Related Experiment Video
Updated: Aug 11, 2026

Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix
Published on: October 20, 2021
Selective detection of human hepatitis B virus surface and core antigens in peripheral blood mononuclear cell subsets
I Chemin1, C Vermot-Desroches, I Baginski
1INSERM U271, Lyons, France.
Insights
Hepatitis B proteins (HBsAg, HBcAg) were found on lymphocytes in chronic hepatitis B patients. Hepatitis B virus (HBV) DNA and RNA replication occurred in B lymphocytes (CD19) and natural killer (NK) cells (CD56).
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Chronic hepatitis B (CHB) is a significant global health concern.
- The role of peripheral mononuclear cells (PBMCs) in hepatitis B virus (HBV) infection is not fully understood.
- Investigating viral protein expression and replication within specific immune cell subsets is crucial for understanding CHB pathogenesis.
Purpose of the Study:
- To investigate the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) on PBMCs in CHB patients.
- To determine if HBV DNA and RNA are present and replicate within specific PBMC subsets.
- To elucidate the cellular tropism of HBV within the immune system.
Main Methods:
- Flow cytometry was used to detect HBsAg and HBcAg on PBMC subsets (CD3, CD4, CD8, CD19, CD56).
- Polymerase chain reaction (PCR) and Southern blotting were employed to detect HBV DNA and RNA in sorted PBMC subsets.
- Primers targeting the HBV S gene were utilized for PCR analysis.
Main Results:
- HBsAg and HBcAg were detected on the surface of PBMCs from most CHB patients.
- B lymphocytes (CD19) and NK cells (CD56) showed the highest expression of HBsAg and HBcAg.
- HBV DNA was detected in CD3, CD4, CD19, and CD56 cells, while HBV RNA was predominantly found in CD19 and CD56 cells, indicating active replication and transcription.
Conclusions:
- HBV can infect and replicate within B lymphocytes and NK cells in patients with chronic hepatitis B.
- The presence of viral antigens on immune cells suggests a complex interplay between HBV and the host immune system.
- These findings highlight potential new targets for therapeutic interventions in chronic hepatitis B.
Abstract:
The presence of hepatitis B surface protein (HBs) and hepatitis B core protein (HBc) was investigated, by flow cytometry, on the surface of peripheral mononuclear cells (PBMC) from cells of the following phenotype: CD3 (T lymphocytes), CD4 (T helper/ inducer), CD8 (T cytotoxic/suppressor), CD19 (B lymphocytes) and CD56 [natural killer (NK) cells] among eight patients suffering from chronic hepatitis B and five healthy HBV-negative subjects. This study demonstrated the presence of HBsAg and HBcAg on the lymphocyte surface for most of the patients. The mean percentage of labelled cells was 17% for HBsAg and 15% for HBcAg. Among the different lymphocyte subsets only B lymphocytes and the NK cells expressed HBsAg for 57% and 26% of cells, respectively. Similarly HBcAg was also detected among CD19 and CD56 cells only. Polymerase chain reaction (PCR) was used to search for the presence of hepatitis B virus (HBV) DNA and RNA in PBMC, using primers located in the S gene. HBV DNA was detected with variable intensity in the CD3, CD4, CD19 and CD56 subsets following their separation with a cell sorter. For HBV RNA the signal obtained after PCR and Southern blotting was higher for CD56 and CD19 cells than for CD3 cells and undetectable for CD4 cells. This study demonstrates that replication and transcription of the HBV can occur in CD19- and CD56-positive cells. Positive signals in CD3 cells may be due to contamination of this subpopulation by NK cells.
More Related Videos
11:34A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
04:11Real-Time Polymerase Chain Reaction-Based Detection and Quantification of Hepatitis B Virus DNA
Published on: December 15, 2023