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PubMed1999

Antiviral treatment for human immunodeficiency virus patients co-infected with hepatitis B virus: combined effect for both infections, an obtainable goal?

A large percentage of human immunodeficiency virus (HIV) patients have serological evidence of a past or present hepatitis B virus infection (HBV). Long-term survival is increasing for HIV patients because of highly active antiretroviral therapy. Therefore, the chronic hepatitis B infection may become an important determinant of disease outcome in these co-infected patients. We describe two HIV/HBV co-infected patients who were treated with extended antiviral therapy, initially indicated for the HIV infection. Lamivudine, a suppressor of viral replication in both infections, was one of these antiviral drugs. One patient showed a severe rebound of the HBV after withdrawal of lamivudine, the other patient developed a mutant hepatitis B virus after 18 months of treatment. This mutation was exclusively induced by lamivudine. These patients show that, with improved HIV-related survival, the HBV infection should be monitored carefully, thereby enabling the physician to interfere with therapy when necessary.

Anti-HIV Agents↗

PubMed1982

Seroepidemiology of infection with hepatitis B virus in Fiji.

A batch of 984 sera obtained from a stratified sample of Melanesians and Indians living in rural and urban areas of Fiji in 1981 were for hepatitis B surface antigen (HBsAg) and antibody to hepatitis B core antigen (anti-HBc) by solid phase radioimmunoassay. The prevalence of hepatitis B infection (as measured by the sum of HBsAg and anti-HBc frequencies of HBsAg negative sera in the two groups) was 81.5% and 17.9%, respectively. No major differences were detected between urban and rural populations. While hepatitis B virus is endemic in Melanesians and Indians, the epidemiology of the infection shows certain differences. Among Melanesians, infection appears to be acquired early in life and peak prevalence of serologic markers of infection occurs during the second decade. Among the Indian population, the prevalence of markers increases steadily with age, presumably as a result of continuous exposure and infection throughout life. the high prevalence of infection and carriers among Melanesians is consistent with previous observations among Pacific populations. The lower prevalence of infection among Indians is remarkable, since they constitute almost half of the total population and live under similar conditions. Since the two populations remain largely separate in terms of housing and schooling, and intermarriage is uncommon, it is no possible to determine whether these differences merely represent different degrees of exposure to the virus or are the reflection of differences in susceptibility or response to infection.

Adult↗

PubMed1999

Interferon gene transfer by a hepatitis B virus vector efficiently suppresses wild-type virus infection.

Hepatitis B viruses specifically target the liver, where they efficiently infect quiescent hepatocytes. Here we show that human and avian hepatitis B viruses can be converted into vectors for liver-directed gene transfer. These vectors allow hepatocyte-specific expression of a green fluorescent protein in vitro and in vivo. Moreover, when used to transduce a type I interferon gene, expression of interferon efficiently suppresses wild-type virus replication in the duck model of hepatitis B virus infection. These data suggest local cytokine production after hepatitis-B-virus-mediated gene transfer as a promising concept for the treatment of acquired liver diseases, including chronic hepatitis B.

Animals↗

PubMed1991

Remission of hepatitis B-associated membranous glomerulonephritis in human immunodeficiency virus infection.

Hepatitis B virus (HBV) infection has been associated with several renal diseases, the most common being membranous glomerulonephritis (MGN). The role of concurrent human immunodeficiency virus (HIV) infection in affecting the course of the renal involvement is largely unknown. We report the case of a HIV-infected adult male with chronic HBV-associated MGN who had complete remission of the nephrotic syndrome associated with spontaneous seroconversion from hepatitis B e antigen (HBeAg)-positive to HBeAg-negative. The present case illustrates that HIV infection does not preclude improvement of chronic HBV infection or an associated membranous nephropathy. Such improvement may be dependent on the ability of the host immune system to clear HBeAg.

Adult↗

PubMed1997

Detection of type 2-like T-helper cells in hepatitis C virus infection: implications for hepatitis C virus chronicity.

