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At least 631 records · Page 35Linked to original sources
PubMed1986

Relationship between hepatitis B virus DNA in blood and serological markers of hepatitis B infection.

The hepatitis B virus (HBV) DNA dot-hybridization assay has been introduced into clinical practice in Australia and its behaviour compared with that of the classic markers of HBV infection. A good correlation exists between the presence of HBV DNA and that of hepatitis B e antigen but the degree of dissociation between HBV DNA and the e:anti-e system was smaller than earlier studies would suggest. Patients who are seronegative for hepatitis B surface antigen (HBsAg), whether they possess anti-HBs, anti-HBc HBc (antibody to the core antigen), or neither antibody, gave uniformly negative results for the presence of HBV DNA. Theses results are different from those that were obtained from earlier studies of patients with chronic liver disease.

Acute Disease↗
PubMed2004

Pediatric fulminant hepatic failure in endemic areas of hepatitis B infection: 15 years after universal hepatitis B vaccination.

To investigate the role of hepatitis B virus (HBV) infection in pediatric fulminant hepatic failure (FHF) after the launch of universal HBV vaccination, the authors analyzed the data from patients with FHF collected from a nationwide collaborative study group. Children aged 1 month to 15 years who were diagnosed with FHF (62 males and 33 females) between 1985-1999 were included. HBV infection (hepatitis B surface antigen [HBsAg] and/or immunoglobulin M hepatitis B core antibody [IgM anti-HBc] seropositive) accounted for 46% (43 of 95 cases) of all the cases of FHF. The average annual incidence of FHF in the time period 1985-1999 was 0.053/100,000 in the group of patients ages 1-15 years and 1.29/100,000 in those patients age < 1 year. Approximately 61% (58 of 95 cases) of all FHF cases were infants. The percentage of HBV infection was found to be higher in infants (57%) compared with children ages 1-15 years (27%) (P = 0.004). The incidence rate ratio of those patients age < 1 year to those ages 1-15 years was 54.2 for HBV-positive FHF and 15.2 for HBV-negative FHF. Maternal HBsAg was found to be positive in 97% of the infants with HBV-positive FHF, and hepatitis B e antigen (HBeAg) was found to be negative in 84% of these infants. Approximately 74% of all HBV-positive FHF patients and 81% of the infantile HBV-positive patients had been vaccinated. In conclusion, within the first 15 years of universal vaccination, HBV was found to rarely cause FHF in children age > 1 year but remained a significant cause of FHF in infants. HBV-positive FHF was prone to develop in infants born to HBeAg-negative, HBsAg-carrier mothers; these infants had not received hepatitis B immunoglobulin according to the vaccination program in place.

Adolescent↗
PubMed2003

Progression of HIV infection and mortality by hepatitis C infection in patients with haemophilia over 20 years.

Hepatitis C virus (HCV) infection is an important cause of mortality in human immune deficiency virus (HIV)-positive haemophiliacs. This study describes progression to AIDS, death from HCV end-stage liver disease (ESLD) and all-cause mortality over 20 years. All HIV-positive haemophiliacs in La Paz University Hospital were included in this cohort. HIV seroconversion was estimated using mathematical techniques for interval-censored data from 1979 to 1985. Poisson regression was used to estimate rates of AIDS, death from ESLD and all causes in different periods: before 1988, 1988-89, 1990-91, 1992-93, 1994-95, 1996-97 and 1998-2001 using competing risk models. Among 383 cohort members, global AIDS incidence was 9.7 per 100 person-years, peaking in 1992-93 and dropping by 87% in 1998-2001 compared with before 1988 [incidence rate ratio (IRR) 0.13; 95% CI: 0.03-0.53]. Overall mortality was 7.5 per 100 person-years, was highest from 1992 to 1997, and fell by 66% in 1998-2001 compared with before 1988 (IRR 0.34; 95% CI: 0.14-0.81). Eighteen (5%) persons died of ESLD which represented 19% of deaths before 1988, 4% during 1988-89, 1990-91 and 1992-93, 2% in 1994-95, 10% in 1996-97 and 33% in 1998-2001. Overall death rate from ESLD was 0.5 cases per 100 person-years with no statistically significant trend observed over time. Important reductions in HIV disease progression to AIDS and death have been observed from 1998 to 2001, and can be attributed to highly active antiretroviral therapy. Although no increase in the rate of HCV-related deaths can be demonstrated, HCV accounts for an increasing proportion of deaths in the recent years.

