摘要
This study examined a signal amplification assay, the Invader assay, for the q uantitation of hepatitis B virus (HBV) covalently closed circularDNA (cccDNA) in liver biopsies and sera. DNA was extracted from liver biopsy and serum samples were collected from 16 hepatitis B e antigen (HBeAg)-positive and 36 antibody- to-HBeAg-positive (anti-HBe-positive) chronic hepatitis B patients. The amou nt of total HBV DNA and cccDNA was measured using the Invader assay. Anti-HBe- positive patients had lower median total intrahepatic HBV DNA (P < .001) and int rahepatic cccDNA levels (P = .001) than HBeAg-positive patients. Intrahepatic c ccDNA correlated positively with the total intrahepatic HBV DNA (r = 0.950, P < .001). However, the proportion of intrahepatic HBV DNA in the form of cccDNA was inversely related to the amount of total intrahepatic HBV DNA (r = -0.822, P < .001). A small amount of cccDNA was detected in 39 of 52 (75%) serum samples. Anti-HBe-positive patients had lower median serum cccDNA levels than HBeAg-po sitive patients (P = .002). Serum HBV DNA correlated positively with intrahepati c total HBV DNA (r = 0.778, P < .001) and intrahepatic cccDNA (r = 0.481, P = .0 02). In conclusion, the Invader assay is a reliable assay for the quantitation o f cccDNA. Serum and intrahepatic total HBV DNA and cccDNA levels become lower as the disease progresses from HBeAg-positive to anti-HBe-positive phase, with cccDNA becoming the predominant form of intrahepatic HBV DNA.
This study examined a signal amplification assay, the Invader assay, for the q uantitation of hepatitis B virus (HBV) covalently closed circularDNA (cccDNA) in liver biopsies and sera. DNA was extracted from liver biopsy and serum samples were collected from 16 hepatitis B e antigen (HBeAg)-positive and 36 antibody- to-HBeAg-positive (anti-HBe-positive) chronic hepatitis B patients. The amou nt of total HBV DNA and cccDNA was measured using the Invader assay. Anti-HBe- positive patients had lower median total intrahepatic HBV DNA (P < .001) and int rahepatic cccDNA levels (P = .001) than HBeAg-positive patients. Intrahepatic c ccDNA correlated positively with the total intrahepatic HBV DNA (r = 0.950, P < .001). However, the proportion of intrahepatic HBV DNA in the form of cccDNA was inversely related to the amount of total intrahepatic HBV DNA (r = -0.822, P < .001). A small amount of cccDNA was detected in 39 of 52 (75%) serum samples. Anti-HBe-positive patients had lower median serum cccDNA levels than HBeAg-po sitive patients (P = .002). Serum HBV DNA correlated positively with intrahepati c total HBV DNA (r = 0.778, P < .001) and intrahepatic cccDNA (r = 0.481, P = .0 02). In conclusion, the Invader assay is a reliable assay for the quantitation o f cccDNA. Serum and intrahepatic total HBV DNA and cccDNA levels become lower as the disease progresses from HBeAg-positive to anti-HBe-positive phase, with cccDNA becoming the predominant form of intrahepatic HBV DNA.
