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PubMed2003

Therapeutic vaccination in the immunotolerant phase of children with chronic hepatitis B infection.

AIM: Hepatitis B virus (HBV) infection is a major global health concern and is the most common cause of chronic liver disease worldwide. Our aim was to investigate the efficacy of specific HBV vaccination as active immunotherapy in treating chronic hepatitis B (CHB) infection during the immunotolerant phase of children with normal aminotransferase values and high viral load. MATERIALS AND METHODS: Seventy-four patients never vaccinated before were randomly and prospectively recruited into two groups. Group 1 included 43 patients vaccinated with three standard injections of the GenHevac B vaccine at 30-day intervals. Group 2 contained 31 patients who did not receive any medication or vaccination (control group). Postvaccination serologic and virologic evaluation was performed 6 months after the first injection and at the end of the 12th month. Response to therapy was defined as loss of HBV DNA in serum and hepatitis B e antigen (HBeAg) seroconversion (loss of HBeAg), development of hepatitis B e antibody (anti-HBe). RESULTS: The mean baseline alanine aminotransferase (ALT) value in Group 1 was 33.0 +/- 9.6 IU/l, 34.6 +/- 13.9 IU/l at 6 months after first injection and 34.3 +/- 17.1 IU/l at end of 12 months (P > 0.05). In Group 1 the HBV DNA load at the start of immunization was 3571 +/- 1292 pg/ml; this value was 3220 +/- 1217 pg/ml at the 6th month and 2931 +/- 1292 pg/ml at the 12th month (P > 0.05). In Group 2 the mean ALT values at the beginning of therapy and at the 6th and 12th months were 32.6 +/- 7.8, 32.3 +/- 8.0 and 30.3 +/- 7.3 IU/l, respectively (P > 0.05), and the mean viral load HBV DNA values were 3909 +/- 1378, 3546 +/- 869 and 3106 +/- 718 pg/ml, respectively (P > 0.05). There was no statistically significant difference between Group 1 and Group 2 at the end of the 6th and 12th months in the mean ALT values and mean viral load of HBV DNA (P > 0.05). Except for one patient in each group, hepatitis B surface antigen and HBeAg clearance or hepatitis B surface antibody and anti-HBe seroconversion were not observed during follow-up (P > 0.05). CONCLUSION: In this multicentered study comparison of vaccinated and unvaccinated groups of immunotolerant children with CHB infection showed no difference in the clearance of HBV DNA or seroconversion from HBeAg to anti-HBe. Different immunization protocols should be considered for future investigations in the immunotolerant phase of children with CHB infection.

Adolescent↗

PubMed2004

Challenges in the management of HIV and hepatitis C virus co-infection.

Hepatitis C virus (HCV) has become a significant contributor to morbidity and mortality to those infected with HIV since the introduction of highly active antiretroviral therapy (HAART). The presence of HIV clearly has a negative effect on the natural history of HCV, although there is some debate over whether HCV influences the natural history of HIV. Given the prevalence of co-infection and the accelerated liver damage from HCV, treatment of chronic HCV infection is an important consideration in patients co-infected with HIV. There are few studies of pegylated interferon and ribavirin in co-infected populations, but it seems that the treatment is well tolerated, although it is possibly less effective in this group. HAART in the setting of HCV infection also requires some special consideration, namely an increased incidence of hepatotoxicity. Treatment of co-infected patients requires close monitoring as current therapies are not ideal in terms of effectiveness, and toxicity may be severe.

AIDS-Related Opportunistic Infections↗

PubMed1980

Viral hepatitis. 2. Prevention and control.

Good personal hygiene is one of the most important measures for control of hepatitis infection. Hepatitis is transmitted by close contact with an infected person or nonhuman primate, exposure to infected food or water, transfusion of infected blood, dialysis, or contact with hepatitis-containing laboratory specimens. Each of these situations necessitates certain precautions to avoid contamination. In some instances, passive immunization with either immune serum globulin (ISG) or hepatitis B immune globulin (HBIG) is recommended. Vaccines now being tested for active immunization against hepatitis B will probably be available soon for use in persons at high risk, but development of a vaccine against hepatitis A seems unlikely in the near future.

