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PubMed2000

Anticardiolipin autoantibodies in serum samples and cryoglobulins of patients with chronic hepatitis C infection.

OBJECTIVE: Chronic hepatitis C virus (HCV) has been linked to extrahepatic autoimmune phenomena. In addition, a variety of autoantibodies are found in patients with HCV. The prevalence, nature, and clinical significance of anticardiolipin (aCL) autoantibodies in serum samples of patients with HCV were therefore investigated. PATIENTS AND METHODS: A prospective study of 48 consecutive patients with chronic HCV with no evidence of previous hepatitis B virus (HBV) infection or any other autoimmune disorder. Thirty patients with HBV and 50 healthy volunteers matched for age and sex served as control groups. Anticardiolipin antibodies in the serum samples and cryoprecipitates were measured by a sensitive enzyme linked immunosorbent assay (ELISA). The beta(2) glycoprotein I (beta(2)-GPI) dependency was determined by carrying out aCL assays in the presence or absence of fetal calf serum samples. RESULTS: High levels of IgG aCL antibodies were detected in serum samples of 21/48 (44%) patients with HCV. These autoantibodies showed no beta(2)-GPI dependency. The control groups had much lower levels of aCL antibodies (20% in the patients with HBV and none in the normal volunteers). Cryoprecipitates from four patients with HCV (three aCL positive; one aCL negative) were further isolated. In two of the three aCL positive patients, specific cardiolipin reactivity was shown in the cryoprecipitates. The group of patients with HCV and aCL antibodies in their serum showed significantly higher total IgG levels, a higher incidence of antinuclear antibodies, and viraemia (HCV RNA) than the aCL negative patients. None of the patients with HCV and aCL antibodies showed any clinical manifestations related to those autoantibodies. CONCLUSIONS: This study clearly shows a high prevalence of IgG aCL antibodies in the serum of patients with HCV and the localisation of these antibodies in some cryoprecipitates. The role of these autoantibodies on the course of HCV infection and their clinical significance has not yet been determined.

Adult↗
PubMedDate not supplied

Hepatitis C infection: a review.

Hepatitis C, transmitted through body fluid exchange, affects approximately 1.8% of the U.S. population, roughly 3.9 million persons. Transfusion of blood and blood products was once an important source of hepatitis C transmission. Since the initiation of the hepatitis C screening program in 1985, however, injection drug use has become a major route. Hepatitis C is a leading cause of chronic liver disease. In 80% to 85% of those infected with the virus, chronic hepatitis C eventually develops, which can lead to cirrhosis and hepatocellular carcinoma, with alcohol abuse and coinfection with hepatitis B as additional risk factors. Screening for hepatitis C can be achieved with serologic assays. Molecular assays are helpful in confirming the diagnosis, assessing viral load, and characterizing the genetic nature of the viruses. Interferon alpha (IFN-alpha) and a combination of IFN-alpha 2B and ribavirin are therapies available in treatment of hepatitis C, but sustained response to the treatment has been unsatisfactory. Further studies are indicated to obtain more effective therapies for eradication of the disease. Hepatitis C is preventable, and clinicians should use every opportunity possible in their practice to assess those at risk and actively engage them in risk factor reductions.

Antiviral Agents↗
PubMed1998

The sequential occurrence of viral mutations in a liver transplant recipient re-infected with hepatitis B: hepatitis B immune globulin escape, famciclovir non-response, followed by lamivudine resistance resulting in graft loss.

