Virologic and Clinical Expressions of Reciprocal Inhibitory Effect of Hepatitis B, C, and Delta Viruses in Patients With Chronic Hepatitis

Sagnelli, E.; Coppola, Nicola; Scolastico, Carlo; Filippini, Pietro; Santantonio, T.; Stroffolini, Tommaso; Piccinino, F

doi:10.1053/jhep.2000.19288

Cited by 210 publications

(198 citation statements)

References 45 publications

(57 reference statements)

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“…In our previous study, the more severe forms of chronic hepatitis were more frequently found in chronic HBV/HCV concurrent infection than in HBV infection alone or in HCV infection alone. 8 In compliance with this, Zarski 7 and Mohamed et al 29 report higher prevalences of cases with histologically proven liver cirrhosis among patients with chronic HBV/HCV concurrent infection than in those with HCV infection alone.…”

Section: Discussionmentioning

confidence: 86%

HBV superinfection in hepatitis C virus chronic carriers, viral interaction, and clinical course

Sagnelli

Coppola

Messina³

et al. 2002

Hepatology

127

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We enrolled 44 patients with hepatitis B virus (HBV) acute infection, 21 anti-hepatitis C virus (HCV)-positive for at least 1 year (case BC group), 20 anti-HCV-negative (control B group), and 3 with HBV/HCV acute concurrent infection. For each case BC, a subject with chronic HCV infection alone was selected (control C group). At the first observation, 85.7% of patients in case BC group and 85% of those in control B group were HBV-DNA-positive (polymerase chain reaction [PCR]), with a similar trend towards a decrease and negativization in about 20 days; in the case BC group, seroconversion to antibody to hepatitis B e antigen (anti-HBe) was more rapid. HCV-RNA (PCR) was undetectable in all case BC patients but 1, who shortly became negative, whereas 85.7% of subjects in control C group were positive (P < .001). Severe acute hepatitis was more frequent in the case BC group than in the control B group (28.6% vs. 0%, P < .05). Of the 14 patients in the case BC group and of the 16 in the control B group followed up for more than 6 months, 1 in the first and 1 in the second group became hepatitis B surface angiten ( P atients with chronic hepatitis B virus (HBV)/hepatitis C virus (HCV) concurrent infection show a reciprocal inhibition of viral genomes, an association with a severe clinical presentation, and an infrequent response to interferon alfa treatment. 1-10 Instead, very little is known about HBV/HCV acute concurrent infection because only a few case reports are available in the literature. 11,12 Also, little is known about HBV acute infection when it develops in chronic HCV carriers, but the few case reports published on the topic suggest an association with a severe clinical presentation. [13][14][15] Acute HBV infection in chronic HCV carriers may be rather frequent in Italy and in other western countries where drug addicts are numerous, frequently anti-HCVpositive, [16][17][18][19] and infrequently vaccinated against HBV.This article reports the data from our study on the clinical presentation, course of the disease, and HBV/ HCV interaction in 21 HCV chronic carriers who developed HBV acute hepatitis (cases), compared with 20 patients with HBV-related acute hepatitis with no HCV infection (controls) observed in the same period. We also report the data on 3 cases of HBV/HCV acute concurrent infection identified in the same investigation. Patients and MethodsWe enrolled all 44 consecutive patients with HBVrelated acute hepatitis hospitalized in our ward from

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Section: Discussionmentioning

confidence: 86%

HBV superinfection in hepatitis C virus chronic carriers, viral interaction, and clinical course

Sagnelli

Coppola

Messina³

et al. 2002

Hepatology

127

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“…The explanation for this fi nding may be in the fact that patients with occult B infection would be infected with low levels of viral particles incapable of stimulating the immune system to form its antibodies (28) , or that, following acute infection patients present a progressive decline of these markers until their becoming undetectable in the serum (35) . Another hypothesis is the existence of mutating HBV strains which do not express neither antigens nor antibodies in the blood of this population of patients (18,32) .…”

Section: Discussionmentioning

confidence: 99%

Occult hepatitis B virus infection in patients with chronic liver disease due to hepatitis C virus and hepatocellular carcinoma in Brazil

Branco

Mattos

Coral

et al. 2007

Arq. Gastroenterol.

