Long-term follow-up of posttransfusion and sporadic chronic hepatitis non-A, non-B and frequency of circulating antibodies to hepatitis C virus (HCV)

Hopf, U.; Möller, B.; Küther, D.; Stemerowicz, R.; Lobeck, H.; Lüdtke-Handjery, A; Walter, Elke; Blum, Hubert E.; Roggendorf, M; Deinhardt, Friedrich

doi:10.1016/0168-8278(90)90075-3

Cited by 214 publications

(69 citation statements)

References 23 publications

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“…Furthermore, a possible link to hepatocellular carcinoma has been proposed for HCV genotype 1b. There is compelling evidence that hepatocellular carcinoma occurs more frequently or emerges earlier among HCV-infected Japanese patients (125,137) than among HCV carriers in western countries (33,55). Because HCV genotype 1b is more common in Japan than in Europe or the United States, the hypothesis relating to genotype is attractive and appears to explain these differences.…”

Section: Progression Of Liver Diseasementioning

confidence: 98%

Clinical Significance of Hepatitis C Virus Genotypes

Zein

2000

Clinical Microbiology Reviews

455

358

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Section: Progression Of Liver Diseasementioning

confidence: 98%

Clinical Significance of Hepatitis C Virus Genotypes

Zein

2000

Clinical Microbiology Reviews

455

358

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“…Acute transfusion-associated non-A, non-B hepatitis (mainly hepatitis C) led to cirrhosis in 8% to 24%, hepatocellular carcinoma in 0% to 1.3%, and liver-related casualties in 1.6% to 6% of the cases within a mean follow-up of 8 to 14 years. [19][20][21][22][23] A prospective US national cohort study on transfusion-associated non-A, non-B and type C hepatitis with matched disease controls indicated a low risk of hepatitis-induced mortality (3%) after 18 years, 24 and in a 20-year update 40% chronicity, 15% cirrhosis, and only 26% recovery. 25 The risks may be underestimated because of the extremely high mortality (51%) caused by nonhepatic, mostly cardiac disease.…”

Section: Discussionmentioning

confidence: 99%

Low frequency of cirrhosis in a hepatitis C(genotype 1b) single-source outbreak in germany: A 20-year multicenter study

et al. 2000

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batches of anti-D immune globulin contaminated with hepatitis C virus (HCV) genotype 1b (20,000-480,000 copies/dose) from a single erythrocyte donor had been administered for prophylaxis of rhesus isoimmunization throughout East Germany. All 2,867 women involved had been recalled after January 12, 1979 for repeated screening of alanine transaminase (ALT). They were prospectively followed in regional centers. We have reexamined a cohort of 1,018 women (median age 24, range 16-38 years at infection) on follow-up for 20 years in 9 representative centers. Within 6 months after anti-D administration, 10% of these women had no evidence of disease and 90% had acute hepatitis C (n ‫؍‬ 917) including 49% with symptomatic and 22% with icteric course. After 20 years, 85% of the 917 affected women still tested positive for HCV antibodies (among them 3% responded to interferon treatment) and 55% were positive for HCV RNA (among them 7% were nonresponders to interferon and 3% were apparent HCV carriers). Only 4 (0.4%) had overt cirrhosis. Two (0.2%) died of superinfected fulminant hepatitis B or alcoholism and cirrhosis, respectively. Histology obtained in 44% of the viremic women showed hepatitis of minimal to moderate grade in 96%, portal fibrosis in 47%, and septal fibrosis in 3% of the cases.

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“…3 is the main causative agent for transfusion-associated and sporadic non-A, non-B hepatitis throughout the world (1). HCV often causes a prolonged and persistent infection (2) and plays an important role in the pathogenesis of virus-associated hepatocellular carcinoma (HCC) (3)(4)(5).…”

Section: Hepatitis C Virus (Hcv)mentioning

confidence: 99%

Hepatitis C Virus NS5A Protein Down-regulates the Expression of Spindle Gene Aspm through PKR-p38 Signaling Pathway

Chang

et al. 2008

Journal of Biological Chemistry

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Hepatitis C virus often causes persistent infection and hepatocellular carcinoma. Studies have demonstrated the roles of viral nonstructural protein 5A (NS5A) in the induction of chromosome aneuploidy, but the molecular mechanisms are not clear. In this study, hydrodynamics-based in vivo transfection was applied to a mouse system. Mouse hepatocytes that successfully expressed NS5A protein were isolated by laser capture microdissection. Gene expression profiles of the NS5A-expressing hepatocytes were examined by an Affymetrix oligonucleotide microarray system. Aspm (abnormal spindle-like, microcephaly associated), which encodes the mitotic spindle protein ASPM, was identified to be differentially expressed in the absence and the presence of NS5A. The down-regulation of Aspm mRNA and ASPM protein was confirmed by real time polymerase chain reaction and Western blot analysis, respectively, both in mouse model systems and in viral subgenomic replicon and in vitro transfection culturing systems. In addition, cultured cells that constitutively expressed NS5A protein showed G 2 /M cell cycle block and chromosome aneuploidy. Overexpression of ASPM relieved the G 2 /M cell cycle block. Furthermore, NS5A protein repressed the promoter activity of Aspm gene in a dose-dependent manner. The regulatory effect was abolished when amino acid substitutions P2209L, T2214A, and T2217G known to interrupt the NS5A-PKR interaction were introduced into the NS5A protein. This indicates that the down-regulation of Aspm expression is via the PKR-p38 signaling pathway. These results suggest that NS5A protein downregulates the expression of the mitotic spindle protein ASPM and induces aberrant mitotic cell cycle associated with chromosome instability and hepatocellular carcinoma.

show abstract

Long-term follow-up of posttransfusion and sporadic chronic hepatitis non-A, non-B and frequency of circulating antibodies to hepatitis C virus (HCV)

Cited by 214 publications

References 23 publications

Clinical Significance of Hepatitis C Virus Genotypes

Clinical Significance of Hepatitis C Virus Genotypes

Low frequency of cirrhosis in a hepatitis C(genotype 1b) single-source outbreak in germany: A 20-year multicenter study

Hepatitis C Virus NS5A Protein Down-regulates the Expression of Spindle Gene Aspm through PKR-p38 Signaling Pathway

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