Mutations of the core promoter and response to interferon treatment in chronic replicative hepatitis B

Erhardt, Andreas; Reineke, Ulf; Blondin, D.; Gerlich, W.H.; Adams, Ortwin; Heintges, Tobias; Niederau, C.; Häussinger, Dieter

doi:10.1016/s0168-8278(00)80468-7

Cited by 52 publications

(53 citation statements)

References 37 publications

(51 reference statements)

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“…[23][24][25][26][27][28][29][30] Various mutations at nt 1753 and nt 1754, which confer the ability to secrete enveloped particles irrespective of the presence of core promoter mutations (A1762T/G1764A) and enhance HBV replication, were found more frequently in FH than in AH. 31,32 T1753A/C and/or T1754C/ G mutations, which were accompanied by the double mutations of A1762T and G1764A in 57% of the patients in this study, occurred signifi cantly more frequently in patients with FH than in those with AH or SAH.…”

Section: Discussionmentioning

confidence: 99%

Initial load of hepatitis B virus (HBV), its changing profile, and precore/core promoter mutations correlate with the severity and outcome of acute HBV infection

et al. 2007

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Section: Discussionmentioning

confidence: 99%

Initial load of hepatitis B virus (HBV), its changing profile, and precore/core promoter mutations correlate with the severity and outcome of acute HBV infection

et al. 2007

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“…Since B and C are the predominant genotypes reported from Asian countries, these studies are restricted to comparison of patients with these two genotypes. Genotypes A and D have been reported from Western Europe and North America [15][16][17], the Mediterranean region [18], the Middle East [19], and Central Asia [20], among which genotype D is dominant. Limited data from India [21][22][23] suggest that genotypes A and D are most prevalent but their relationship to disease severity is not known.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Hepatitis B Virus Genotype D in Precore Mutants Among Chronic Liver Disease Patients from New Delhi, India

et al. 2007

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Hepatitis B is one of the most important causes of chronic viral hepatitis world wide. Mutations in the precore region of the hepatitis B virus (HBV) genome are frequently found in hepatitis B envelope antigen-negative cases. Data from India on the HBV genotype-associated distribution of precore mutations are limited. Our objective in this study was to genotype and detect the precore mutant with a point mutation from G to A at nucleotide 1896 using ligase chain reaction (LCR) and direct sequencing. A total of 115 cases of chronic liver disease were screened. The cases were evaluated on the basis of history, clinical examination, liver function profile, and serological test for HBV infection, which includes HBsAg, anti HBcIgG, HBeAg using commercially available ELISA kits. The cases, which were HBeAg+, HBeAg-, and HBV DNA+, were subjected to LCR and confirmed by direct sequencing. Of 115 chronic liver disease cases, 50 (43.5%) cases were HBV DNA positive. All cases were subjected to LCR; 11 (22%) cases confirmed the presence of precore mutants, while the remaining 39 (78%) were classified as the wild form of the virus. HBV genotyping by direct sequencing revealed that genotype D was predominant in both wild and mutant forms of the virus. We conclude that the HBV genotype distribution was not significantly different between precore mutants and the wild form of the virus (P>0.05). North Indian patients with genotype D were more likely to have persistent HBV infection with precore mutants. HBV genotypes correlate with the clinical outcome of chronic HBV infection.

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“…The level of sensitivity of HBV to IFN-α may be genotypespecific, with genotypes C and D more resistant than genotypes A and B. (26,54,55). Other factors that improve the chances of a good therapeutic response are (i) high serum ALT levels, (ii) no cirrhosis, (iii) no co-infection with HIV or hepatitis D virus (HDV), and (iv) age (56,57).…”

Section: Interferon Alpha (Ifn-α)mentioning

confidence: 99%

Drug Delivery Systems and Liver Targeting for the Improved Pharmacotherapy of the Hepatitis B Virus (HBV) Infection

et al. 2010

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In spite of the progress made in vaccine and antiviral therapy development, hepatitis B virus (HBV) infection is still the most common cause of liver cirrhosis and hepatocellular carcinoma, with more than 400 million people chronically infected worldwide. Antiviral therapy with nucleos(t)ide analogues and/or immunomodulating peptides is the only option to control and prevent the progression of the disease in chronic hepatitis B (CHB)-infected patients. So far, the current antiviral monotherapy remains unsatisfactory because of the low efficacy and the development of drug resistance mutants. Moreover, viral rebound is frequently observed following therapy cessation, since covalent closed circular DNA (cccDNA) is not removed from hepatocytes by antiviral therapy. First, this review describes the current pharmacotherapy for the management of CHB and the new drug candidates being investigated. Then, the challenges in the development of drug delivery systems for the targeting of antiviral drugs to the liver parenchyma are discussed. Finally, perspectives in the design of a more efficient pharmacotherapy to eradicate the virus from the host are addressed.

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Mutations of the core promoter and response to interferon treatment in chronic replicative hepatitis B

Cited by 52 publications

References 37 publications

Initial load of hepatitis B virus (HBV), its changing profile, and precore/core promoter mutations correlate with the severity and outcome of acute HBV infection

Initial load of hepatitis B virus (HBV), its changing profile, and precore/core promoter mutations correlate with the severity and outcome of acute HBV infection

Prevalence of Hepatitis B Virus Genotype D in Precore Mutants Among Chronic Liver Disease Patients from New Delhi, India

Drug Delivery Systems and Liver Targeting for the Improved Pharmacotherapy of the Hepatitis B Virus (HBV) Infection

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