Viral replication in patients with concomitant hepatitis B and C virus infections

Crespo, Javier; Lozano, Juanita; Carte, Beatriz; Heras, Begoña de las; Cruz, Fernando de la; Pons‐Romero, F.

doi:10.1007/bf02471908

Cited by 50 publications

(42 citation statements)

References 45 publications

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“…Negative samples were confirmed qualitatively by polymerase chain reaction (PCR) with nested primers directed at the surface and precore/core gene regions of HBV as previously described. 19,20 …”

Section: Serologic Testingmentioning

confidence: 99%

Liver transplantation with allografts from hepatitis B core antibody-positive donors: A new approach

Fábrega

García-Suárez

Guerra

et al. 2003

Liver Transplantation

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The enduring shortfall of organ donors has inspired the widespread utilization of hepatic allografts from donors with hepatitis B core antibodies in spite of the potential risk of transmitting hepatitis B virus (HBV) infection to the recipient. Here we report a protocol of naive recipients receiving livers from hepatitis B core antibody-positive donors. From November, 1999 to March, 2002, 77 liver transplantations were performed in 73 patients at our institution, 7 of whom received livers from hepatitis B core antibody-positive donors. All recipients received 10,000 U/d of intravenous HBIg for 7 days and 100 mg /d of lamivudine until we could obtain the HBV-DNA from the donor samples (serum and liver tissue). If the results of the HBV-DNA from the donor samples were positive, the patient would continue with prophylaxis and if they were negative we would finish the combined prophylaxis. After transplantation, HBV serologic markers and HBV-DNA by polymerase chain reaction (PCR) in serum and lymphocytes were tested in the recipients on the seventh, fifteenth, thirtieth, and ninetieth days as well as every 3 months after transplantation. All seven donor organs were negative for HBV-DNA in serum and liver tissue. Thus, we stopped the combined prophylaxis in all recipients (range, 7 to 10 days). None of the 7 patients developed de novo HBV infection over the 3-year study period (range, 9 to 36 months). Our approach is reasonably safe, and it appears to be very effective in the prevention of de novo HBV infection after liver transplantation. (Liver Transpl 2003;9:916-920.) D e novo hepatitis B virus (HBV) after orthotopic liver transplantation (OLT) has been reported in recipients negative for hepatitis B surface antigen (HBsAg) from hepatitis B core antibody (anti-HBc)-positive donors. Several studies have reported a 16.6% to 95% increased incidence for HBV infection in these patients. 1-12 As a result, many centers do not use antiHBc-positive donors for recipients without previous HBV infection. 11 These results were derived mostly from studies performed in geographic regions with a low prevalence (3% to 5%) of anti-HBc-positive liver donors. However, in a recent study, anti-HBc positivity was found in 10% of the Spanish adults in the 26 to 65 age range and in 27% of donors older than 60. 2 For this reason, the prevalence of anti-HBc positivity in Spanish liver donors and, thus, the incidence of de novo HBV infection after liver transplantation would be greater in our area than in areas of lower prevalence.In an attempt to prevent transmission of HBV infection to recipients from donors positive for anti-HBc, polyclonal hepatitis B immunoglobulin (HBIg) has been administered to the recipients almost universally. Many centers use HBIg either continuously or for an indefinite amount of time, usually 2 or more years after OLT. 10 Recent studies have suggested that lamivudine, a nucleoside analog that inhibits HBV replication, can be used in addition to or as an alternative to HBIg in such cases. [13][14][15] However, thi...

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Section: Serologic Testingmentioning

confidence: 99%

Liver transplantation with allografts from hepatitis B core antibody-positive donors: A new approach

Fábrega

García-Suárez

Guerra

et al. 2003

Liver Transplantation

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“…22,23 Elevated expression has also been reported in hepatitis B virus-related cirrhosis. 24 In addition, intrahepatic lymphocytes express FasL and show FasL-dependent cytolytic activity in patients with chronic hepatitis C. 21 However, little information was obtained about the role of the Fas system in the pathogenesis of recurrent HCV liver disease in patients who underwent OLT for HCV-related cirrhosis.…”

Section: H Epatitis C Virus (Hcv)-related Cirrhosis Currentlymentioning

confidence: 99%

“…3,24 The linear range of quantitative PCV ranges from 10 4 to 10 10 RNA molecules/mL (4 to 10 logs HCV RNA/mL) by comparisons with end point dilution analysis. Genotyping of HCV was performed by PCV amplification; amplified DNA and complementary DNA sequences were detected by an EIA procedure.…”

Section: Hcv Rna Studymentioning

confidence: 99%

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Involvement of the Fas System in Hepatitis C Virus Recurrence After Liver Transplantation

