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16th International HIV Drug Resistance Workshop12-16 June 2007, Barbados |
DOES TREATMENT OF HEPATITIS B VIRUS REDUCE HEPATITIS DELTA VIRAEMIA IN HIV CO-INFECTED PATIENTS?
Antivir Ther. 2007; 12:S39 (abstract no. 34)
J Sheldon, B Ramos, P Ríos, J Martínez-Alarcón, C Toro and V Soriano
Department of Infectious Diseases, Hospital Carlos III, Madrid, Spain
BACKGROUND: Studies have shown a more severe course of Delta hepatitis in HIV-positive patients. Treatment of chronic hepatitis Delta virus (HDV) infection is currently limited to intensive interferon-a therapy. However, the role of nucleos(t)ide analogues against chronic HDV infection (particularly using drugs other than lamivudine) has not been well examined. The aim of this study was to quantify and compare the HDV and HBV viral loads, and hepatic biochemical and serological markers in chronic HDV patients coinfected with HIV undergoing anti-HBV antiviral treatment.
METHODS: A longitudinal study was carried out in all HIV-positive patients chronically infected with HBV and HDV whom attended our hospital. Serum HBV DNA for each patient was longitudinally determined using Cobas HBV Taqman PCR (Roche, LLD 10 cop/ml), and serum HDV RNA was quantified using an in-house, real-time PCR assay (LLD, 100 cop/ml) at yearly intervals. Treatment regimens, plasma HIV RNA, CD4 counts, ALT/AST levels and HCV infection were also assessed. All statistical analyses were made using SPSS v12.
RESULTS: A total of 15 HIV+ patients with chronic hepatitis Delta were identified. Median follow-up was 6 years. All had detectable serum HDV RNA before receiving any anti-HBV treatment (mean: 6.1 log10 cop/ml). A statistical significant correlation between HBV and HDV viral load was found (r=0.32, P=0.006). Anti- HBV drugs used were lamivudine (n=14), tenofovir (n=9) and/or emtricitabine (n=4).
Overall, 11 patients showed good response to anti-HBV therapy with achievement of undetectable HBV DNA. Moreover, all of them showed a statistically significant decrease (mean: 2 log10 cop/ml) in plasma HDV RNA (P=0.0004). In fact, three of these patients achieved undetectable HDV RNA (<100 cop/ml) after a mean of 5.6 years of HBV antiviral therapy. However, six patients with detectable HBV DNA due to either removal of anti-HBV treatment or selection of drug resistance showed a significant rebound in serum HDV RNA (P=0.0004).
CONCLUSION: In patients undergoing successful anti- HBV antiviral therapy there is an indirect benefit suppressing Delta virus replication, albeit not very efficient. Hypothetically, a significant and sustained reduction in serum HDV RNA may only be seen when a reduction in HBV cccDNA is achieved, which may require long periods of successful anti-HBV therapy. In our knowledge, this is the first evidence of benefit of potent anti-HBV nucleos(t)ide analogue therapy in chronic Delta hepatitis.
2007-06-12
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