Hepatitis A↗

PubMed1997

Nucleic acid-based antiviral and gene therapy of chronic hepatitis B infection.

Persistent hepatitis B virus (HBV) infection often leads to the development of chronic hepatitis, cirrhosis and hepatocellular carcinoma. There is a need to develop new antiviral approaches for the treatment of this disease. We have explored various nucleic acid-based strategies designed to inhibit HBV replication including: the use of antisense RNA and DNA constructs, DNA-based immunization techniques to stimulate broad-based cellular immune responses with particular emphasis on the generation of cytotoxic lymphocyte (CTL) activity to viral structural proteins, hammerhead ribozymes to cleave HBV pregenomic RNA in vitro and dominant negative HBV core mutant proteins as inhibitors of nucleocapsid formation within cells. In order to optimize these antiviral effects, various novel expression vectors have been developed to deliver such DNA constructs to cells. For example, adenoviral vectors carrying genes that encode for dominant negative proteins have been employed to transfect hepatocytes in vitro and in vivo. In addition, plasmid vectors have been produced to promote expression of HBV structural genes following injection into muscle cells as a means to stimulate the host's cellular and humoral immune response in the context of histocompatibility antigen (HLA) class I and II antigen presentation. These experimental approaches may have important implications for the generation of efficient antiviral effects during chronic HBV infection.

Antiviral Agents↗

PubMed2000

Immunobiology of hepatitis C virus (HCV) infection: the role of CD4 T cells in HCV infection.

Hepatitis C virus (HCV) is yet another example of a pathogen that persists in the presence of a readily apparent immune response. As evidence for both humoral and cellular immune responsiveness is quite strong, our studies have begun to examine whether qualitative defects in CD4 T-cell responses to viral antigens may help to explain why HCV is not eliminated in the vast majority of infections. Direct evidence that CD4 T cells play a role in HCV persistence is lacking, but several observations are consistent with this possibility. Importantly, it does not exclude the role of antibody or killer T cells in the immunopathogenesis of HCV infection. In addition, we discuss the consequences of viral mutation and how naturally occurring variants in immunodominant viral epitopes can effectively suppress helper T-cell responses to wild type virus.

Antigen Presentation↗

PubMed2000

Subgenomic negative-strand RNA function during mouse hepatitis virus infection.

Mouse hepatitis virus (MHV)-infected cells contain full-length and subgenomic-length positive- and negative-strand RNAs. The origin and function of the subgenomic negative-strand RNAs is controversial. In this report we demonstrate that the synthesis and molar ratios of subgenomic negative strands are similar in alternative host cells, suggesting that these RNAs function as important mediators of positive-strand synthesis. Using kinetic labeling experiments, we show that the full-length and subgenomic-length replicative form RNAs rapidly accumulate and then saturate with label, suggesting that the subgenomic-length negative strands are the principal mediators of positive-strand synthesis. Using cycloheximide, which preferentially inhibits negative-strand and to a lesser extent positive-strand synthesis, we demonstrate that cycloheximide treatment equally inhibits full-length and subgenomic-length negative-strand synthesis. Importantly, following treatment, previously transcribed negative strands remain in transcriptionally active complexes even in the absence of new negative-strand synthesis. These findings indicate that the subgenomic-length negative strands are the principal templates of positive-strand synthesis during MHV infection.

Animals↗

PubMed1998

New therapies for the treatment of chronic hepatitis B infection.

Persistent hepatitis B virus infection can lead to the development of chronic liver disease, cirrhosis and primary hepatocellular carcinoma. The only therapy of confirmed benefit in chronic hepatitis B is interferon alpha, which can lead to long-term benefit in only a third of highly selected patients. A number of new therapeutic approaches are being actively developed for treating chronic hepatitis B, including the use of nucleoside analogues, cytokines, antisense oligonucleotides, ribozymes, dominant negative mutants and DNA-based vaccines. Recent clinical trials with the nucleoside analogues have identified several important challenges for future drug development, in which the gene therapy-based approach may prove useful either alone or most probably in various combinations. Future clinical trials should aim to address these challenges using the new therapies so that the goal of substantial and sustained inhibition of viral replication with the accompanying improvement in the underlying liver disease can be achieved.

