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Serum HBV-DNA (hepatitis B virus DNA) in acute and chronic hepatitis B infection
1Department of Medicine, Mount Sinai Hospital, University of Toronto, Canada.
Insights
Hepatitis B virus (HBV) DNA is often detected in patients with acute and chronic hepatitis B. Persistent HBV DNA indicates chronic infection, while its absence in carriers suggests lower risk.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Hepatitis B virus (HBV) infection is a global health concern.
- Accurate detection of HBV DNA is crucial for diagnosing and managing HBV infection.
- Understanding HBV DNA presence across different clinical presentations is essential.
Purpose of the Study:
- To investigate the presence and persistence of HBV DNA in patients with various hepatitis B manifestations.
- To correlate HBV DNA levels with disease activity and histological findings.
- To assess the relationship between HBeAg and HBV DNA in different stages of HBV infection.
Main Methods:
- Serum samples from 69 patients with hepatitis B virus infections were analyzed.
- Patients were categorized into acute hepatitis B, chronic active hepatitis (CAH), chronic persistent hepatitis (CPH), cirrhosis, and asymptomatic carriers.
- HBV DNA levels were quantified, and HBeAg status was determined.
Main Results:
- HBV DNA was transient in acute hepatitis B but persisted in chronic cases.
- 23 of 24 CAH patients showed persistent HBV DNA; all 13 with CAH and cirrhosis were positive.
- HBV DNA was detected in 2/6 CPH patients, and absent in cirrhosis without CAH and asymptomatic carriers.
- HBeAg and HBV DNA were not always concurrently present.
Conclusions:
- Persistent HBV DNA is a hallmark of chronic hepatitis B, including CAH and cirrhosis.
- HBV DNA detection is valuable across different HBV infection stages.
- The study highlights the complex interplay between HBeAg and HBV DNA detection.
Abstract:
HBV DNA was measured in the sera of 69 patients with hepatitis B virus infections. Sixteen patients had acute hepatitis B, 24 had chronic active hepatitis (CAH), 6 had chronic persistent hepatitis (CPH), 5 had cirrhosis without CAH and 18 were asymptomatic HBsAg carriers. In patients with acute hepatitis B who recovered, HBV DNA was present in the serum transiently early in the illness. HBV DNA persisted in the serum in the two patients who developed chronic hepatitis. Sera of 23 of 24 patients with CAH were persistently positive for HBV DNA. There was no relationship between the quantity of HBV DNA in the serum and the histological intensity of activity. Thirteen of the 24 patients with CAH had histological evidence of cirrhosis in addition to CAH and HBV DNA was detected in the sera of all 13. The sera of 2 of 6 patients with CPH were positive for HBV DNA. In one it was positive only where there was clinical evidence of reactivation of HBV infection. The other patient subsequently developed CAH. Sera of 5 patients with established HBsAg positive cirrhosis but without evidence of CAH were negative for HBV DNA. Two of these patients had hepatocellular carcinoma. Sera of 18 asymptomatic anti-HBe positive carriers with normal ALT were negative for HBV DNA. HBeAg and HBV DNA were not always found in the serum together. In acute hepatitis 5 patients with HBV DNA in the serum were HBeAg positive, but in 6 patients the sera were HBeAg positive inthe absenceof HBV DNA.