Crespo¹

2000

Liver Transplantation

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To date, there have been no reports of the involvement of the Fas system in recurrent hepatitis C virus (HCV) infection after orthotopic liver transplantation (OLT). In 25 patients who underwent OLT for HCV-related liver cirrhosis, we evaluated the expression of the Fas antigen (FasAg) on hepatocytes, apoptic hepatocytes, and serum levels of soluble Fas (sFas). The level of HCV viremia and HCV genotype were determined by polymerase chain reaction. Serum sFas levels were determined by an enzyme immunoassay procedure. DNA fragmentation was determined by the terminal deoxynucleotidyl transferasemediated deoxyuridine triphosphate nick end-labeling (TUNEL) technique on deparaffinized liver samples. FasAg expression was evaluated by an immunoperoxidase method. Sixteen patients had evidence of recurrent HCV disease. The number of hepatocytes expressing FasAg and the percentage of apoptotic hepatocytes was greater among patients who developed recurrent hepatitis than among those who did not (P < .01 and P < .0001, respectively). There was a correlation between hepatic expression of FasAg, intensity of lobular inflammation (P ‫؍‬ .007), and TUNEL index (P < .001). The levels of sFas were greater among the patients with recurrent HCV hepatitis than those without recurrent hepatitis (P < .04). We conclude that (1) Fas expression is up-regulated in recurrent HCV after OLT and is related to the grading of liver disease; likewise, levels of sFas were greater in the patients with recurrent HCV hepatitis; and (2) the demonstration of hepatocytes with FasAg expression and the labeling of the nuclei by TUNEL assay suggest that hepatic apoptosis mediated by the Fas system may have a role in the pathogenesis of recurrent HCV hepatitis after OLT. (Liver Transpl 2000;6:562-569.) H epatitis C virus (HCV)-related cirrhosis currently accounts for approximately 25% to 40% of the indications for orthotopic liver transplantation (OLT). 1,2 Despite the nearly universal recurrence of HCV viremia, the degree to which recurrent hepatitis is recognized histologically varies markedly. [3][4][5][6] Factors that determine the frequency and severity of the disease have not been clearly identified, but a number of interrelated variables are probable, including level of HCV viremia, HCV genotype, and degree and type of immunosuppression. 2,3-6,7-9 However, the mechanism of liver cell damage in the patients with recurrent HCV liver disease is unknown.The apoptotic process, or programmed cell death, can be induced by stimuli of the so-called death receptors, such as the tumor necrosis factor (TNF) receptor-1, DR-3, DR-4, or Fas (APO-1, CD95). The Fas receptor or Fas antigen (FasAg) is a 45-kd cell-surface type 1 plasma membrane protein expressed in lymphoid and many other tissues. The receptor is activated through oligomerization on binding of its ligand (FasL) to its extracellular domain, and the apoptotic signal is transduced through the so-called death domain. [10][11][12] FasAg is one of the best-identified cell-surface molecules that mediate exter...

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“…15,16 If the amplification product of surface gene was not visible on the ethidium bromide-stained agarose gel after the first PCR, the serum samples were amplified in a nested PCR. The sensitivity of this PCR assay was evaluated using serial dilutions of recombinant entire HBV DNA as template.…”

Section: Polymerase Chain Reaction and Direct Sequencing Of Hbv Dnamentioning

confidence: 99%

Severe clinical course of de novo hepatitis B infection after liver transplantation

et al. 1999

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The aim of this study is to determine the origin, clinical outcome, allograft histological characteristics, and virological outcome of de novo hepatitis B virus (HBV) infection after orthotopic liver transplantation (OLT). We studied 136 hepatitis B surface antigen (HBsAg)-negative liver transplant recipients. HBV DNA was detected by dot-blot hybridization and polymerase chain reaction (PCR). The S gene was sequenced. Hepatitis C virus (HCV) RNA was assessed by PCR. The long-term clinical and histological outcome was determined. Six of 136 HBsAg-negative patients (4.4%) became HBsAg positive after transplantation. The source of HBV infection was reactivation of latent HBV infection in 2 patients and was not identified in 4 patients. Two donors had isolated core antibody. Two of these 6 patients developed acute liver failure related to hepatitis B. The 4 other patients had severe chronic hepatitis related to hepatitis B. All patients had high-level HBV replication. No significant mutations in the S gene were found. These data suggest that de novo hepatitis B infection is not a mild disease and might represent a significant cause of graft dysfunction. This is the first report of fulminant hepatitis caused by de novo hepatitis B infection after OLT.

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Viral replication in patients with concomitant hepatitis B and C virus infections

Cited by 50 publications

References 45 publications

Liver transplantation with allografts from hepatitis B core antibody-positive donors: A new approach

Liver transplantation with allografts from hepatitis B core antibody-positive donors: A new approach

Involvement of the Fas System in Hepatitis C Virus Recurrence After Liver Transplantation

Severe clinical course of de novo hepatitis B infection after liver transplantation

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