Acquired Immunodeficiency Syndrome↗
PubMed1998

GBV-C/HGV infection in hepatitis C virus-infected deferred Swedish blood donors.

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.

Adult↗
PubMed2004

Anti-soluble liver antigen (SLA) antibodies in chronic HCV infection.

Hepatitis C infection is associated with autoimmune disorders, such as the production of autoantibodies. Anti-LKM1 and anti-LC1, immunomarkers of type 2 autoimmune hepatitis, have been previously associated with a HCV infection. Anti-Soluble-Liver-Antigen autoantibodies (SLA) are specifically associated with type 1 and type 2 autoimmune hepatitis and more closely related to patients who relapse after steroid therapy. The recent molecular cloning of the soluble liver antigen provides the opportunity to develop more specific tests for the detection of antibodies against it. The aim of this work is to characterize anti-soluble-liver autoantibodies in sera from patients chronically infected by HCV. A recombinant cDNA from activated Jurkat cells coding for the full length tRNP(Ser)Sec/SLA antigen was obtained. ELISA, Western Blot and immunoprecipitation tests were developed and used to search for linear and conformational epitopes recognized by anti-SLA antibodies in sera from patients chronically infected by HCV. Anti-soluble liver antigen antibodies were found in sera from 10.4% of HCV-infected patients. The prevalence was significantly increased to 27% when anti-LKM1 was also present. Most anti-SLA reactivity was directed against conformational epitopes on the antigen. The means titers by ELISA were lower than those obtained in type 2 AIH. The result of autoantibody isotyping showed a subclass restriction to IgG1 and also IgG4. This study shows the presence of anti-SLA antibodies in approximately 10% of HCV infected patients. The prevalence of SLA autoantibodies in HCV infected patients increases when LKM1 autoantibodies are also present. The relationship between the prevalence of this characteristic autoimmune hepatitis autoantibody and the implication of an autoimmune phenomenon in the liver injury of patients chronically infected by HCV needs further investigation.

Autoantibodies↗
PubMed1993

Spontaneous reactivation of chronic hepatitis B infection leading to fulminant hepatic failure. Report of two cases and review of the literature.

Reactivation of chronic hepatitis B viral (HBV) infection, defined as conversion from the low level replicative phase (HBV-DNA negative) to the high level replicative phase (HBV-DNA positive) with continued hepatitis B surface antigen positivity, occurs after immunosuppressive therapy, chemotherapy, and rarely spontaneously. Development of hepatic failure after spontaneous reactivation of chronic HBV is rare. We report two patients with chronic HBV infection and stable cirrhosis in whom spontaneous reactivation lead to hepatic failure. In one, spontaneous reactivation lead to severe jaundice, ascites, and encephalopathy. Treatment with alpha-interferon resulted in transient improvement, but the patient ultimately died with hepatorenal syndrome. In the second, severe liver failure required orthotopic liver transplantation. Spontaneous reactivation is an unusual cause of hepatic decompensation in patients with chronic HBV infection and may lead to fulminant hepatic failure. The role of interferon or liver transplantation in the management of spontaneous reactivation remains to be clarified.

Adult↗
PubMed2001

Hepatitis C virus core and envelope proteins do not suppress the host's ability to clear a hepatic viral infection.

