Ling-Bo Liang1, Xia Zhu2, Li-Bo Yan2, Ling-Yao Du2, Cong Liu2, Juan Liao2, Hong Tang3. 1. Center of Infectious Disease, State Key Laboratory of Biotherapy, West China Hospital, West China School of Medicine, Sichuan University, 37# Guoxue Lane, 610041 Chengdu, China; Division of General Practice, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, China. 2. Center of Infectious Disease, State Key Laboratory of Biotherapy, West China Hospital, West China School of Medicine, Sichuan University, 37# Guoxue Lane, 610041 Chengdu, China. 3. Center of Infectious Disease, State Key Laboratory of Biotherapy, West China Hospital, West China School of Medicine, Sichuan University, 37# Guoxue Lane, 610041 Chengdu, China. Electronic address: htang6198@hotmail.com.
Abstract
BACKGROUND: The aim of this study was to determine the role of baseline hepatitis B virus (HBV) forming covalently closed circular DNA (HBV cccDNA) in liver inflammation in patients infected with HBV with serum alanine aminotransferase (ALT) levels under two times the upper limit of normal (2×ULN). METHODS: After liver biopsy and serum virological and biochemical marker screening, patients diagnosed with chronic HBV infection with serum ALT levels under 2×ULN and histological liver inflammation of less than grade G2 were prospectively recruited into this study. Recruitment took place between March 2009 and November 2010 at the Center of Infectious Disease, Sichuan University. Patient virological and biochemical markers, as well as markers of liver inflammation, were monitored. RESULTS: A total of 102 patients were recruited and 68 met the inclusion criteria; the median follow-up was 4.1 years (range 3.9-5.2 years). During follow-up, 41 patients (60.3%) exhibited signs of inflammation. Baseline HBV cccDNA >1 copy/cell (odds ratio 9.43, p=0.049) and liver inflammation grade ≥G1 (odds ratio 5.77, p=0.046) were both independent predictors of liver inflammation. CONCLUSIONS: A higher baseline intrahepatic HBV cccDNA level may increase the risk of liver inflammation. Further investigations will be required to validate HBV cccDNA as an intrahepatic virological marker of patients who require extended outpatient management.
BACKGROUND: The aim of this study was to determine the role of baseline hepatitis B virus (HBV) forming covalently closed circular DNA (HBVcccDNA) in liver inflammation in patients infected with HBV with serum alanine aminotransferase (ALT) levels under two times the upper limit of normal (2×ULN). METHODS: After liver biopsy and serum virological and biochemical marker screening, patients diagnosed with chronic HBV infection with serum ALT levels under 2×ULN and histological liver inflammation of less than grade G2 were prospectively recruited into this study. Recruitment took place between March 2009 and November 2010 at the Center of Infectious Disease, Sichuan University. Patient virological and biochemical markers, as well as markers of liver inflammation, were monitored. RESULTS: A total of 102 patients were recruited and 68 met the inclusion criteria; the median follow-up was 4.1 years (range 3.9-5.2 years). During follow-up, 41 patients (60.3%) exhibited signs of inflammation. Baseline HBVcccDNA >1 copy/cell (odds ratio 9.43, p=0.049) and liver inflammation grade ≥G1 (odds ratio 5.77, p=0.046) were both independent predictors of liver inflammation. CONCLUSIONS: A higher baseline intrahepatic HBVcccDNA level may increase the risk of liver inflammation. Further investigations will be required to validate HBVcccDNA as an intrahepatic virological marker of patients who require extended outpatient management.
Authors: Miao Liu; Lingyao Du; Xing Cheng; Man Yuan; Jin Shang; Ying Shi; Hailing Yang; Hong Tang Journal: Front Microbiol Date: 2022-06-06 Impact factor: 6.064
Authors: Valentina Svicher; Romina Salpini; Lorenzo Piermatteo; Luca Carioti; Arianna Battisti; Luna Colagrossi; Rossana Scutari; Matteo Surdo; Valeria Cacciafesta; Andrea Nuccitelli; Navjyot Hansi; Francesca Ceccherini Silberstein; Carlo Federico Perno; Upkar S Gill; Patrick T F Kennedy Journal: Gut Date: 2020-12-21 Impact factor: 31.793