BACKGROUND/AIMS: The purpose of this study was to characterize the clinical, histological and virological events in an orthotopic liver transplant (OLT) recipient with recurrent hepatitis B infection who was initially managed with hepatitis B immune globulin (HBIg) and when viral recurrence occurred, with nucleoside analogue salvage therapy. The aims were to document the mutations occurring in the hepatitis B virus (HBV) polymerase gene as a consequence of HBIg escape, famciclovir non-response and subsequent lamivudine resistance. METHODS: Throughout the follow-up of 796 days, the patient was seen at least at 4-week intervals. Clinical, biochemical and virological data were registered according to protocol. HBV DNA was quantified throughout the treatment period. The viral polymerase gene was sequenced from serum samples collected at representative time intervals. Consecutive liver biopsies were scored according to the modified Knodell classification. RESULTS: Clinically, the patient was in excellent condition until the development of acute hepatitis during the lamivudine therapy period, 765 days post-OLT. Until this terminal event, serum transaminase activity was only 1-2 times the upper limit of normal with serum bilirubin and prothrombin time within the normal range. Subsequent liver biopsies showed chronic active hepatitis with no signs of fibrosis. The post-mortem biopsy showed severe acute hepatitis B with massive necrosis. The HBV polymerase gene was sequenced during HBIg, famciclovir and lamivudine treatment. One mutation I533L was detected during HBIg treatment. No amino acid changes were selected during famciclovir treatment. Three amino acid changes were selected while the patient was on lamivudine treatment, which include L533I, S559T and M550I. CONCLUSIONS: We have documented HBV recurrence in a liver transplant recipient with the emergence of a multidrug resistant HBV which caused graft loss. The primary resistance to famciclovir in spite of therapeutic penciclovir levels may be as a result of a combination of the mutations found in the polymerase region. After 300 days of lamivudine treatment, a drug-resistant population emerged which was associated with a greater than three log increase in HBV DNA and contributed to loss of graft function. This is the first report of such an adverse clinical outcome due to the emergence of a mutant virus as a consequence of immunoprophylactic and antiviral therapy in a liver transplant recipient.

2-Aminopurine↗
PubMed2005

Evolutionary dynamics of hepatitis C virus envelope genes during chronic infection.

Hepatitis C virus (HCV) envelope glycoproteins E1 and E2 are important targets for the host immune response. The genes encoding these proteins exhibit a high degree of variability that gives rise to differing phenotypic traits, including alterations in receptor-binding affinity and immune recognition and escape. In order to elucidate patterns of adaptive evolution during chronic infection, a panel of full-length E1E2 clones was generated from sequential serum samples obtained from four chronically infected individuals. By using likelihood-based methods for phylogenetic inference, the evolutionary dynamics of circulating HCV quasispecies populations were assessed and a site-by-site analysis of the d(N)/d(S) ratio was performed, to identify specific codons undergoing diversifying positive selection. HCV phylogenies, coupled with the number and distribution of selected sites, differed markedly between patients, highlighting that HCV evolution during chronic infection is a patient-specific phenomenon. This analysis shows that purifying selection is the major force acting on HCV populations in chronic infection. Whilst no significant evidence for positive selection was observed in E1, a number of sites under positive selection were identified within the ectodomain of the E2 protein. All of these sites were located in regions hypothesized to be exposed to the selective environment of the host, including a number of functionally defined domains that have been reported to be involved in immune evasion and receptor binding. Dated-tip methods for estimation of underlying HCV mutation rates were also applied to the data, enabling prediction of the most recent common ancestor for each patient's quasispecies.

Amino Acid Sequence↗
PubMed2005

The significance of transfusion in the past as a risk for current hepatitis B and hepatitis C infection: a study in endoscopy patients.

BACKGROUND: The objective was to determine the contribution of transfusion in the past to the risk of current infection with hepatitis B or C among patients attending a large hospital for endoscopic procedures. STUDY DESIGN AND METHODS: Blood samples had been tested for hepatitis markers by routine methods. Patients completed a comprehensive risk factor questionnaire and results were analyzed using computer software. RESULTS: Twenty-seven percent of the 2120 participants in the study received transfusions in the past. There was no increase in prevalence of hepatitis B among those transfused. Compared with nontransfused participants, recipients of blood before the implementation of hepatitis C virus (HCV) screening in 1990 had a 4.6-fold increased risk of HCV infection, whereas those transfused with screened blood had a 3-fold increased risk. The difference between the odds ratios for patients before and after screening was not significant. CONCLUSIONS: Because screening has almost completely eliminated HCV from the blood supply, our finding of a continuing association of HCV infection with transfusion was unexpected. It implies that there are significant other nosocomial risks for hepatitis C transmission associated with the clinical situations where patients received blood. These should be actively investigated.

Adult↗
PubMed1996

Hepatitis virus infection and liver disease in injecting drug users who died suddenly.