Several hepatitis C virus (HCV) proteins have been shown in vitro to interact with host cellular components that are involved in immune regulation. However, there is a paucity of data supporting the relevance of these observations to the in vivo situation. To test the hypothesis that such an interaction suppresses immune responses, we studied a line of transgenic C57BL/6 mice that express the HCV core and envelope proteins in the liver. The potential effects of these proteins on the hepatic immune response were evaluated by challenging these mice with a hepatotropic adenovirus. Both transgenic and nontransgenic mice developed similar courses of infection and cleared the virus from the liver by 28 days postinfection. Both groups of mice mounted similar immunoglobulin G (IgG), IgG2a, interleukin-2, and tumor necrosis factor alpha responses against the virus. Additionally, BALB/c mice were able to clear infection with recombinant adenovirus that does or does not express the HCV core and envelope 1 proteins in the same manner. These data suggest that HCV core and envelope proteins do not inhibit the hepatic antiviral mechanisms in these murine experimental systems and thus favor a model in which HCV circumvents host responses through a mechanism that does not involve general suppression of intrahepatic immune responses.

Animals↗
PubMed2005

Recurrence of hepatitis C infection: Where are we now?

1. Hepatitis C-associated liver failure is the most common indication for liver transplantation, and approximately 10% of HCV-infected recipients will die or lose their allograft secondary to recurrent HCV infection. 2. Risk factors associated with histological recurrence of HCV include donor (age, fat content, ischemic time, and living donor), recipient (age and non-Caucasian race), clinical (rejection and CMV), and viral (viral load and quasispecies). 3. Treatment of recipients with histological recurrence is with pegylated IFN (+/- ribavirin). The role of hepatitis C immunoglobulin in the management of postransplant HCV is still evolving. (

Antiviral Agents↗
PubMed2001

Genetic susceptibility in chronic viral hepatitis.

Infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) may result in a number of different clinical outcomes. There is strong evidence in HBV infection that host genetic factors play a major role in determining the outcome of infection. A number of approaches may be used to determine the specific genetic factors involved but the principal method which has been used to date is the disease association study. Disease association studies have a number of drawbacks but trials with well-constructed designs and large numbers of cases have recently produced compelling and reproducible results. In particular alleles in the MHC class II loci and interleukin 10 promoter have been demonstrated to influence the outcome of these infections.

Disease Susceptibility↗
PubMed1997

Host-derived intracellular immunization against mouse hepatitis virus infection.

Mouse hepatitis virus (MHV) utilizes the murine biliary glycoprotein receptor (BgpA) for entry into susceptible cells. The Bgp1 gene was transfected into a murine DBT cell clone that expressed little if any BgpA receptor and resisted wild-type MHV infection. Clones which expressed low levels of receptor were efficient hosts for MHV-A59 replication. Clones which expressed 20- to 69-fold more BgpA receptor than controls were also susceptible to MHV-A59 infection, yet few infectious progeny virions were released. Pretreatment of clones with monoclonal antibody CC1, which binds to the N-terminus of BgpA, blocked MHV-A59 replication in DBT clones that expressed wild-type levels of receptor protein. In the overexpressing cell clones, however, CC1 pretreatment reversed the BgpA overexpression blockade and increased virus titers by 3-4 logs. BgpA overexpression inhibited the formation of infectious extracellular and intracellular virions, but levels of virus transcription were equivalent to those of controls. Ultrastructural studies revealed normal cell cytopathology in both the MHV-A59-infected controls and the overexpressing cell clones. Although equivalent numbers of virions were released compared with the control, peplomer spike glycoproteins were rarely evident in virions derived from the BgpA-overexpressing cell clones. Consonant with these findings, purified virions from BgpA-overexpressing cell clones demonstrated a 70% reduction in the amount of S glycoprotein, but not of N or M proteins. These data suggest that BgpA receptor overexpression establishes an intracellular trap which blocks MHV replication during the maturation and release of infectious progeny virions.