Journal Article↗

PubMed1995

Global programme for control of hepatitis B infection.

The hepatitis B virus (HBV) has infected more than 2000 million persons alive today and 350 million persons are chronically infected carriers of the virus, at high risk of death from active hepatitis, cirrhosis and primary hepatocellular cancer. Each year approximately 1 million people die from the acute and chronic sequelae of HBV infection, making it one of the major causes of morbidity and mortality in man. In May 1992, the World Health Assembly, the governing body of the World Health Organization, endorsed recommendations stating that countries with an HBV carrier prevalence of 8% or more should have hepatitis B vaccine integrated into their national immunization programmes by 1995 and that all countries should have such immunization in place by 1997. At present, 50 countries have a national policy of including hepatitis B vaccine as a routine part of their infant immunization programme--up from 25 countries in 1990. These countries represent 32% of the world's 145 million newborns, but 56% of the world's carriers. Several countries of 'low' endemicity are also recommending hepatitis B immunization of all newborns or adolescents (or both), realising that the strategy of 'high-risk group' immunization has failed to control HBV infection even in areas of low endemicity and that addition of hepatitis B vaccine to routine immunization schedules is highly cost-effective. All countries should establish working groups to examine the burden of disease due to HBV infection and the cost-effectiveness of adding hepatitis B vaccine to routine and/or adolescent immunization programmes.

Adolescent↗

PubMed2003

Viral and clinical factors associated with the fulminant course of hepatitis A infection.

Fulminant hepatitis is a severe complication of hepatitis A virus infection. Its mechanism is unknown. Liver transplantation can be necessary, but spontaneous recovery is frequent. There are no data on the level of viral replication according to the clinical form of hepatitis A. We reviewed the files of 50 patients with acute hepatitis A. Nineteen patients had fulminant hepatitis (defined by encephalopathy and factor V <50%), and, from them, 10 patients underwent transplantation. Hepatitis A virus (HAV) RNA was quantified by real-time PCR on sera obtained at admission. The genotype was determined by phylogenetic analysis of HAV RNA. HAV RNA was detected in serum by RT-PCR in 39 out of 50 patients. Encephalopathy and low factor V level were significantly related to female gender, HAV PCR negativity (9/19 vs. 5/31, respectively; P =.03), a low serum HAV RNA level (log, 3.6 +/- 0.6 vs. 4.4 +/- 0.9, respectively; P =.02), genotypes other than IA, and acetaminophen intake. In multivariate analysis, low or undetectable HAV viral load and a high bilirubin level were independently associated with both low factor V levels and fulminant hepatitis and also with death or transplantation. In conclusion, HAV-related liver failure is due to an excessive host response associated with a marked reduction in viral load. Serum HAV RNA assay could be of help in the management of severe hepatitis A.

Acetaminophen↗

PubMed1998

Clinical and molecular virological differences between fulminant hepatic failures following acute and chronic infection with hepatitis B virus.

Clinical and molecular biological characteristics were compared between patients who presented with fulminant hepatic failure following acute infection with hepatitis B virus (HBV) and those who developed hepatic failure during they carried HBV. The 11 patients with acute HBV infection had higher levels of alanine aminotransferase (mean +/- SD: 4943 +/- 2867 vs 1157 +/- 678 IU/L, P < 0.01), more often with a single peak (91% vs. 0%, P < 0.001), and lower total bilirubin level (15.3 +/- 4.4 vs 28.1 +/- 14.3 mg/1000 ml, P < 0.01) than the 13 patients with chronic HBV infection. Hepatitis B surface antigen was detected less often (55% vs. 100%, P < 0.05) and viral DNA polymerase less frequently (0% vs. 46%, P < 0.05) in the patients with acute than chronic HBV infection. Hepatitis B e antigen was detected in one (9%) patient with acute infection, less frequently than in six (46%) patients with chronic infection (P < 0.05). Mutations in the precore region was detected in HBV DNA clones from ten (91%) patients with acute infection and only in those from eight (62%) patients with chronic infection. All HBV DNA clones from the five (38%) patients with chronic infection that did not have precore mutations, however, possessed mutations in the core promoter. These results indicate that HBV mutants incapable of translating hepatitis B e antigen would play a major role in fulminant hepatic failure occurring after acute HBV infection. In contrast, HBV variants with core promoter mutations for reducing the transcription of hepatitis B e antigen would play an additional role in fulminant hepatic failure developing during chronic infection.