AIM: To determine the extent of liver damage resulting from infection with hepatitis B, C and D viruses (HBV, HCV and HDV) in intravenous drug users (IDUs). METHODS: Liver sections taken at necropsy performed to investigate the cause of sudden death in 48 IDUs were scored for necroinflammatory activity and fibrosis. Evidence of infection was by detection of viral antibodies in serum, hepatitis B surface antigen (HBsAg) and HCV RNA by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Evidence of HCV infection was present in 43 (90%) of 48 serum samples. Six (12%) HBsAg positive serum samples had markers indicative of chronic HBsAg carriage, including three with antibody directed against HDV. Evidence of past HBV infection was found in 27 (69%) of 39 HBsAg negative serum samples. HIV was detected in one (2%) of 48 samples. In five (10%) of 48 samples there was no evidence of current or past infection with HCV, HBV or HIV. All 43 liver sections from HCV positive IDUs scored > or = 1 for necroinflammatory activity, whereas three IDUs without HCV scored 0. Scores for stage of fibrosis were > or = 1 in 15 (35%) of 43 and zero of five IDUs, respectively. Fibrosis scores of > or = 3 were seen only in three IDUs positive for HBV, HDV and HCV. CONCLUSION: Inflammatory activity in the liver is present in a high proportion of IDUs in Glasgow and is strongly associated with HCV infection. Severe chronic liver damage was limited to HBsAg carriers superinfected with HDV and HCV.

Adolescent↗
PubMed1998

Chronic hepatitis virus infection in children.

Hepatitis B and C viruses (HBV and HCV) are the two main hepatitis viruses causing chronic liver diseases in children. In hyperendemic areas, nearly half of the primary infection in chronic HBV carriers occurs during the perinatal period through the transmission from hepatitis B e antigen (HBeAg)-positive mothers. The other half are from horizontal transmission mainly through intrafamilial spread or injection using unsterilized needles. During the natural course of chronic HBV infection, spontaneous HBeAg/anti-HBe seroconversion occurs very rarely (2% annually) before 3 years of age. After 3 years of age, the HBeAg seroconversion rate increases gradually to 5% per year. Those with mothers who are hepatitis B carriers tend to clear HBeAg slower than those whose mothers are non-carriers. Transplacental HBeAg may cause T cell tolerance in infected children. Universal HBV immunization programmes have been effective in reducing the hepatitis B carrier rate more than 10-fold, and the incidence of hepatocellular carcinoma in children has also been decreased significantly. Hepatitis C virus infection occurs mainly in high-risk children, such as those who received blood products (blood diseases, malignancies, post-open heart surgery etc.), children of HCV-infected mothers, and in hyperendemic areas, from injection using unsterile needles. Mother-to-infant transmission occurs on average in 5% of infants of viraemic mothers. The maternal HCV-RNA titre is the most important factor determining the infectivity. Chronicity developed in 60-80% of HCV-infected children. Although transient or persistent elevation of aminotransferases occurs frequently in chronically HCV-infected children, liver histology showed minimal or mild changes only. The most prevalent genotype of HCV in children is Ib. Screening of the blood products for HCV antibody has markedly reduced the rate of HCV infection in children at risk. However, vaccine development is needed to prevent mother-to-infant transmission and other routes of infections.

Adolescent↗
PubMedDate not supplied

Hepatitis delta virus infection and Labrea hepatitis. Prevalence and role in fulminant hepatitis in the Amazon Basin.

To define more exactly the epidemiology of delta virus infection and confirm its role in causing fulminant Labrea hepatitis in the Amazon Basin, we studied the prevalence of delta virus infection among persons with acute and chronic hepatitis B virus infection in the Boca do Acre district of the southern Amazon Basin. Delta virus infection was found in 24% of asymptomatic hepatitis B virus carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. Chronic delta virus infection occurred primarily in older children and adults, while acute and fulminant delta virus infection occurred in young children as well. In fulminant hepatitis cases, delta virus superinfection of hepatitis B virus carriers was the most common serological pattern; histopathologic examination showed features identical to those described in fulminant hepatitis cases of similar etiology in Colombia and Venezuela. Delta virus infection is highly endemic in the southern Amazon Basin and is the principal cause of Labrea hepatitis.

Acute Disease↗
PubMed1996

Hepatitis G virus infection in patients with hepatitis C virus infection undergoing liver transplantation.

