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Journal articles on the topic 'Hepatitis B; human haemopoietic cells'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Delaney, William E., and Harriet C. Isom. "Hepatitis B virus replication in human HepG2 cells mediated by hepatitis B virus recombinant baculovirus." Hepatology 28, no. 4 (October 1998): 1134–46. http://dx.doi.org/10.1002/hep.510280432.

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2

Herrscher, Charline, Philippe Roingeard, and Emmanuelle Blanchard. "Hepatitis B Virus Entry into Cells." Cells 9, no. 6 (June 18, 2020): 1486. http://dx.doi.org/10.3390/cells9061486.

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Hepatitis B virus (HBV), an enveloped partially double-stranded DNA virus, is a widespread human pathogen responsible for more than 250 million chronic infections worldwide. Current therapeutic strategies cannot eradicate HBV due to the persistence of the viral genome in a special DNA structure (covalently closed circular DNA, cccDNA). The identification of sodium taurocholate co-transporting polypeptide (NTCP) as an entry receptor for both HBV and its satellite virus hepatitis delta virus (HDV) has led to great advances in our understanding of the life cycle of HBV, including the early steps of infection in particular. However, the mechanisms of HBV internalization and the host factors involved in this uptake remain unclear. Improvements in our understanding of HBV entry would facilitate the design of new therapeutic approaches targeting this stage and preventing the de novo infection of naïve hepatocytes. In this review, we provide an overview of current knowledge about the process of HBV internalization into cells.

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3

Xia, Y., A. Carpentier, Z. Zhang, U. Protzer, and T. J. Liang. "Hepatitis B Virus Infection of Human Stem Cells-Derived Hepatocyte-Like Cells." Journal of Hepatology 64, no. 2 (2016): S398. http://dx.doi.org/10.1016/s0168-8278(16)00625-5.

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4

Chou, C. K., T. S. Su, C. M. Chang, C. P. Hu, M. Y. Huang, C. S. Suen, N. W. Chou, and L. P. Ting. "Insulin suppresses hepatitis B surface antigen expression in human hepatoma cells." Journal of Biological Chemistry 264, no. 26 (September 1989): 15304–8. http://dx.doi.org/10.1016/s0021-9258(19)84826-3.

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5

Zeldis, J. B., H. Mugishima, H. N. Steinberg, E. Nir, and R. P. Gale. "In vitro hepatitis B virus infection of human bone marrow cells." Journal of Clinical Investigation 78, no. 2 (August 1, 1986): 411–17. http://dx.doi.org/10.1172/jci112591.

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6

Chou, Chen Kung. "Scutellariae radix suppresses hepatitis B virus production in human hepatoma cells." Frontiers in Bioscience E2, no. 4 (2010): 1538–47. http://dx.doi.org/10.2741/e213.

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7

Balmasova, I. P., R. I. Sepiashvili, and E. S. Malova. "MOLECULAR BIOLOGY OF HEPATITIS B VIRUS AND IMMUNOPATHOGENESIS OF CHRONIC VIRAL HEPATITIS B." Journal of microbiology, epidemiology and immunobiology, no. 2 (April 28, 2016): 119–26. http://dx.doi.org/10.36233/0372-9311-2016-2-119-126.

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Hronic hepatitis B belongs to a category of socially significant diseases due to its wide abundance in the world and high frequency of unfavourable outcomes of this disease. Features of interaction of hepatitis B virus with human immune system, accompanying development of mechanisms of escape from immunological control, is the basis of development of chronic hepatitis B. Molecular-biological features of hepatitis B virus are the basis of the indicated mechanisms, and the content of this review is their examination. Herewith, stages of immunopathogenesis of this disease is the basis of characteristics of interaction of viral proteins with cells of immune system, and isolation of those is accepted in contemporary foreign literature.

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8

Protzer, U., and H. Abken. "Can Engineered “Designer” T Cells Outsmart Chronic Hepatitis B?" Hepatitis Research and Treatment 2010 (September 21, 2010): 1–9. http://dx.doi.org/10.1155/2010/901216.

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More than 350 million people worldwide are persistently infected with human heptatitis B virus (HBV) and at risk to develop liver cirrhosis and hepatocellular carcinoma making long-term treatment necessary. While a vaccine is available and new antiviral drugs are being developed, elimination of persistently infected cells is still a major issue. Recent efforts in adoptive cell therapy are experimentally exploring immunotherapeutic elimination of HBV-infected cells by means of a biological attack with genetically engineered “designer” T cells.