Acute Disease↗

PubMed1987

Genetic variation between woodchuck populations with high and low prevalence rates of woodchuck hepatitis virus infection.

Woodchuck hepatitis virus (WHV) infection is known to be endemic in areas of the mid-Atlantic states but is apparently absent from populations in New York and much of New England. Blood samples of 40 woodchucks (Marmota monax) from New York and from Delaware were examined by starch gel electrophoresis, and 18 monomorphic and six polymorphic protein-coding genetic systems were identified. Mendelian inheritance of variants of the six polymorphic systems was confirmed in 52 laboratory offspring of the original samples. Average heterozygosity of 0.066 in New York woodchucks and 0.039 in Delaware woodchucks were high values for mammals, although similar to those of other sciurids. Significant heterogeneity between samples from New York and Delaware woodchucks was observed at two loci (peptidase with glycyl leucine-4 and phosphogluconate dehydrogenase), suggesting that these populations were genetically distinct. Whether there are genetically determined differences in response to WHV infection remains to be determined experimentally.

Alleles↗

PubMed2006

Epidemiology of hepatitis C virus (HCV) infection.

Hepatitis C virus remains a large health care burden to the world. Incidence rates across the world fluctuate and are difficult to calculate given the asymptomatic, often latent nature of the disease prior to clinical presentation. Prevalence rates across the world have changed as well with more countries aware of transfusion-related hepatitis C and more and more evidence supporting intravenous drug use as the leading risk factor of spread of the virus. This article reviews current hepatitis C virus prevalence and genotype data and examines the different risk factors associated with the virus.

Journal Article↗

PubMed2004

Practical management of chronic hepatitis B infection.

Chronic hepatitis B virus (HBV) infection is a complex disease. In recent years, there has been a marked increase in new knowledge regarding its virology, epidemiology, and natural history. In addition, more sensitive molecular diagnostic tests and relatively effective therapies for many individuals with chronic HBV infection have been developed and are available to practicing physicians. On the other hand, the influx of new immigrants from HBV hyperendemic areas such as the Asia-Pacific region, Indochina, and Eastern Europe has increased the demand for management of HBV infection in these populations. Physicians thus need to be able to identify persons at risk for hepatitis B and to evaluate and monitor them appropriately. Counseling on precautions to prevent transmission of HBV is also important for patients, as is education regarding the natural course of HBV infection and patient prognosis. Clinicians need to balance the treatment options carefully for their patients. This article provides up-to-date information on management of HBV infection for practicing physicians.

Adenine↗

PubMed2000

Posttranscriptional inhibition of class I major histocompatibility complex presentation on hepatocytes and lymphoid cells in chronic woodchuck hepatitis virus infection.

Woodchuck hepatitis virus (WHV), similar to human hepatitis B virus, causes acute liver inflammation that can progress to chronic hepatitis and hepatocellular carcinoma. WHV also invades cells of the host lymphatic system, where it persists for life. We report here that acute and chronic hepadnavirus hepatitis is characterized by a profound difference in the expression of class I major histocompatibility complex (MHC) molecules on the surface of infected hepatocytes and, notably, lymphoid cells. While acute WHV infection is accompanied by the enhanced hepatocyte surface presentation of class I MHC antigen and upregulated transcription of the relevant hepatic genes, inhibition of class I antigen display on liver cells is a uniform hallmark of chronic WHV infection. This inhibition in chronic hepatitis occurs despite augmented (as in acute infection) expression of hepatic genes for class I MHC heavy chain, beta(2)-microglobulin, and transporters associated with antigen processing (TAP1 and TAP2). Further, the class I antigen inhibition is not related to the histological severity of hepatocellular injury, the extent of lymphocytic infiltrations, the level of intrahepatic gamma interferon induction, or the hepatic WHV load. Importantly, the antigen expression is also inhibited on organ lymphoid cells of chronically infected hosts. The results obtained in this study demonstrate that the defective presentation of class I MHC molecules on cells supporting persistent WHV replication is due to viral posttranscriptional interference. This event may diminish the susceptibility of infected hepatocytes to virus-specific T-cell-mediated elimination, hinder virus clearance, and deregulate the class I MHC-dependent functions of the host immune system. This multifarious effect could be critical for perpetuation of liver damage and evasion of the antiviral immunological surveillance in chronic infection and therefore could be supportive of hepadnavirus persistence.