BACKGROUND & AIMS: Hepatitis G virus (HGV) is transmissible by blood transfusion, but its role in chronic liver disease is unknown. The aim of this study was to determine the prevalence of HGV infection in patients infected with hepatitis C virus (HCV) undergoing transplantation and evaluate the effects of HGV coinfection on the course of posttransplantation HCV infection. METHODS: One hundred twenty-four patients infected with HCV undergoing liver transplantation were studied. Serum samples were tested for HCV and HGV RNA; HCV RNA was quantitated by branched DNA assay, and HCV genotype was determined. RESULTS: The prevalence of pretransplantation and posttransplantation HGV infection was 24% and 28%, respectively. Pre-transplantation HGV infection was positively correlated with posttransplantation HGV infection (P < 0.001). Pretransplantation clinical features were not different in patients infected with HCV with and without HGV infection. Posttransplantation HCV RNA levels were not significantly different in patients with and without HGV coinfection, but HCV genotype 1b was more frequent in patients with HGV coinfection. There were no differences in the histological severity of posttransplantation liver disease, graft, and patient survival between patients with and without HGV infection. CONCLUSIONS: Although HGV coinfection is frequent in patients with end-stage HCV disease undergoing liver transplantation, there is no association between the presence of HGV coinfection and the severity of liver disease post-transplantation, graft, or patient survival.

Adult↗
PubMed1998

High prevalence of infection with hepatitis G virus in patients with hepatic and extrahepatic malignancies.

BACKGROUND/AIMS: The pathogenic role of hepatitis G virus, the recently discovered blood-borne agent, is controversial. Our aim was to ascertain the prevalence of hepatitis G virus infection in hepatic and in extrahepatic malignancies. METHODS: We studied 166 Italian patients (112 male, 54 female, mean age 61.8+/-9.3, mean+/-SD, range 34-85). One hundred and eighteen had cirrhosis, which was complicated by hepatocellular carcinoma in 66 cases. Forty-eight patients had extra-hepatic malignancies. Circulating HGV RNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) of both the nonstructural-3 and 5'noncoding regions of the hepatitis G virus genome. Antibodies to the E2 protein of hepatitis G virus were detected by means of an enzyme-linked immunosorbent assay. RESULTS: Ongoing HGV infection was detected in 30/66 (46%) patients with hepatocellular carcinoma, 12/52 (23%) patients with cirrhosis, and 14/48 (29%) patients with extrahepatic malignancies (p<0.05). Evidence of exposure to hepatitis G virus (detection of either HGV RNA or anti-E2 antibodies) was found in 46% of patients with cirrhosis, 66% of patients with hepatocellular carcinoma, and 39% of patients with extrahepatic malignancies. Serum HGV RNA positivity was associated with a hematocrit value < or = 0.35 and with history of exposure to blood products (p<0.005). CONCLUSIONS: Ongoing hepatitis G virus infection is detected at a very high rate in patients with hepatocellular carcinoma, but is also fairly common in extrahepatic malignancies. Hepatitis G virus infection in these patients is likely to originate from exposure to blood products, and to persist because of deficient immune surveillance.

Adult↗
PubMed1986

The intensity of experimental schistosome infections modulates hepatic pathology.

Groups of mice infected with Schistosoma japonicum were killed 7, 10 or 15 weeks after infection. The size of hepatic granulomas and degree of hepatic fibrosis in individual mice were examined in relation to the number of worm pairs present using regression analysis. Mice with heavy S. japonicum infections had smaller circumoval granulomas in their livers than did mice with lighter infections. Hepatic fibrosis per unit infection, i.e., per worm pair or per egg, also decreased as the intensity of infection increased. These trends were similar in 8 strains of mice examined. No clear trends were found in rabbits or monkeys infected with S. japonicum. Hepatic fibrosis in S. haematobium-infected mice decreased with increasing intensity of infection, although this trend was significant only in infections of 1 year duration. C57BL/6 mice infected with S. mansoni often showed trends similar to those in S. japonicum-infected mice; however the findings in C3H and ICR mice infected with S. mansoni were more variable. Most of the data for the present report were from animals also described in previous publications. The relevance of these findings to schistosome infections in humans is unknown but the results are clearly pertinent to the analysis of hepatic pathology in experimental infections. Overall egg production by the worms was not affected and the number of eggs per worm pair recovered from the tissues was not generally influenced by the number of worm pairs present.