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9

Deng, Cun-Liang. "Chronic hepatitis B serum promotes apoptotic damage in human renal tubular cells." World Journal of Gastroenterology 12, no. 11 (2006): 1752. http://dx.doi.org/10.3748/wjg.v12.i11.1752.

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10

Bchini, R., F. Capel, C. Dauguet, S. Dubanchet, and M. A. Petit. "In vitro infection of human hepatoma (HepG2) cells with hepatitis B virus." Journal of Virology 64, no. 6 (1990): 3025–32. http://dx.doi.org/10.1128/jvi.64.6.3025-3032.1990.

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11

Paganelli, M., D. N. Khuu, M. Najimi, I. Malla, B. Kabamba, P. Goubau, and E. M. Sokal. "PP41 HEPATITIS B VIRUS IN VITRO INFECTION OF HUMAN LIVER PROGENITOR CELLS." Digestive and Liver Disease 41 (October 2009): S219. http://dx.doi.org/10.1016/s1590-8658(09)60498-9.

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12

Jin, Yan, Feng Ye, Juanzi Shi, Hongtao Qiu, Yingren Zhao, Shumei Lin, Tianyan Chen, Min Liu, Yingli He, and Shulin Zhang. "Hepatitis B virus infection and replication in primary cultured human granulosa cells." Archives of Virology 156, no. 1 (September 29, 2010): 1–7. http://dx.doi.org/10.1007/s00705-010-0808-8.

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13

Chou, Chen-Kung, Li-Hsien Wang, Hsing-Mei Lin, and Chin-Wen Chi. "Glucocorticoid stimulates hepatitis B viral gene expression in cultured human hepatoma cells." Hepatology 16, no. 1 (July 1992): 13–18. http://dx.doi.org/10.1002/hep.1840160104.

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14

Hsia, Chu Chieh, Ritva P. Evarts, Harushige Nakatsukasa, Elizabeth R. Marsden, and Snorri S. Thorgeirsson. "Occurrence of oval-type cells in hepatitis B virus—associated human hepatocarcinogenesis." Hepatology 16, no. 6 (December 1992): 1327–33. http://dx.doi.org/10.1002/hep.1840160604.

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15

Cox, Charlotte V., Roger S. Evely, and Allison Blair. "Detection of a CD133+/CD38− SL-IC Population in Childhood B Cell Precursor ALL." Blood 106, no. 11 (November 16, 2005): 1369. http://dx.doi.org/10.1182/blood.v106.11.1369.1369.

