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Abstract Details
Eradication of Chronic HCV Infection: Improvement of Dysbiosis Only in Patients Without Liver Cirrhosis
Hepatology. 2021 Jul;74(1):72-82. doi: 10.1002/hep.31700. Epub 2021 Jun 15.
Freya Wellhöner1, Nico Döscher1, Franziska Woelfl1, Marius Vital2, Iris Plumeier2, Silke Kahl2, Andrej Potthoff1, Michael Peter Manns13, Dietmar Helmut Pieper23, Markus Cornberg13, Heiner Wedemeyer13, Benjamin Heidrich123
Author information
1Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
2Microbial Interactions and Processes Research Group, Helmholtz Center for Infection Research, Braunschweig, Germany.
3German Center for Infection Research (DZIF), Partner Site Hannover-Braunschweig, Braunschweig, Germany.
Abstract
Background and aims: It is well accepted that liver diseases and their outcomes are associated with intestinal microbiota, but causality is difficult to establish. The intestinal microbiota are altered in patients with hepatitis C. As chronic HCV infection can now be cured in almost all patients, it is an ideal model to study the influence of liver disease on the microbiota.
Approach and results: We aimed to prospectively analyze the changes in the gut microbiome in patients who received direct-acting antivirals (DAA) and achieved sustained virological response (SVR). Amplicon sequencing of the V1-V2 region in the 16S ribosomal RNA gene was performed in stool samples of patients with chronic hepatitis C. Patients in the treatment group received DAA (n = 65), whereas in the control group, no DAA were given (n = 33). Only patients achieving SVR were included. The alpha diversity increased numerically but not significantly from baseline to SVR at week 24 or 48 (SVR24/48; 2.784 ± 0.248 vs. 2.846 ± 0.224; P = 0.057). When stratifying for the presence of liver cirrhosis, a significant increase in diversity was only seen in patients without cirrhosis. Differences in the microbial community structure induced by the achievement of SVR were only observed in patients without liver cirrhosis. In patients with liver cirrhosis and in the control group, no significant differences were observed.
Conclusions: In conclusion, the achievement of SVR24/48 in patients with chronic HCV was associated with changes in the intestinal microbiota. However, these changes were only seen in patients without liver cirrhosis. A major role of liver remodeling on the intestinal microbiota is indicated by the dynamics of the intestinal microbial community structure depending on the stage of fibrosis in patients resolving chronic hepatitis C.