Animals↗
PubMed2002

Hepatitis e virus infection in fulminant hepatitis patients and an apparently healthy population in Bangladesh.

This is the first study comparing hepatitis E virus (HEV) infection in Bangladesh in fulminant hepatitis (FH) patients presumed to have a viral cause and in the apparently healthy population. Sera from 22 FH patients were analyzed for antibodies to hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C and D viruses, and HEV and for hepatitis B surface antigen (HBsAg). Anti-HEV immunoglobulin M (IgM) was detected in the sera of 63.6% of patients, whereas 35.7% were positive for HBsAg. A high prevalence of HEV infection (83.3%) was noted in the HBV carriers. Serum samples from 273 apparently healthy individuals were tested for antibodies to HAV and HEV. Anti-HEV IgM was detected in 7.3% of the samples. The seroprevalence of HAV differed from that of HEV in the same population because all samples were negative for anti-HAV IgM. These data indicate that HEV infection is highly endemic in Bangladesh.

Adolescent↗
PubMed2005

Natural history of hepatitis C virus infection: from chronic hepatitis to cirrhosis, to hepatocellular carcinoma.

Hepatitis C is a heterogeneous disease and is responsible for considerable mortality and morbidity. The hepatitis C virus (HCV) infects nearly 170 million people world-wide. More than 80% of infected individuals develop chronic infection; the remaining 10-20% develop spontaneous clearance with natural immunity. Acute hepatitis is icteric in only 20% of patients and is rarely severe. The majority of patients who develop chronic HCV infection are asymptomatic; but 60-80% develop chronic hepatitis as indicated by elevated alanine aminotransferase (ALT), around 30% maintain persistently normal ALT levels despite having detectable HCV-RNA in serum. One-third of chronically infected patients develop progressive liver injury, fibrosis and cirrhosis over a period of 20-30 years. The relationship between virus load, HCV genotype, quasi-species variability and progression of liver disease is controversial. Acquired infection after age 40, male sex, excessive alcohol-consumption, hepatitis B virus (HBV) or HIV co-infection, steatosis, and immunosuppressed state have been identified as co-factors associated with progression of fibrosis and development of cirrhosis. In patients with cirrhosis, the incidence of hepatocellular carcinoma is 2-5% per year. At present, HCV-related end-stage cirrhosis is the first cause of liver transplantation.

AIDS-Related Opportunistic Infections↗
PubMed1996

[Increased possibility for HIV-associated retinal microangiopathy syndrome in patients with concomitant hepatitis C infection].

BACKGROUND: The etiology of HIV-related retinal microangiopathy syndrome is yet unknown. Several authors postulate direct endothelial-cell infection, an immunocomplex vasculitis caused by HIV-related hypergammaglobulinemia or an increased serum concentration of endothelin as its origin. PATIENTS: 118 patients infected by HIV-1 have been examined (CDC I: 1; CDC II: 42; CDC III: 7; CDC IV: 68). 49 out of them were also infected by hepatitis-C-virus (CDC I: 0; CDC II: 16; CDC III: 4; CDC IV: 29). RESULTS: 26 out of 49 patients with hepatitis-C-co-infection showed HIV-related retinal microangiopathy syndrome (CDC I: 0/0; CDC II: 8/16; CDC III: 2/4; CDC IV: 16/29). In 69 patients without hepatitis-C-infection, HIV-related retinal microangiopathy syndrome was found five times (CDC I: 0/1; CDC II: 2/26; CDC III: 0/3; CDC IV: 3/39). CONCLUSION: Co-infection with hepatitis-C-virus is supposed to enhance the development of retinal microangiopathy syndrome in patients infected by HIV-1.

AIDS-Related Opportunistic Infections↗
PubMed2001

Influence of human immunodeficiency virus type 1 infection on acute hepatitis A virus infection.