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Abstract Clonality studies of immunoglobulin rearrangements in B cell precursor acute lymphoblastic leukaemia (BCP ALL) has suggested that the disease may arise in cells already committed to the B cell lineage. In contrast, Ph+ ALL, which has a less favourable prognosis, is thought to arise in a more primitive haemopoietic cell. This was confirmed recently by studies that demonstrated only the CD34++/CD38− subfraction from Ph+ cases could engraft NOD/SCID mice. However, more recently there has been an increasing body of evidence to suggest that pre B and common ALL may also arise in a cell with a primitive phenotype. We have previously demonstrated that in childhood BCP ALL, the cells capable of long term proliferation in vitro in suspension culture and in vivo to engraft NOD/SCID mice are CD34+/CD10−, CD19−. We then attempted to further define these ALL progenitor cells by investigating the expression of CD133, the primitive stem cell marker. ALL cells capable of long term proliferation in vitro and NOD/SCID engrafting capacity were derived from the CD133+/CD19− subfraction only. These cells were capable of secondary NOD/SCID repopulation, demonstrating they had self-renewal ability. Here, we have attempted to further characterise these ALL progenitor cells to address the question as to whether BCP ALL arises in a common lymphoid progenitor cell or in a more primitive haemopoietic cell. ALL cells from five patients were sorted for CD133+/CD38+ and CD133+/CD38− populations, the sorted subfractions were analysed by cytogenetics and their functional ability was assessed in the NOD/SCID mouse model. Cytogenetic analyses by FISH revealed that both CD133+/CD38+ and CD133+/CD38− subfractions contained the BCR/ABL and ETV6/RUNX1 gene fusions, which had been detected in the patients at diagnosis, and in 1 case with del 17p, this deletion was also noted in the sorted subfractions. These sorted ALL subfractions and unsorted cells were injected intravenously into sublethally irradiated NOD/SCID mice. Bone marrow was harvested at 8–10 weeks post inoculation and analysed for the presence of human cells by flow cytometry. Engraftment was achieved in every case using 2.5x106–107 unsorted cells (0.1–4.5% CD45+). There was no evidence of human cell engraftment in recipients of the CD133+/CD38+ subfraction. However, in each case, engraftment was observed with the CD133+/CD38− subfraction, 0.6–3.2% CD45+ using as few as 6x102–4x104 cells. Using this sorting strategy, we were able to enrich NOD/SCID leukaemia engrafting cells by at least 4 logs compared to the bulk ALL population. Cytogenetic analyses demonstrated that the engrafted cells had the same karyotype as the patients at diagnosis, confirming engraftment of leukaemic cells. These findings suggest that the leukaemia has arisen in a cell with a primitive phenotype, similar to that described for normal haemopoietic stem cells and adds further support to the evidence for a primitive cell origin for B cell precursor ALL. Studies are ongoing to determine whether these primitive ALL cells have the same IgH rearrangements that are detected in the bulk ALL population at diagnosis. This primitive ALL population may be resistant to current chemotherapeutic strategies that are targeted against generic properties of the malignant blasts and subsequent relapses may arise from these cells. Hence, identification and characterisation of these putative ALL stem cells is essential for the development of more effective therapeutic strategies.

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16

Bai, Jian-ying, Yong-tao Yang, Rong Zhu, Yi-qin Wang, Yin Tian, Xiao-huan Li, and Rong-quan Wang. "CpG oligodeoxynucleotides discriminately enhance binding capacity of human naïve B cells to Hepatitis B virus epitopes." Canadian Journal of Microbiology 58, no. 6 (June 2012): 752–59. http://dx.doi.org/10.1139/w2012-045.

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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.

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17

Bunce, C. M., P. J. French, P. Allen, J. C. Mountford, B. Moor, M. F. Greaves, R. H. Michell, and G. Brown. "Comparison of the levels of inositol metabolites in transformed haemopoietic cells and their normal counterparts." Biochemical Journal 289, no. 3 (February 1, 1993): 667–73. http://dx.doi.org/10.1042/bj2890667.

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We have compared the levels of inositol metabolites in three pairs of normal and transformed cells which have been matched with respect to their cell lineage, differentiation and proliferation status: (i) normal human myeloid blast cells and the human promyelocytic leukaemic cell line, HL60; (ii) human umbilical-cord T-helper cells and C8166 cells, a HTLV-1-transformed T-helper cell line; and (iii) an interleukin 3-dependent long-term culture of murine pro-B-cells (BAF3) and BAF3 cells transformed by transfection with the bcr-abl oncogene. Complex patterns of inositol metabolites were present in each of the cell populations. Although there were a number of differences in the levels of certain inositol metabolites between individual cell populations in the paired groups, we did not observe any consistent difference in the levels of inositol metabolites between the proliferating normal and transformed cells. In particular, our data do not support the reported correlation between elevated glycerophosphoinositol (GroPIns) levels and transformation of cells by membrane and cytoplasmic oncogenes which has been reported by other workers. All the cells contained high concentrations of Ins(1,3,4,5,6)P5 (between 12 and 55 microM) and InsP6 (between 37 and 105 microM). The HTLV1-transformed T-helper cells had particularly high levels of total inositol phosphates (predominantly GroPIns, an unidentified inositol bisphosphate and InsP6). The observations are discussed with reference to cell transformation and to the differentiation status of the paired populations.

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18

Coto-Llerena, Mairene, Marco Lepore, Julian Spagnuolo, Daniela Di Blasi, Diego Calabrese, Aleksei Suslov, Glenn Bantug, et al. "Interferon lambda 4 can directly activate human CD19+ B cells and CD8+ T cells." Life Science Alliance 4, no. 1 (November 6, 2020): e201900612. http://dx.doi.org/10.26508/lsa.201900612.

