pi, the levels of viral antigens in all tissues decreased and were undetectable by 15 days pi. This viral hepatitis of chickens is possibly a useful model for other viral infections where a cell-free viremic phase is important for spread of virus from primary sites to target organs, such as the liver.
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PMID:Pathogenesis of an acute viral hepatitis: inclusion body hepatitis in the chicken. 184 68

We have developed animal models of viral hepatitis E using cynomolgus and rhesus monkeys. They developed acute biochemical and histological hepatitis after the inoculation of virus particles with identical kinetics and magnitude for the sixth subpassage. Virus particles multiplied in hepatocytes and were excreted into feces via bile. Additionally, a transient viremia was recognized. Molecular cloning of virus gene cDNA was successfully accomplished from two separate libraries (HT3 and NE). These clones were expressed into polypeptides having immunological epitopes, which were used for antibody assay of sera of monkeys and patients with positive results.
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PMID:Animal model, virology and gene cloning of hepatitis E. 190 55

Hepatitis C virus (HCV) is the major etiologic agent associated with non-A, non-B hepatitis. This study was designed to assess virologic and serologic markers in hemophiliacs exposed to non-heat-treated and/or virus-inactivated plasma derivatives. Serial bleeds from 48 hemophilic patients were analyzed for the presence of HCV viral RNA sequences as detected by polymerase chain reaction (PCR) and antibodies to structural (core) and nonstructural (C-100 and 33C) proteins by specific dot immunoblot assay. All patients exposed to non-heat-treated products, and four of six patients exposed only to virus inactivated products, had evidence of HCV infection. However, over the 5-yr study period, six exposed patients (13%) consistently lacked detectable anti-C-100 and seven (15%) lost this antibody. HCV viremia (PCR positive) was found in 91% of exposed patients, and was significantly more frequent in HIV seropositive hemophiliacs (P less than 0.05). Six patients had high antibody level to HCV and elevated ALT, but appeared to clear viremia. Four hemophiliacs were HCV seropositive but lacked detectable viremia. These data indicate that hemophiliacs remain persistently infected by HCV and that antibody to the core antigen of HCV is a reliable marker of this transfusion transmissible agent.
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PMID:Evidence for persistent hepatitis C virus (HCV) infection in hemophiliacs. 193 52

Sequential serum samples from previously untreated haemophiliacs in whom non-A, non-B hepatitis (NANBH) developed after they received factor VIII concentrate contaminated with hepatitis C virus (HCV) were tested by a commercial assay for the presence of antibodies to the C100 protein of HCV (anti-C100) and by "nested" PCR for the presence of HCV RNA sequences. Three temporal patterns of viraemia were observed: transient viraemia in acute resolving NANBH; viraemia lasting for several years in chronic NANBH; and intermittent viraemia in chronic NANBH, with an initial transient phase followed by recurrence after many months. In three of five cases the initial detection of serum HCV RNA was made before the onset of liver function test abnormality, many weeks or months before anti-C100 seroconversion. Diagnosis of acute HCV infection may therefore be possible much earlier by PCR than by existing serological techniques, but the timing of samples may be critical.
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PMID:Demonstration of viraemia patterns in haemophiliacs treated with hepatitis-C-virus-contaminated factor VIII concentrates. 197 17

The study of two major risk factors in the development of hepatocellular carcinoma, namely persistent hepatitis virus infection and exposure to dietary aflatoxins, has been hampered by lack of an experimental system. To this end we have used a Pekin duck model to examine the effect of congenital duck hepatitis B virus (DHBV) infection and aflatoxin B1 (AFB1) exposure in the induction and development of liver cancer. AFB1 was administered to DHBV infected or noninfected ducks at two doses (0.08 and 0.02 mg/kg) by i.p. injection once a week from the third month posthatch until they were sacrificed (2.3 years later). Two control groups of ducks not treated with AFB1 (one of which was infected with DHBV) were observed for the same period. Each experimental group included 13-16 ducks. Higher mortality was observed in ducks infected with DHBV and treated with AFB1 compared to noninfected ducks treated with AFB1 and other control ducks. In the groups of noninfected ducks treated with high and low doses of AFB1, liver tumors developed in 3 of 10 and 2 of 10 ducks; in infected ducks treated with the high dose 3 of 6 liver tumors were observed and none in the low dose of AFB1. No liver tumors were observed in the two control groups. Ducks infected with DHBV and treated with AFB1 showed more pronounced periportal inflammatory changes, fibrosis, and focal necrosis compared to other groups. All DHBV carrier ducks showed persistent viremia throughout the observation period. An increase of viral DNA titers in livers and sera of AFB1 treated animals compared to infected controls was frequently observed. No DHBV DNA integration into the host genome was observed, although in one hepatocellular carcinoma from an AFB1 treated duck, an accumulation of viral multimer DNA forms was detected. The metabolism of AFB1 in infected and noninfected duck liver was also examined. The study on the role of DHBV infection and AFB1 in the etiopathogenesis of liver tumors may help to clarify some of the basic mechanisms of carcinogenesis.
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PMID:Contribution of aflatoxin B1 and hepatitis B virus infection in the induction of liver tumors in ducks. 210 70

A 'blind' recombinant immunoscreening approach, of general application to studies of infectious diseases, was used to clone and identify the genome of the previously uncharacterized non-A, non-B hepatitis (NANB) virus. This agent is a positive-stranded RNA virus that appears to be distantly related to the flaviviridae family. A recombinant viral antigen (C100-3) was used to develop a capture assay for circulating antibody. Data obtained using this assay indicate that this agent, termed the hepatitis C virus (HCV), is the major cause of post-transfusion, community-acquired and cryptogenic, NANB. Anti-C100-3 antibody appears to be directed towards dominant, non-structural viral epitopes. It is a non-neutralising antibody that develops generally late in infection and is a particularly good marker of chronic, persistent viraemia. Many asymptomatic but infectious blood donors can now be detected using this antibody assay. HCV is associated with the development of hepatocellular carcinoma and possibly, other liver diseases.
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PMID:Hepatitis C virus: the major causative agent of viral non-A, non-B hepatitis. 211 12

To assess the role of immunization against hepatitis delta antigen in the prevention of hepatitis delta virus infection, woodchuck carriers of woodchuck hepatitis virus were immunized with a 64 amino acid portion of hepatitis delta antigen from its N-terminal region. The protein was expressed in Escherichia coli and contained a major immunogenic epitope. A significant anti-hepatitis delta response was observed that did not, however, protect the animals from hepatitis delta virus superinfection. Unexpectedly, the period of detectable viremia was longer in the immunized than in the control animals. We conclude that immunization with this recombinant hepatitis delta antigen does not afford protection against subsequent hepatitis delta virus exposure.
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PMID:Immunization of woodchucks with recombinant hepatitis delta antigen does not protect against hepatitis delta virus infection. 222 8


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