To assess the possible influence of human immunodeficiency virus type 1 (HIV-1) infection on the clinical course of acute hepatitis A virus (HAV) infection, 15 HIV-1-infected homosexual men and 15 non-HIV-infected age-matched subjects were compared. HAV load was higher in HIV-1-infected than in non-HIV-infected patients (P<.001). Duration of viremia in HIV-1-infected patients (median, 53 days) was significantly (P<.05) longer than in non-HIV-infected patients (median, 22 days). HIV-1-infected patients had lower elevations in alanine aminotransferase levels than did non-HIV-infected patients (P<.01) but had higher elevations in alkaline phosphatase levels than did non-HIV-infected patients (P<.001). Some HIV-1-infected patients still had HAV viremia when clinical symptoms had disappeared and alanine aminotransferase levels had returned to normal (60-90 days after the onset of symptoms). HIV-1 infection was associated with prolongation of HAV viremia, which might cause a long-lasting outbreak of HAV infection in HIV-1-infected homosexual men.

Acute Disease↗
PubMed1998

Pilot study to estimate survivors to 1995 of 1983-1984 prevalent hepatitis C infections in Lothian patients who tested positive or negative for hepatitis B surface antigen in 1983-1984.

OBJECTIVE: To estimate Hepatitis C prevalence in 1983-1984, and survivorship to 1 January 1995, of patients who tested were for Hepatitis B surface antigen in 1983-1984; and to do so according to risk of blood-borne virus transmission, including injector status. SETTING: Regional Virus Laboratory in Edinburgh. SAMPLES: Sera from 1983-1984 which were originally received for hepatitis B surface antigen testing and were classified as being at high, medium, or low risk for blood-borne virus transmission. RESULTS: Available 1983-1984 sera were tested from: (i) all 246 patients aged 15-55 years who were Hepatitis B surface antigen positive in 1983-1984; and (ii) a 10% systematic sample of 355 patients aged 15-55 years who had tested Hepatitis B surface antigen negative in 1983-1984. Patients' survival status at 1 January 1995 was established via the records of the Registrar General for Scotland. A Hepatitis C prevalent case cohort of 500 survivors to 1 January 1995- who were already infected with Hepatitis C in 1983-1984--could be established from group (i) and high or medium risk group (ii) patients with, as controls, 1460 individuals of similar age and risk group whose 1983-1984 sample was negative when tested retrospectively for Hepatitis C antibodies. Two hundred out of these 500 cases are not known to be injecting drug users, and the total would rise to 300 out of 600 if the case cohort were expanded to include low risk group (ii) surviving patients who were Hepatitis C antibody positive in 1983-1984. Between 82% (40/49) and 97% of injectors (57/59 if also HIV-infected) who were Hepatitis B surface antigen positive in 1983-1984 were already Hepatitis C antibody positive; and 72% (95% confidence interval (CI) 51%-93%) of injectors who were Hepatitis B surface antigen negative in 1983-1984 were nonetheless infected with Hepatitis C. Known drug user/contacts (excluding the major group of 59 identified HIV-infecteds) had Hepatitis C prevalence in 1983-1984 of 79% (53/67, with 95% CI 69%-89%), substantially higher than our prior assumption, which was 50%. Hepatitis C prevalence in 1983-1984 for patients who were not known to be injectors, were Hepatitis B surface antigen negative and were rated as moderate risk for blood-borne virus transmission was 13% (95% CI 4%-23%) and 8% (95% CI 3%-14%) even for low risk patients. Deaths by end December 1994 in 1983-1984 prevalent Hepatitis C infections were low: 2/35 (6%) for patients who were Hepatitis B surface antigen negative in 1983-1984 and 2/40 (5%) for Hepatitis B surface antigen positive injectors who were not HIV-infected. The latter rate with upper 95% confidence limit of 12% is modest when compared to the 10% mortality that would be expected of injectors over 11 years. CONCLUSION: Retrospective Hepatitis C testing of 1700 stored sera from high or medium risk group (ii) patients who were not known to be injectors will identify an estimated 200 (11.7%) who were already Hepatitis C infected in 1983-1984 and still alive on 1 January 1995. Retrospective Hepatitis C testing of 1300 low risk samples is expected to yield 100 (7.6%) apparently non-injector patients who were already Hepatitis C infected in 1983-1984 and still alive on 1 January 1995.

Adolescent↗