One striking clinical feature of hepatitis C virus (HCV) infection is that more than 50% of patients with acute hepatitis C will develop chronic infection. To investigate its possible mechanisms, we examined the activation of type 2-like T-helper (Th2-like) cells relating to the development of chronicity. Peripheral blood CD4+ T-cell proliferation and cytokine secretion in response to a panel of recombinant HCV antigens including core (C22), envelope 1 (E1), E2, nonstructural (NS) protein 4 (C100), fusion protein of NS3 and NS4 (C200), and NS5 were assayed in 17 patients with acute hepatitis C. All six patients with self-limited disease had a significant CD4+ T-cell proliferation to C22, E1, C100, C200, and NS5, running parallel with the antigen-stimulated secretion of interleukin (IL)-2 and interferon gamma (IFN-gamma), but not with interleukin (IL)-4 and IL-10, indicating predominant Th1 responses. Among the remaining 11 patients who developed chronicity, 6, 2, and 9 cases showed a specific CD4+ T-cell response to C22, C100, and C200, respectively, and the responses were significantly lower than those of cases with recovery in terms of stimulation index (SI) (P < .05) and of antigen-stimulated IL-2 and IFN-gamma production. Importantly, IL-4 and IL-10 (Th2 responses) were detectable, and C22-specific Th2-like T-cell clones could be generated from patients with chronicity. The data suggested that activation of Th2 responses in acute hepatitis C patients may play a role in the development of chronicity.

Adult↗

PubMed2001

Impaired allostimulatory function of dendritic cells in chronic hepatitis C infection.

BACKGROUND & AIMS: Dendritic cells (DC), which play an essential role in the triggering of primary antiviral immune reactions, may also contribute, in some viral models, to the propagation of viral infection and the pathogenesis of viral disease. During natural infection with hepatitis C virus (HCV), the interactions between the virus and DC may contribute to viral persistence, a general feature of HCV infection. METHODS: We compared the phenotypical and biological functions of monocyte-derived DC from patients with chronic hepatitis C (HCV-DC; n = 6), seronegative individuals (naive-DC; n = 8), long-term responders to antiviral therapy (LTR-DC; n = 8), and a group of patients with non-HCV-hepatic disorders (n = 11). The presence and the nature of HCV sequences during the DC cultures was assessed by reverse transcription-polymerase chain reaction and the analysis of the viral quasispecies distribution. RESULTS: Although HCV-DC displayed a normal morphology, phenotype, and capacity to capture antigen, their ability to stimulate the proliferation of allogeneic T cells was dramatically impaired in comparison with naive-DC (P = 0.0013). Mixing experiments revealed that HCV-DC did not affect the proliferation of T cells induced by naive-DC. Remarkably, the allostimulatory function of LTR-DC or DC from patients with non-HCV-hepatic disorders did not show any impairment. The presence of HCV genomic sequences could be documented for 5 of 6 HCV carriers either in the cells and/or the supernatants of the DC cultures. The presence of HCV sequences was found in the DC cultures from one patient showing a dramatic allostimulation defect. For that patient, extensive analysis of the viral quasispecies distribution revealed the presence, in the DC cultures, of genomic sequences of a unique nature, distinct from those identified in the patient's mononuclear cells, serum, or liver. CONCLUSIONS: Overall, these results indicate that chronic infection by HCV is associated with an allostimulatory defect of monocyte-derived DC, possibly because these cells constitute an extrahepatic reservoir for the virus. Although the exact mechanism responsible for such an alteration remains to be unraveled, our observations argue against an active immunosuppression-based mechanism.

Adenovirus E2 Proteins↗

PubMed1987

Cellular changes associated with persistent hepatitis A infection in vitro.

The rate of division, morphology and ultrastructure of BSC-1 cells, persistently infected with hepatitis A virus (HAV), were compared with uninfected cells for 60 days after splitting of the cells. Both control and infected cells showed a biphasic growth pattern marked firstly by increasing cell density and high mitotic rate (exponential phase) and then high constant cell density and little mitosis (stationary phase). Immunoperoxidase studies showed that hepatitis A antigen (HAAg) appeared as cytoplasmic granules approximately one third of the way through the exponential phase in infected cells. The percentage of cells with HAAg rose until the early stationary phase when virtually all cells contained antigen. Radioimmunoassay demonstrated an increase in HAAg per cell in the stationary phase. Radioimmunofocus assay and immune electron microscopy confirmed the presence of HAV in infected cells in the stationary phase. Thin sectioning electron microscopy showed cytoplasmic annulate lamellae in infected cells of both phases but not in control cells.

Animals↗

PubMed2007

Comparative study between occult hepatitis C virus infection and chronic hepatitis C.

