scholarly journals Impaired generation of hepatitis B virus-specific memory B cells in HIV infected individuals following vaccination

Vaccine ◽  
2010 ◽  
Vol 28 (21) ◽  
pp. 3672-3678 ◽  
Author(s):  
Nishaki Mehta ◽  
Coleen K. Cunningham ◽  
Patricia Flynn ◽  
Joyce Pepe ◽  
Stephen Obaro ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
Memory B Cells ◽  
Specific Memory ◽  
B Virus

scholarly journals Potent human broadly neutralizing antibodies to hepatitis B virus from natural controllers

2020 ◽  
Vol 217 (10) ◽  
Author(s):  
Verena Hehle ◽  
Maxime Beretta ◽  
Maryline Bourgine ◽  
Malika Ait-Goughoulte ◽  
Cyril Planchais ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
Neutralizing Antibodies ◽  
Humoral Response ◽  
Neutralizing Antibody ◽  
Memory B Cells ◽  
Chronic Hepatitis B Virus ◽  
B Virus

Rare individuals can naturally clear chronic hepatitis B virus (HBV) infection and acquire protection from reinfection as conferred by vaccination. To examine the protective humoral response against HBV, we cloned and characterized human antibodies specific to the viral surface glycoproteins (HBsAg) from memory B cells of HBV vaccinees and controllers. We found that human HBV antibodies are encoded by a diverse set of immunoglobulin genes and recognize various conformational HBsAg epitopes. Strikingly, HBsAg-specific memory B cells from natural controllers mainly produced neutralizing antibodies able to cross-react with several viral genotypes. Furthermore, monotherapy with the potent broadly neutralizing antibody Bc1.187 suppressed viremia in vivo in HBV mouse models and led to post-therapy control of the infection in a fraction of animals. Thus, human neutralizing HBsAg antibodies appear to play a key role in the spontaneous control of HBV and represent promising immunotherapeutic tools for achieving HBV functional cure in chronically infected humans.

scholarly journals Hepatitis B virus‐induced hyperactivation of B cells in chronic hepatitis B patients via TLR4

2020 ◽  
Vol 24 (11) ◽  
pp. 6096-6106
Author(s):  
Yang Li ◽  
Shengxia Yin ◽  
Yuxin Chen ◽  
Quan Zhang ◽  
Rui Huang ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
B Virus

scholarly journals Molecular Basis for the Interaction of the Hepatitis B Virus Core Antigen with the Surface Immunoglobulin Receptor on Naive B Cells

2001 ◽  
Vol 75 (14) ◽  
pp. 6367-6374 ◽  
Author(s):  
Una Lazdina ◽  
Tinghua Cao ◽  
Juris Steinbergs ◽  
Mats Alheim ◽  
Paul Pumpens ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
Light Chain ◽  
Molecular Basis ◽  
Cell Surface Receptor ◽  
Core Antigen ◽  
Binding Motif ◽  
Linear Motif ◽  
B Virus

ABSTRACT The nucleocapsid of the hepatitis B virus (HBV) is composed of 180 to 240 copies of the HBV core (HBc) protein. HBc antigen (HBcAg) capsids are extremely immunogenic and can activate naive B cells by cross-linking their surface receptors. The molecular basis for the interaction between HBcAg and naive B cells is not known. The functionality of this activation was evidenced in that low concentrations of HBcAg, but not the nonparticulate homologue HBV envelope antigen (HBeAg), could prime naive B cells to produce anti-HBc in vitro with splenocytes from HBcAg- and HBeAg-specific T-cell receptor transgenic mice. The frequency of these HBcAg-binding B cells was estimated by both hybridoma techniques and flow cytometry (B7-2 induction and direct HBcAg binding) to be approximately 4 to 8% of the B cells in a naive spleen. Cloning and sequence analysis of the immunoglobulin heavy- and light-chain variable (VH and VL) domains of seven primary HBcAg-binding hybridomas revealed that six (86%) were related to the murine and human VH1 germ line gene families and one was related to the murine VH3 family. By using synthetic peptides spanning three VH1 sequences, one VH3 sequence, and one VLκV sequence, a linear motif in the framework region 1 (FR1)complementarity-determining region 1 (CDR1) junction of the VH1 sequence was identified that bound HBcAg. Interestingly, the HBcAg-binding motif was present in the VL domain of the HBcAg-binding VH3-encoded antibody. Finally, two monoclonal antibodies containing linear HBcAg-binding motifs blocked HBcAg presentation by purified naive B cells to purified HBcAg-primed CD4+ T cells. Thus, the ability of HBcAg to bind and activate a high frequency of naive B cells seems to be mediated through a linear motif present in the FR1-CDR1 junction of the heavy or light chain of the B-cell surface receptor.

