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Updated: Jul 11, 2026

"Liver-on-a-Chip" Cultures of Primary Hepatocytes and Kupffer Cells for Hepatitis B Virus Infection
Published on: February 19, 2019
Viral load speaks little about toll on liver
Mamun-Al Mahtab1, Salimur Rahman, Mobin Khan
1Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh. shwapnil@agni.com
Background:
Bangladesh is situated in the intermediate prevalence region of hepatitis B virus (HBV). The lifetime risk of acquiring HBV infection in Bangladesh is greater than 40%. It has been estimated that this virus is responsible for 10%-35% cases of acute viral hepatitis, 35.7% cases of fulminant hepatic failure, 33.3%-40.5% cases of chronic hepatitis and 46.8% cases of hepatocellular carcinoma in Bangladesh. The aim of this study is to compare the correlation between HBV DNA load and grade and stage of liver disease in patients with chronic hepatitis B (CHB).
Methods:
Percutaneous liver biopsies done in 159 CHB patients revealed 62.9% (100 patients) had wild type HBV infection and the rest 37.1% (59) had pre-core/core promoter mutant HBV infection. HBV DNA load was measured using PCR in all patients.
Results:
In the wild type CHB group, 97% (97 patients) had moderate to high HBV DNA load and 3% (3) had low to moderate HBV DNA. In the pre-core/core promoter mutant group, 74.6% (44 patients) had moderate to high HBV DNA and the rest 25.4% (15) had low to moderate HBV DNA. The patients with moderate to high HBV DNA of the patients with wild type CHB, 78.4% (76 patients) had minimal to mild chronic hepatitis (HAI-NI 0-8) and 21.6% (21) had moderate to severe chronic hepatitis (HAI-NI 9-18). 66.6% (2 patients) and 33.3% (1) patients with low to moderate HBV DNA load had minimal to mild and moderate to severe chronic hepatitis respectively. In the moderate to high HBV DNA group, 77.3% (75 patients) patients had minimal to moderate fibrosis (HAI-F 0-2) and 22.7% (22) (HAI-F 3-4) had severe fibrosis to cirrhosis. These figures were 33.3% (1 patient) and 66.6% (2) respectively in the patients with low to moderate HBV DNA load. On the other hand in case of patients with pre-core/core promoter mutant type CHB, in the moderate to high HBV DNA group, 79.5% (35 patients) had minimal to mild chronic hepatitis (HAI-NI 0-8) and 20.5% (9) had moderate to severe chronic hepatitis (HAI-NI 9-18). 93.3% (14) and 6.7% (1) patients with low to moderate HBV DNA load had minimal to mild and moderate to severe chronic hepatitis respectively. In the moderate to high HBV DNA group, 68.2% (30 patients) had minimal to moderate fibrosis (HAI-F 0-2) and 31.8% (14) (HAI-F 3-4) had severe fibrosis to cirrhosis. These figures were 86.7% (13) and 13.3% (2) respectively in patients with low to moderate HBV DNA load.
Conclusions:
The study shows that high HBV DNA load does not correlate with necro-inflammatory activity or extent of fibrosis in the liver in patients with either wild type or pre-core mutant type CHB.
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