Fulminant hepatitis B: Induction by hepatitis B virus mutants defective in the precore region and incapable of encoding E antigen

Kosaka, Yoshitane; Takase, Kohjiro; Kojima, Mineo; Shimizu, Masaru; Inoue, Katsumi; Yoshiba, Makoto; Tanaka, Satoshi; Akahane, Yoshihiro; Okamoto, Hiroaki; Tsuda, Fumio; Miyakawa, Yuzo; Matsui, Makoto

doi:10.1016/0016-5085(91)90286-t

Cited by 252 publications

(137 citation statements)

References 34 publications

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“…3 Moreover, primary infection with HBV mutants that cannot encode HBeAg can induce fulminant hepatitis. [4][5][6] Hence, HBeAg has a significant bearing on the clinical status of the individuals infected with HBV.…”

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confidence: 99%

A Case–Control Study for Clinical and Molecular Biological Differences Between Hepatitis B Viruses of Genotypes B and C

et al. 2001

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Clinical and molecular virological differences were evaluated in 50 Japanese patients chronically infected with HBV of genotype B and C who were matched for age and sex as well as the severity of liver disease in a case-control study. Hepatitis B e antigen (HBeAg) was significantly less frequent (16% vs. 42%, P < .01), whereas antibody to HBeAg (anti-HBe) was significantly more common (84% vs. 56%, P < .01) in genotype B than C patients. The predominance of mutants with G-to-A mutation at nucleotide (nt) 1896 in the precore region (A1896) over the wild-type was comparable between genotype B and C patients (60% and 62%, respectively), and it correlated with anti-HBe. The double mutation in the basic core promoter (A-to-T at nt 1762 and G-to-A at nt 1764), however, was significantly more frequent in genotype C than B patients (58% vs. 16%, P < .01), and it did not correlate with anti-HBe or HBeAg. By the multiple logistic regression analysis, the double mutation in the basic core promoter (T1762/A1764) was significantly associated with genotype C [odds ratio (OR), 9.3; 95% confidence interval (

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confidence: 99%

A Case–Control Study for Clinical and Molecular Biological Differences Between Hepatitis B Viruses of Genotypes B and C

et al. 2001

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“…The culture negative ascitic fluids also had bacterial peritonitis as indicated by high absolute neutrophil count. 15,16 Of the 10 patients who did not have diagnostic paracentesis, five had bacteremia. Result of the blood culture in patients with AH in 2006 and 2007 showed high incidence of bacteremia in patients with AH which was significantly higher in patients with complications (Table 3).…”

Section: Laboratory Findingsmentioning

confidence: 99%

“…Hepatitis B virus variants with mutation in the precore region and/or the core promoter [16][17][18][19] were implicated in AHF. Similarly nucleotide substitution in the 5'UTR of HAV genome was considered a possible cause of severity in hepatitis A.…”

Section: Thus the Question Arises What Is This Entity Called Sahf? Anmentioning

confidence: 99%

Subacute Hepatic Failure: Its Possible Pathogenesis

Shrestha¹

2012

Euroasian Journal of Hepato-Gastroenterology

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“…46 There are reports that these pre-core mutants could induce resistance to interferon therapy, 47 increase incidence of fibrosing cholestatic hepatitis in liver transplant patients, 48 increase susceptibility to hepatitis D co-infection 49 and cause fulminant hepatic failure. 50 Despite the high HBV endemicity in Saudi Arabia and the reported high prevalence of the pre-core mutant in the Mediterranean basin, very little is known about HBV pre-core mutants in this country.…”

Section: Hbv Pre-core Mutantsmentioning

confidence: 99%

Hepatitis B Surface Gene Mutants and their Emerging Role in the Efficacy of HBV Vaccination Programs

Shobokshi

Serebour²,

Skakni³

1999

Ann Saudi Med

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The advances in molecular biology techniques in the past decade have led to the clarification of hepatitis B viral DNA sequences. However, much remains to be established regarding the emerging hepatitis B mutants. Several putative forms of hepatitis B virus have been isolated, but their epidemiology, natural course of infection and clinical significance remain sketchy. Compounding these problems are factors created by human interventions, such as HBsAg mass immunization, chemotherapy of chronic HBV patients and HBIg prophylaxis of orthotopic liver transplant (OLT) patients, which tend to encourage new mutants to emerge.Despite the availability of HBsAg vaccines and the mass immunization schemes implemented in over 80 countries worldwide, HBV infection continues to be a major public health problem. There are over 350 million chronic carriers worldwide, out of which about 10% die of cirrhosis and hepatocellular carcinoma.

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Fulminant hepatitis B: Induction by hepatitis B virus mutants defective in the precore region and incapable of encoding E antigen

Cited by 252 publications

References 34 publications

A Case–Control Study for Clinical and Molecular Biological Differences Between Hepatitis B Viruses of Genotypes B and C

A Case–Control Study for Clinical and Molecular Biological Differences Between Hepatitis B Viruses of Genotypes B and C

Subacute Hepatic Failure: Its Possible Pathogenesis

Hepatitis B Surface Gene Mutants and their Emerging Role in the Efficacy of HBV Vaccination Programs

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