A higher frequency of IL-10-producing B cells in Hepatitis B virus-associated membranous nephropathy

2016 ◽  
Vol 43 (4) ◽  
pp. 417-427 ◽  
Author(s):  
Yong Liu ◽  
Haifeng Wang ◽  
Xintong Hu ◽  
Zhihui Qu ◽  
Huimao Zhang ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
Membranous Nephropathy ◽  
B Virus

CpG oligodeoxynucleotides discriminately enhance binding capacity of human naïve B cells to Hepatitis B virus epitopes

2012 ◽  
Vol 58 (6) ◽  
pp. 752-759 ◽  
Author(s):  
Jian-ying Bai ◽  
Yong-tao Yang ◽  
Rong Zhu ◽  
Yi-qin Wang ◽  
Yin Tian ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
Binding Capacity ◽  
Class Ii ◽  
Class I ◽  
Cpg Odn ◽  
Cpg Oligodeoxynucleotides ◽  
Class Ii Mhc ◽  
B Virus

CpG oligodeoxynucleotides (CpG ODN) have the potential to enhance the antigen-presenting cells function of human naïve B cells. In this study, we aim to define the effect of CpG ODNs on the binding capacity of human naïve B cells for different Hepatitis B virus (HBV) epitopes. Three HLA-A2 restricted epitopes were selected to incubate with CpG ODN-primed human naïve B cells. Binding capacity for each epitope and expression of CD80, CD86, class I major histocompatibility complex (MHC), and class II MHC of naïve B cells was tested, respectively, by flow cytometry. CpG ODNs, especially ODN 2216, enhanced the binding capacity of human naïve B cells for HBV epitopes (p < 0.01), and induced markedly higher expression of CD80, CD86, class I MHC, and class II MHC. The binding capacity of CpG-treated naive B cells for each epitope was significantly different. In all the 3 subjects, CpG ODN 2216-primed naïve B cells showed the highest binding ability for Env172–180 compared with the other epitopes with a high expression of co-stimulatory and MHC molecules. CpG ODN showed the potential to selectively enhance the binding capacity of human naïve B cells for HBV epitopes. These results suggest new strategies for development of vaccine design.

scholarly journals Re-evaluation of hepatitis B virus clinical phases by systems biology identifies unappreciated roles for the innate immune response and B cells

Hepatology ◽  
2015 ◽  
Vol 62 (1) ◽  
pp. 87-100 ◽  
Author(s):  
Thomas Vanwolleghem ◽  
Jun Hou ◽  
Gertine van Oord ◽  
Arno C. Andeweg ◽  
A.D.M.E. Osterhaus ◽  
...  
Keyword(s):  
Immune Response ◽  
Systems Biology ◽  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
Innate Immune Response ◽  
Innate Immune ◽  
B Virus

scholarly journals Hepatitis B virus particles activate B cells through the TLR2–MyD88–mTOR axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Qian Li ◽  
Jun Wang ◽  
Heba Islam ◽  
Carsten Kirschning ◽  
Hongzhou Lu ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
B Cells ◽  
Hepatitis B ◽  
B Cell ◽  
Cell Function ◽  
Hepatitis Virus ◽  
Transcriptional Profiling ◽  
Cell Types ◽  
Mrna Accumulation ◽  
B Virus

AbstractHost immune control plays a pivotal role in resolving primary hepatitis-B-virus (HBV) infections. The complex interaction between HBV and host immune cells, however, remains unclear. In this study, the transcriptional profiling of specimens from animals infected with woodchuck hepatitis virus (WHV) indicated TLR2 mRNA accumulation as most strongly impacted during WHV infection resolution as compared to other mRNAs. Analysis of blood transcriptional modules demonstrated that monocytes and B-cells were the predominantly activated cell types in animals that showed resolution of infection, which was similar to the response of TLR2-stimulated PBMCs. Further investigation of TLR2-stimulated B-cells pointed at interactions between activated TLR signaling, Akt-mTOR, and glucose metabolic pathways. Moreover, analysis of B-cells from Tlr2−/−, Trif−/−, Myd88−/−, and Trif/Myd88−/− mice challenged with HBV particles indicated B-cell function and glucose metabolism alterations is TLR2-MyD88-mTOR axis dependent. Overall, our study implicates B-cell TLR2 activation in HBV infection resolution.

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