Animals↗
PubMed2004

[Is endemic hepatitis E infection present in developed countries?--Accumulating information about the hepatitis E virus and hepatitis E infection].

There are several new data on the acute viral hepatitis particularly on infectious non-A-non-C hepatitis viruses. The hepatitis E virus infection was originally thought to be limited only for certain geographic areas and humans. Recently, it has been demonstrated the genetic diversity and worldwide distribution of hepatitis E virus in human population, as well as, the circulation of the virus in many species of animals. It is evident, that hepatitis E virus can spread by fecally contaminated water (waterborne transmission), by meat of infected animals (food-borne transmission), by animal-human contact (zoonotic transmission), and even by transfusion (blood-borne transmission). The frequency of hepatitis E virus infections among the acute hepatitis cases with unknown origin is supposed to be more than 10%. In the differential diagnosis of hepatitis, possible hepatitis E virus infection must be now taken into account even in those areas and countries, like in Hungary, where the infection was previously thought to be non-endemic. To confirm the clinical diagnosis of hepatitis E virus infection, virus specific ELISA and molecular methods are now available. In the near future, a molecular epidemiological study will be organized for the detection of hepatitis E virus in Hungary in collaboration with 9 European countries.--This review covers all aspects of the hepatitis E virus infection including the characteristics and transmission of the etiological agent, the clinical symptoms, its epidemiology, laboratory diagnosis, and some possible control measures.

Developed Countries↗
PubMed1987

Evidence of hepatitis A infection in immature rhesus monkeys.

Forty immature (less than 2 years old) rhesus monkeys (Macaca mulatta) with marked increases in aspartate and alanine aminotransferase activities were examined. Serological and histopathological evaluations were done to determine if affected animals were infected with hepatitis A virus. Although no clinical signs of illness were noted in any of the monkeys, an excellent correlation was found between the increased serum aminotransferase values and seropositivity with the acute phase (IgM) HAVAB-M antibody. Histopathological evaluations of livers of selected animals revealed hepatic lesions consistent with those in chimpanzees and marmosets infected with hepatitis A virus: generalized activation of sinusoidal lining cells, focal hepatocellular necrosis with occasional acidophilic bodies, and cuffs of mononuclear cells in the portal areas. Although no animals were seropositive for HAVAB upon receipt from the breeding colony, a total of ten of 18 animals for which serological data were available had seroconverted to HAVAB positivity during the 4-month observation period. These results are consistent with hepatitis A infection in immature rhesus monkeys and indicate the potential significance of serological testing in animals in which hepatic function is being evaluated.

Alanine Transaminase↗
PubMed2005

Peginterferon-alpha 2a for the treatment of hepatitis B infection.

Chronic hepatitis B is one of the world's most common serious diseases with > 300 million patients worldwide. Currently recommended treatments include conventional interferon (IFN), lamivudine and adefovir. Recently, peginterferon-alpha2a (PEG-IFN-alpha2a, Pegasys; Hoffmann-La Roche & Co.) has been approved for use in patients with chronic hepatitis B in the US, the EU, Switzerland, Turkey and in several countries in the Asia-Pacific region. Several trials have been carried out using PEG-IFN-alpha2a (40 kDa) compared with conventional IFN, lamivudine monotherapy and a combination of PEG-IFN-alpha2a and lamivudine in patients with hepatitis Be antigen- (HBeAg) positive chronic hepatitis B, and patients with HBeAg-negative chronic hepatitis B. PEG-IFN-alpha2a was shown to be superior to conventional IFN in HBeAg-positive disease and to lamivudine in both HBeAg-positive and HBeAg-negative chronic hepatitis B. Although there was greater suppression of virus while on therapy, the combination of lamivudine and PEG-IFN-alpha2a did not enhance sustained response at the end of the 24-week follow-up period, compared with PEG-IFN monotherapy. In addition, approximately 3% of patients underwent hepatitis B surface antigen (HBsAg) seroconversion - the ultimate marker of therapeutic response, which is rarely seen following treatment with antiviral agents. The side effect profile was reasonable. PEG-IFN-alpha2a could become the treatment of choice in many patients with both HBeAg-positive and HBeAg-negative disease and, in those who fail to respond, consideration could then be given to the use of antiviral agents.