We have recently described the presence of occult hepatitis C virus (HCV) infection (HCV-RNA in liver in the absence of anti-HCV and serum HCV-RNA) in patients with persistently abnormal liver function tests of unknown aetiology. The aim of this study was to compare the characteristics of patients with occult HCV infection vs those of patients with chronic hepatitis C. We compared clinical features of 68 patients with occult HCV infection and 69 untreated chronic HCV patients (anti-HCV and serum HCV-RNA positive), matched for age, gender, duration of abnormal liver function tests and body mass index. Aspartate aminotransferase and alanine aminotransferase were higher (P < 0.001) in chronic HCV, but cholesterol and triglycerides were significantly higher in patients with occult HCV infection (P < 0.001 and P = 0.002). Chronic HCV patients had higher gamma-globulin (P = 0.005), alpha-foetoprotein (P < 0.001) and iron (P < 0.001) levels. Percentage of patients with necroinflammatory activity and fibrosis was higher (P < 0.001) in chronic HCV than in occult HCV infection. Mean percentage of infected hepatocytes was higher (P = 0.001) in chronic HCV (10.1%) than in occult HCV infection (5.3%). This occult HCV infection is a milder disease than chronic HCV, and this could be related to the significantly lower number of infected hepatocytes observed in occult HCV.

Adult↗

PubMedDate not supplied

Peginterferon alpha/ribavirin combination therapy for the treatment of hepatitis C infection.

Chronic infection with the hepatitis C virus is widespread in the United States. This disease is associated with a progression of fibrosis of the liver leading to liver cirrhosis in as many as 20% of cases. The current standard of care for the treatment of chronic hepatitis C infection is combination therapy with pegylated interferon alpha plus ribavirin. In more than 50% of patients, this regimen has been shown to induce a sustained viral response, defined as undetectable hepatitis C viral ribonucleic acid (RNA) for 6 months after the end of treatment. Typically, patients are treated for 24 or 48 weeks. A number of possible adverse events are associated with combination therapy, and patient empowerment through supportive nursing care is critical to facilitating patient adherence to treatment. This article provides an update on information concerning the diagnosis and treatment of chronic hepatitis C infection. This information can be tailored to provide patient-focused assessment, education, and treatment.

Antiviral Agents↗

PubMed2004

Synergic effect of chronic hepatitis C infection and beta thalassemia major with marked hepatic iron overload on liver fibrosis: a retrospective cross-sectional study.

BACKGROUND: Increased hepatic iron is assumed to potentiate progression towards liver fibrosis in chronic hepatitis C virus (HCV) infection. In this study we have evaluated the potentiating effect of marked hepatic iron overload and chronic HCV infection on hepatic fibrosis in thalassemic patients. METHODS: Liver biopsies of one group of patients with beta thalassemia major and chronic HCV infection (group 1) was compared with two groups of patients (groups 2&3) with either chronic HCV infection or thalassemia major, respectively (20 patients in each group). Necroinflammation, fibrosis, and iron overload were graded and compared. RESULTS: Stage of fibrosis in group 1 patients was significantly higher than the other two groups (p < 0.05). Necroinflammatory grade was significantly lower, but iron score was significantly higher in thalassemic patients (group 3) in comparison to groups 1 and 2 (p < 0.05). CONCLUSION: Our results indicate that marked liver iron overload and HCV infection in thalassemic patients have potentiating effect on hepatic fibrogenesis.

Adolescent↗

PubMed2001

Long-term clinical impact of occult hepatitis B virus infection in chronic hepatitis B patients.

BACKGROUND/AIMS: Long-term clinical outcomes of occult hepatitis B virus (HBV) infection were studied. METHODS: Fifteen chronic hepatitis B patients were monitored for a median of 4.4 years (range 0.9-15.3) after hepatitis B surface antigen (HBsAg) seroclearance. Serum HBV DNA was measured by real-time detection polymerase chain reaction. Thirteen patients underwent liver biopsies at the end of follow-up and liver histology was evaluated by Ishak score. Liver HBV DNA was also measured for 12 patients. RESULTS: At the end of follow-up, HBV viremia was absent in 13 (87%) patients, and antibody titers to hepatitis B core antigen showed an inverse correlation with time from HBsAg seroclearance (r=-0.554; P=0.0040). However, all patients retained liver HBV DNA and tested positive for the covalently closed circular HBV DNA replicative intermediate. The hepatic HBV DNA loads had no relation to liver histology. Paired biopsies from 11 patients disclosed that each necroinflammatory score significantly improved after HBsAg seroclearance. Amelioration of liver fibrosis was also evident in eight (73%) patients (P=0.0391 by signed rank test). CONCLUSIONS: A long-standing but strongly suppressed HBV infection may confer histological amelioration after HBsAg seroclearance.

