Abstract
The aim of this study was to assess the effect of 48-week entecavir therapy on serum and intrahepatic hepatitis B virus, covalently closed circular DNA (HBV cccDNA) levels in hepatitis B e antigen (HBeAg)-positive patients. A total of 120 patients with HBeAg-positive chronic hepatitis were treated with entecavir for 48 weeks. Serum HBV markers, total HBV DNA, and HBV cccDNA levels were measured at baseline and week 48. Biopsies from 20 patients were available for both intrahepatic total HBV DNA and cccDNA testing at these timepoints. HBV cccDNA levels were decreased from a median level of 5.1×106 copies/mL at baseline to a median level of 2.4×103 copies/mL at week 48. Reduction magnitudes of HBV cccDNA in patients with normalized alanine aminotransferase levels and those undergoing HBeAg seroconversion were significantly greater than those in alanine aminotransferase-abnormal and HBeAg positive patients. Intrahepatic HBV cccDNA was decreased significantly after 48 weeks of treatment, but could not be eradicated. In conclusion, treatment of HBeAg-positive hepatitis B patients with entecavir for 48 weeks decreased serum and intrahepatic HBV cccDNA significantly, and the magnitude of HBV cccDNA reduction was related to total HBV DNA decrease, alanine aminotransferase normalization, and HBeAg seroconversion.
Highlights
Hepatitis B virus (HBV) infection affects more than 350 million individuals worldwide, causing acute and chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma [1]
A peculiarity of the HBV life cycle is that the HBV genome is either encapsulated to produce virions and be secreted into the blood, or recycled back to the nucleus to maintain a pool of closed circular DNA (cccDNA), resulting in accumulation of HBV cccDNA in hepatocyte nuclei at a level of about 5–-50 copies per cell during chronic
We evaluated the effect of entecavir treatment on serum and intrahepatic HBV cccDNA levels in Chinese patients with hepatitis B e antigen (HBeAg)-positive chronic hepatitis B using a TaqMan real-time polymerase chain reaction (PCR) assay
Summary
Hepatitis B virus (HBV) infection affects more than 350 million individuals worldwide, causing acute and chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma [1]. When HBV enters hepatocytes, the partially double-stranded, relaxed circular DNA (rcDNA) genome will convert into a covalently closed circular DNA (cccDNA) episome in the nucleus of infected cells [2]. A peculiarity of the HBV life cycle is that the HBV genome is either encapsulated to produce virions and be secreted into the blood, or recycled back to the nucleus to maintain a pool of cccDNA, resulting in accumulation of HBV cccDNA in hepatocyte nuclei at a level of about 5–-50 copies per cell during chronic. Persistence of cccDNA in hepatocytes plays a key role in viral persistence, reactivation of viral replication after cessation of antiviral therapy, and resistance to therapy [4]
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