Acute Disease↗

PubMed2006

Functional and clinical significance of hepatitis D virus genotype II infection.

Hepatitis D virus (HDV) infection is one of the important etiologies of fulminant hepatitis and may aggravate the clinical course of chronic HBV infection to cirrhosis and liver failure. HDV was classified into three genotypes. Recent molecular phylogenetic analysis of HDV suggests at least seven major clades. The genotype I HDV is widely spread, genotype II is found in East Asia and genotype III HDV is prevalent in South America. The genomic size is 1682-1685 nucleotides (nt) for genotype II, and 1676 nt for genotype IV (IIb). The divergence in HDV nucleic acid sequences between genotype II and other genotypes varies from 13.8% to 35.3%. The divergences in the HDAg-coding region may range from 17.8% to 29.8% between genotype II and other genotypes. There is no genotypic or size restriction on the interactions of either the small or the large hepatitis delta antigens (HDAgs) between genotypes I and II, and there is also no genotypic incompatibility during co-package of HDAgs of different genotypes into virus like particles. There appears no apparent universal genotypic restriction of the transactivation of genotype I HDV RNA replication by small HDAg of genotype II. In contrast, there appears more genotypic restriction for genotype I small HDAgs to transactivate genotype II HDV RNA replication. Of the functional domains of HDAg, the 19 amino acids at the carboxyl-end of the large HDAg show the greatest divergences (70%-80%) between genotypes I and II. The viral packaging efficiencies of genotype I HDV isolates are usually higher than those of genotype II. The 19 amino acids at the carboxyl-end seem to be the most important determinant for viral packaging efficiencies. The editing efficiencies of the genotype I HDV are also higher than those of the genotype II. Genotype II HDV infection is relatively less frequently associated with fulminant hepatitis at the acute stage and less unfavorable outcomes [cirrhosis or hepatocellular carcinoma (HCC)] at the chronic stage as compared to genotype I. It appears that the clinical manifestations and outcomes of patients with genotype IV (IIb) HDV infection are more like those of patients with genotype II HDV infection. Persistent replication of HBV or HDV was associated with higher adverse outcomes (cirrhosis, HCC or mortality) compared to those who cleared both viruses from the sera. HBV of the genotype C is also a significant factor associated with adverse outcomes (cirrhosis, HCC or mortality) in patients with chronic hepatitis D in addition to genotype I HDV and age. However, most patients with chronic HDV infection have low or undetectable hepatitis B virus DNA levels. During longitudinal follow-up, genotype I HDV is the most important determinant associated with survival.

Genotype↗

PubMed2001

Is nausea associated with chronic hepatitis C infection?