Hepatitis B virus↗
PubMed2000

Hepatic dysfunction in childhood dengue infection.

Hepatic functions of 61 children, diagnosed to have dengue infection (DI), aged 2 months to 12 years comprising 37 cases of dengue fever (DF), 16 with dengue hemorrhagic fever (DHF), and eight with dengue shock syndrome (DSS) were prospectively studied during the acute attack. Hepatomegaly (74 per cent), epistaxis (26 per cent), jaundice (25 per cent), and petechial rashes (18 per cent) were the common clinical manifestations of DI. On admission, levels of serum aspartate transaminase (AST), serum alanine transaminase (ALT) and serum alkaline phosphatase (AP) were raised in 80-87 per cent of children with hepatomegaly (group I) and 81 per cent of cases without hepatomegaly (group II). During the second week of hospitalization the proportion of cases with raised levels of AST, ALT, AP and serum bilirubin increased and the mean levels were significantly higher (p < 0.05) in both the groups. These levels gradually declined over the next 2-3 weeks. All the cases with DSS and DHF had raised AST, ALT and AP levels and the mean levels of these enzymes were significantly higher (p < 0.05) as compared to DF. Our results suggest a transient derangement of liver functions in childhood DI, more so in DSS and DHF, with or without hepatomegaly.

Child↗
PubMed1997

The molecular basis of hepatitis B e antigen (HBeAg)-negative infections.

Hepatitis B e antigen (HBeAg)-negative infections are an unusual form of chronic hepatitis B virus (HBV) infection in which viral replication and liver damage persist despite antibodies against HBeAg. This form of HBV may be associated with fulminant hepatitis. The molecular basis for an HBeAg-minus phenotype has been extensively studied and is most often a result of mutations in the precore region. However, other mutations can give rise to this phenotype and their investigation and characterization may reveal new insights into the pathogenesis of chronic viral hepatitis.

Codon, Terminator↗
PubMed2006

Chronic hepatitis C infection in children.

Hepatitis C virus infection may differ in the pediatric age group with respect to transmission, natural history and response to treatment. Most infected children develop chronic hepatitis but with a relatively mild course of the disease. The most efficient transmission of hepatitis C virus is through direct percutaneous exposure to infected blood or blood products. However, the major risk factor for acquisition of hepatitis C virus in children at present is maternal-infant transmission. The rate of progression to advanced liver disease seems to be more rapid in post transfusional and vertically acquired hepatitis C virus infection than in sporadic hepatitis C virus infection acquired postnatally, or in those without known risk factors. There is a wide variety of histopathological expression, depending on the geographical distribution of the different countries. Treatment for hepatitis C virus in children has not yet been approved. However, combination treatment with peginterferon-alpha-2b with ribavirin shows encouraging results and is generally well tolerated. More randomized controlled trials are needed in the future to optimize the approach to hepatitis C virus infection in children.

Child↗
PubMed2001

Thiamine treatment of chronic hepatitis B infection.

OBJECTIVE: Chronic hepatitis B is an international health concern that causes cirrhosis, hepatocellular carcinoma, liver failure, and death. Current treatment options are expensive and associated with side effects; however, indirect evidence suggests a relationship between relative thiamine deficiency and chronic hepatitis B infection. METHODS: The authors present three case studies wherein multiple crossovers of daily thiamine administration were used to evaluate a hypothesized association between thiamine treatment and aminotransferase levels. RESULTS: In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels. Analyses by t test demonstrated a statistically significant reduction in aminotransferase levels in all three cases. CONCLUSIONS: The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection.

Cross-Over Studies↗