Adult↗

PubMed2006

Effects on gene expression and viral load of a medicinal extract from Agaricus blazei in patients with chronic hepatitis C infection.

Extracts from the mushroom Agaricus blazei Murill (AbM) are used extensively as a non-prescription remedy against cancer and infections, including hepatitis. We previously demonstrated a potent immunomodulating effect of a particular preparation on monocytes in vitro, and a protective effect on bacterial infections in mice. Here we report the effect on gene expression in peripheral blood cells from four chronic hepatitis C patients, using global (29 k) oligo-based, single channel microarrays. The viral load was slightly, but not significantly, decreased after 1 week of AbM treatment. The cytokine genes most strongly induced in vitro were not induced in vivo. The more notable changes in mRNA levels were related to genes involved in the G-protein coupled receptor signalling pathway, in cell cycling, and in transcriptional regulation. The results suggest that the beta-glucans of the extract, which presumably are responsible for cytokine induction, did not readily enter the blood, while other components, such as substances proposed to have anticancer effects, were active in the blood.

Administration, Oral↗

PubMed2006

Treating hepatitis C infection in liver transplant recipients.

Chronic infection with hepatitis C virus (HCV) is a growing problem worldwide, with up to 300 million individuals infected, and those with chronic infection are at risk for cirrhosis and hepatocellular carcinoma. HCV infection is the most common indication for liver transplantation in the United States and Europe. Unfortunately, although transplantation is effective for treating decompensated cirrhosis and limited hepatocellular carcinoma associated with hepatitis C, HCV reinfection is virtually the rule among transplant recipients. Reinfection of the graft is associated with more rapidly progressive disease, with a median time to cirrhosis of 8 to 10 yr. Unfortunately, treatment of chronic HCV in liver transplant recipients is suboptimal. Combination therapy with interferon (pegylated and nonpegylated forms) plus ribavirin appears to provide maximum benefits. Drug therapy is usually administered for recurrent disease. No prophylactic therapy is available. Preemptive regimens offer no distinctive advantages over treatments begun for recurrent disease. Overall, treatment is poorly tolerated, with frequent need for dose reductions, especially from cytopenias, and drug discontinuations in up to 50% of patients. Optimizing drug doses is important in maximizing sustained virological response rates. Future therapies may include ribavirin alternatives with lower rates of anemia, alternative interferons with lower rates of cytopenias, and new antiviral drugs that can be used alone or in combination with either interferon or ribavirin to enhance sustained virological response rates and improve tolerability. Liver Transpl 12:1192-1204, 2006. (c) 2006 AASLD.

Antiviral Agents↗

PubMed1978

Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage.

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.

Carrier State↗

PubMed1995

Glomerulonephritis in renal allografts associated with hepatitis C infection: a possible relationship with transplant glomerulopathy in two cases.

Chronic infection with hepatitis C virus (HCV) has been identified as a cause of type I membranoproliferative glomerulonephritis (MPGN). HCV infection is common in patients with end-stage renal disease and may persist in renal allograft recipients. MPGN in the allograft may therefore be a manifestation of persistent HCV infection. We report two cases of glomerulopathy with features of both MPGN and transplant glomerulopathy in renal transplant patients chronically infected with HCV. We discuss the course of interferon alfa therapy in both patients as well as a possible relationship of HCV infection with transplant glomerulopathy.

Chronic Disease↗

PubMed2006

Assessment of peripheral DNA damage by alkaline comet assay in maintenance hemodialysis subjects with hepatitis C infection.

