New hepatitis C virus research from Technical University of Munich discussed
2009 JUL 13 - (NewsRx.com) -- According to recent research published in the journal Genetic Testing and Molecular Biomarkers, "Hepatic stellate cells express all components of the renin-angiotensinogen (AGT) system and secrete active angiotensin II. Animal studies provided evidence that angiotensin II stimulates the accumulation of extracellular matrix by enhancing transforming growth factor beta 1 production." "A functional genetic alteration in the human AGT promoter (c.1-44G >A) has been linked to accelerated progression of fibrosis in hepatitis C virus infection. We enrolled 2154 patients with chronic liver disease of various etiologies, including 1286 individuals with chronic hepatitis C virus infection as well as 207 healthy volunteers. We performed genotyping for two AGT variants, c.1-44G >A and c.803T >C (p.M268T), by melting curve analysis using fluorescence resonance energy transfer probes. Allele frequencies and genotype distributions of both variants did not differ between patients and controls. Genotype frequencies of the c.1-44G >A variant were GG 31.0%, GA 45.6%, and AA 23.4% in patients and GG 30.0%, GA 47.8%, and AA 22.2% in controls. The genotype frequencies of p. M268T, which is in strong linkage disequilibrium with c.1-44G >A, were MM 30.8%, MT 45.5%, and TT 23.4% in patients and MM 29.0%, MT 48.8%, and TT 22.2% in controls. Both variants were associated with neither higher stages of fibrosis nor requirement for liver transplantation in any of the diagnosis subgroups. Particularly, these genetic alterations were not associated with progressive fibrosis in chronic HCV infection," wrote J. Halangk and colleagues, Technical University of Munich. The researchers concluded: "In contrast to previous reports, both AGT variants do not predispose to the progression of fibrosis in chronic liver disease." Halangk and colleagues published their study in Genetic Testing and Molecular Biomarkers (Evaluation of Angiotensinogen c.1-44G>A and p.M268T Variants as Risk Factors for Fibrosis Progression in Chronic Hepatitis C and Liver Diseases of Various Etiologies. Genetic Testing and Molecular Biomarkers, 2009;13(3):407-414). For additional information, contact H. Witt, Technical University Munich TUM, Klin & Poliklin Kinder & Jugendmed, Kolner Pl 1, D-80804 Munich, Germany. The publisher's contact information for the journal Genetic Testing and Molecular Biomarkers is: Mary Ann Liebert Inc., 140 Huguenot Street, 3RD FL, New Rochelle, NY 10801, USA. Keywords: Germany, Munich, Angiotensin, Chronic Hepatitis C, Chronic Liver Disease, Enzyme Research, Fibrosis, Gastroenterology, Genetics, HCV, Hepatitis C Virus, Hepatology, Infectious Disease, Renin, Viral, Virology, Technical University of Munich. This article was prepared by Hepatitis Weekly editors from staff and other reports. Copyright 2009, Hepatitis Weekly via NewsRx.com.
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