OBJECTIVES: Hepatitis C virus is a common chronic infection that is widely associated with symptoms of fatigue and pain in the right upper quadrant. Nausea may be an underrecognized symptom. This study was designed to study the frequency of nausea in patients with hepatitis C virus infection compared to controls. METHODS: A cross-sectional study design with consecutive outpatients was used. Three groups were administered a dyspepsia and a previously validated Nausea Profile questionnaire. Univariate and multivariate analysis was performed. RESULTS: A total of 64 hepatitis C virus (HCV) patients, 53 liver disease controls (LC), and 64 normal controls (NC) were studied. An increased period prevalence of nausea was found in HCV patients 43% versus 29.7% in NC and 18.9% in LC (p = 0.009). There was an increased frequency of fatigue and abdominal pain in HCV patients over 1 month compared to LC and NC combined (p = 0.0001 and 0.0065 respectively). The Nausea Profile score revealed statistically higher total scores and higher subscale scores in the HCV group compared to controls. The total NP score expressed as a percentage of the maximum was 27% in HCV versus 12.7% for LC and 9.2% for NC (p = 0.0005). The odds of nausea using logistic regression were 2.1 CI (1.0-4.5) in HCV patients compared to controls (p = 0.05). Using linear regression, higher Nausea Profile scores were found to be independently associated with the diagnosis of HCV (.0005), fatigue (p = 0.0003), and abdominal pain (p = 0.0001). CONCLUSIONS: HCV infection is associated with an increased risk for nausea. The strong association between abdominal pain and nausea may be a clue to the etiology of nausea in these patients. Further etiological studies are needed.

Abdominal Pain↗

PubMed2006

Clinical presentation and course of acute hepatitis C infection in HIV-infected patients.

Hepatitis C virus (HCV) has become a significant source of morbidity and mortality in HIV-infected patients. However, little is known about the clinical presentation and course of acute HCV infection in this population. This study reports the outcomes of acute HCV infection in 9 HIV-infected men. Sex with men was the only reported risk factor for HCV infection in 6 of the subjects. Clinical presentation of acute HCV ranged from incidentally discovered elevated transaminases to severe liver dysfunction requiring hospitalization. At the time of HCV diagnosis, 8 of 9 patients had CD4+ counts >250 cells/mm(3), and 6 had HIV viral loads of < or =5000 copies/mL. Eight patients were receiving antiretroviral therapy. Outcome of these acute HCV infections varied. Five patients experienced virologic clearance, 2 in whom virus cleared spontaneously and 3 who were treated with pegylated interferon and ribavirin. Four patients developed chronic infection, one of whom had a relapse during HCV treatment and 3 of whom were untreated. All 4 patients to whom HCV therapy was administered experienced significant anemia or neutropenia, necessitating dose reduction or support with growth factors. Prompt recognition of acute HCV infection may minimize antiretroviral treatment interruption and will allow early treatment, which may improve virologic clearance. Unexplained transaminase elevations in HIV-infected patients, including men who have sex with men, should trigger an evaluation for acute HCV infection.

Acute Disease↗

PubMed2006

Introduction to chronic hepatitis B infection.

Chronic hepatitis B virus (HBV) infection affects over 350 million people worldwide and over 1 million die annually of HBV-related chronic liver disease. Although many individuals eventually achieve a state of nonreplicative infection, the prolonged immunologic response to infection leads to the development of cirrhosis, liver failure, or hepatocellular carcinoma (HCC) in up to 40% of patients. In endemic areas, where carrier rates are >5%, most individuals are infected perinatally, by vertical transmission, or in early childhood. In the United States, where prevalence is low except in particular areas and populations (e.g., Alaskan natives, immigrants from highly endemic areas), transmission is generally horizontal, percutaneous, or via sexual contact in adulthood. A variety of host (age at infection, gender, immune status); viral (viral load, genotype, mutation); and external (concurrent viral infections, alcohol consumption, chemotherapy) factors influence disease progression. Several variables (age at infection, gender, ethnicity, immune status) also influence the risk of chronic infection. Perinatal transmission, the most common mode of infection worldwide, can be reduced by appropriate prophylaxis (vaccination of the infant at birth together with hepatitis B immune globulin); anti-viral therapy in late pregnancy may also be beneficial. Five drugs are now FDA-approved for the treatment of HBV (interferon, lamivudine, adefovir, entecavir, and peginterferon alfa-2a), and suppressive anti-viral therapy improves the natural history of HBV. Patients with decompensated cirrhosis or HCC are highly likely to die unless they successfully undergo liver transplantation. While novel anti-viral drugs have improved the management of cirrhosis, strategies to prevent and treat HCC remain inadequate.

Antiviral Agents↗