Despite the high prevalence of hepatitis C infection among hemodialysis subjects, there is no information concerning the DNA damage of hepatitis C (+) hemodialysis subjects. We aimed to find out if there is any additional effect of hepatitis C infection on peripheral DNA damage in maintenance hemodialysis subjects. Fifteen hepatitis C (+) and 22 hepatitis C (-) hemodialysis subjects, 21 hepatitis C subjects without renal disease, and 22 healthy controls were enrolled. Peripheral DNA damage was assayed using alkaline comet assay. Median DNA damage levels of the study groups were as follows: hepatitis C (+) maintenance hemodialysis subjects, 88 (0-232); hepatitis C (-) maintenance hemodialysis subjects, 58 (0-228); hepatitis C (+) subjects without renal disease, 112 (44-252); controls, 26 (0-72). DNA damage level was significantly higher among hepatitis C (+) subjects without renal disease than hepatitis C (-) maintenance hemodialysis subjects and healthy controls (both p<0.05/6). Both maintenance hemodialysis subjects with and without HCV infection had significantly higher DNA damage level than healthy controls (both p<0.05/6). DNA damage level was comparable between hepatitis C (+) subjects without renal disease and HCV (+) hemodialysis subjects, and between hemodialysis subjects with and without hepatitis C infection (all p>0.05/6). Linear regression analysis revealed that hepatitis C infection was the only independent factor in predicting the peripheral DNA damage (p<0.05, beta=0.395). Each one of end-stage renal disease and hepatitis C infection significantly increases DNA damage level. However, in hemodialysis subjects, hepatitis C infection does not cause significant additional increase in DNA damage level, and it may be partly due to protective effect of hemodialysis on hepatitis C infection.

Adult↗

PubMed1997

The clinical course of transplantation-associated de novo hepatitis B infection in the liver transplant recipient.

Transmission of hepatitis B infection from hepatitis B surface antigen (HBsAg)-negative antibody to hepatitis B core (anti-HBc)-positive liver donors has been previously described. The long-term outcome of these transplant-associated de novo hepatitis B patients has not been well described and may affect future use of donor organs that are anti-HBc-positive. We describe the experience in our first 332 transplants, performed before exclusion of anti-HBc-positive liver donors. Nine of these 332 (3%) donors were anti-HBc positive. Three of these 9 (33%) recipients developed transplant-associated de novo hepatitis B infections compared with only 2 of 323 (0.5%) recipients who received anti-HBc-negative donor livers (P = .00014). Of our 9 recipients of anti-HBc-positive livers, 6 (67%) are alive, and no deaths or allograft failures have been related to complications of hepatitis B. Only 1 of 5 patients (20%) with de novo hepatitis B has developed significant graft dysfunction with an average follow-up of more than 7 years (range 63-124 months). The 1 recipient with allograft dysfunction related to de novo hepatitis B has significantly elevated viremia levels (average HBV DNA 460 pg/mL) compared with the other de novo hepatitis B recipients (average HBV DNA 23-58 pg/mL). In summary, anti-HBc-positive donors are more likely to transmit hepatitis B infections to recipients, but these de novo infections usually have a mild clinical course and do not seem to adversely affect long-term patient survival. Hepatitis B-related allograft dysfunction, when it occurs, is associated with higher levels of viral replication. With our current donor shortage, perhaps anti-HBc-positive donors could be used in very selected recipient populations.

Biopsy↗

PubMed1995

Epidemiology and natural history of hepatitis C infections in liver transplant recipients.

Hepatitis C infection is common in patients undergoing liver transplantation. Few studies have focused on the prevalence and epidemiology of hepatitis C infection among liver transplant recipients since the implementation of donor screening for antibodies against the hepatitis C virus (anti-HCV). Using reverse transcription-polymerase chain reaction (RT-PCR) and genomic sequencing methods, we sought to determine the prevalence, epidemiology, and natural history of hepatitis C infections among 44 consecutive liver transplant patients between January and December 1991. All patients and donors were screened for antibodies against HCV with a first-generation test. Laboratory tests and liver biopsies were routinely done 12 months after transplantation. Serum samples from all organ donors and transplant recipients were analyzed for the presence of HCV-RNA. From four of the six HCV-RNA-positive patients, pre- and post-transplant serum samples were available for sequence analysis. No donor had detectable HCV-RNA. Six of 44 (13.6%) patients had detectable HCV-RNA before and after liver transplantation. Recurrent infection was documented in all who were infected before transplantation and was confirmed by genotype analysis in the four patients who were analyzed. No acquired infections were identified. After transplantation, the HCV-RNA-positive recipients had higher mean alanine aminotransferase (207 +/- 85 U/l vs 37 +/- 7 U/l; p < 0.0001) and were more likely to have chronic hepatitis (50% vs 6%; p < 0.03) than the HCV-RNA-negative recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