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-Background -The prevalence and consequences of occult HBV infection in patients with chronic liver disease by HCV remain unknown. Aims -To evaluate the prevalence of occult HBV infection in a population of HCV-infected patients with hepatocellular carcinoma. Methods -The serum samples were tested for HBV DNA by nested PCR and liver tissue analysis was carried out using the immunohistochemical technique of 66 HBsAg-negative patients: 26 patients with chronic hepatitis by HCV (group 1), 20 with hepatocellular carcinoma related to chronic infection by HCV (group 2) and 20 with negative viral markers for hepatitis B and C (control group). Results -Occult HBV infection was diagnosed in the liver tissue of 9/46 (19.5%) HCV-infected patients. Prevalence of occult B infection was evaluated in the HCV-infected patients with and without hepatocellular carcinoma, and there were seven (77.7%) of whom from group 2, conferring a 35% prevalence of this group. No serum sample was positive for HBV DNA in the three groups. Conclusion -Occult infection B is frequently detected in liver tissue of HCV-infected patients, especially in cases of hepatocellular carcinoma. However large studies are needed to confi rm that co-infection could determine a worse progress of chronic liver disease in this population.

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“…Coinfection with HBV and HCV is associated with severe forms of liver disease including fulminant hepatitis [8]. Patients with concurrent HBV and HCV infection have a high propensity to progress toward liver cirrhosis and, compared with monoinfected patients, are at an increased risk of developing hepatocellular carcinoma (HCC) [4,[9][10][11][12]. Notably, viral interference is evident between HBV and HCV.…”

Section: Hbv and Hcvmentioning

confidence: 99%

“…Notably, viral interference is evident between HBV and HCV. Mostly, HCV exerts a suppressive effect on HBV and may enhance seroclearance of HBV antigens or even replace the preexisting virus as the agent for continuing hepatitis [4,10,12,13]. As the newcomer, HBV may also suppress the preexisting HCV [4,14].…”

Section: Hbv and Hcvmentioning

confidence: 99%

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Chien

2008

Hepatol Int

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Concurrent hepatitis C virus (HCV), hepatitis delta virus (HDV), or human immunodeficiency virus (HIV) infection with chronic hepatitis B virus (HBV) appears to increase the risk of progressive liver disease including liver cirrhosis and hepatocellular carcinoma. There is a 10% prevalence of HCV infection in chronic HBV or HDV infection. Serological evidence of previous exposure to HBV is found in more than 80% of HIVpositive patients in the high risk group. Notably, the most recently acquired virus tends to suppress the pre-existing virus. In chronic HBV infection acquired perinatally or in early childhood, usually HCV is dominant and may suppress or even displace HBV and HDV. Less frequently, HBV or HDV suppresses HCV. It is generally agreed that the dominant virus should be identified in order to make appropriate treatment decisions. Studies with standard interferon (IFN) to treat patients with HCV dominantly dual HBV/HCV infection have showed only limited virological response. But high dose of IFN has been demonstrated with better response rate. Combined ribavirin with standard or pegylated IFN therapy could achieve a sustained HCV clearance rate comparable with those infected with HCV alone. On the contrary, patients with HBV dominantly dual viral infection might indicate more appropriate addition of lamivudine to IFN than ribavirin. Additionally, patients with concurrent infection of HBV and HDV, IFN seems to be the only effective agent. However, the efficacy of IFN is related to the dose. High dose of IFN [9 MU tiw (thrice per week)] and longer treatment duration (at least 2 years) have been shown to achieve adequate virological response. In patients with concurrently infected HBV and HIV, anti-HBV therapy should be considered for all patients with evidence of liver disease, irrespective of the CD4 cell count. In patients not requiring antiretroviral therapy, HBV therapy should be preferentially based on IFN, adefovir, or telbivudine. In contrast, in patients with CD4 cell counts \350 cells/ll or those already on antiretroviral therapy, agents with double anti-HBV and anti-HIV activity are preferred. At present, the evidence of therapeutic efficacy is not sufficient to make a recommendation in treating patients with dual HBV/HCV or HBV/HDV or HBV/HIV infection. Further studies of the well-designed, larger scale are needed to elucidate the role of different regimens or combination in the treatment of dual viral infection.

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Virologic and Clinical Expressions of Reciprocal Inhibitory Effect of Hepatitis B, C, and Delta Viruses in Patients With Chronic Hepatitis

Cited by 210 publications

References 45 publications

HBV superinfection in hepatitis C virus chronic carriers, viral interaction, and clinical course

HBV superinfection in hepatitis C virus chronic carriers, viral interaction, and clinical course

Occult hepatitis B virus infection in patients with chronic liver disease due to hepatitis C virus and hepatocellular carcinoma in Brazil

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

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