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Compared with the ubiquitous expression of type I (IFNα and IFNβ) interferon receptors, type III (IFNλ) interferon receptors are mainly expressed in epithelial cells of mucosal barriers of the of the intestine and respiratory tract. Consequently, IFNλs are important for innate pathogen defense in the lung and intestine. IFNλs also determine the outcome of hepatitis C virus (HCV) infections, with IFNλ4 inhibiting spontaneous clearance of HCV. Because viral clearance is dependent on T cells, we explored if IFNλs can directly bind to and regulate human T cells. We found that human B cells and CD8+ T cells express the IFNλ receptor and respond to IFNλs, including IFNλ4. IFNλs were not inhibitors but weak stimulators of B- and T-cell responses. Furthermore, IFNλ4 showed neither synergistic nor antagonistic effects in co-stimulatory experiments with IFNλ1 or IFNα. Multidimensional flow cytometry of cells from liver biopsies of hepatitis patients from IFNλ4-producers showed accumulation of activated CD8+ T cells with a central memory-like phenotype. In contrast, CD8+ T cells with a senescent/exhausted phenotype were more abundant in IFNλ4–non-producers. It remains to be elucidated how IFNλ4 promotes CD8 T-cell responses and inhibits the host immunity to HCV infections.

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19

Lee, Young Ik, Jung Me Hwang, Jee Hye Im, Yoon Ik Lee, Nam Soon Kim, Dae Gon Kim, Dae Yeul Yu, Hyung Bae Moon, and Sook Kyung Park. "Human Hepatitis B Virus-X Protein Alters Mitochondrial Function and Physiology in Human Liver Cells." Journal of Biological Chemistry 279, no. 15 (January 14, 2004): 15460–71. http://dx.doi.org/10.1074/jbc.m309280200.

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20

Nitschke, Katja, Hendrik Luxenburger, Muthamia M. Kiraithe, Robert Thimme, and Christoph Neumann-Haefelin. "CD8+ T-Cell Responses in Hepatitis B and C: The (HLA-) A, B, and C of Hepatitis B and C." Digestive Diseases 34, no. 4 (2016): 396–409. http://dx.doi.org/10.1159/000444555.

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Approximately 500 million people are chronically infected with the hepatitis B virus (HBV) or hepatitis C virus (HCV) worldwide and are thus at high risk of progressive liver disease, leading to liver fibrosis, cirrhosis and ultimately hepatocellular cancer. Virus-specific CD8+ T-cells play a major role in viral clearance in >90% of adult patients who clear HBV and in approximately 30% of patients who clear HCV in acute infection. However, several mechanisms contribute to the failure of the adaptive CD8+ T-cell response in those patients who progress to chronic infection. These include viral mutations leading to escape from the CD8+ T-cell response as well as exhaustion and dysfunction of virus-specific CD8+ T-cells. Antiviral efficacy of the virus-specific CD8+ T-cell response also strongly depends on its restriction by specific human leukocyte antigens (HLA) class I alleles. Our review will summarize the role of HLA-A, B and C-restricted CD8+ T-cells in HBV and HCV infection. Due to the current lack of a comprehensive database of HBV- and HCV-specific CD8+ T-cell epitopes, we also provide a summary of the repertoire of currently well-described HBV- and HCV-specific CD8+ T-cell epitopes. A better understanding of the factors that contribute to the success or failure of virus-specific CD8+ T-cells may help to develop new therapeutic options for HBV eradication in patients with chronic HBV infection (therapeutic vaccination and/or immunomodulation) as well as a prophylactic vaccine against HCV infection.

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21

Hagn, Magdalena, Julia Maier, Tatjana Syrovets, Thomas Simmet, and Bernd Jahrsdoerfer. "Specific Induction of Granzyme B in Human B Cells by Viral Antigens." Blood 112, no. 11 (November 16, 2008): 1556. http://dx.doi.org/10.1182/blood.v112.11.1556.1556.

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Abstract B cells are not currently known to produce granzyme B (GrB) in (patho-) physiological settings. We recently reported that B-chronic lymphocytic leukemia cells and normal B cells treated with interleukin-21 (IL-21) and anti-B cell receptor antibodies (anti-BCR) produce functional GrB. Here we demonstrate for the first time that viral antigens can also induce specific peripheral B lymphocytes to produce and secrete substantial amounts of active GrB. Using FACS, ELISpot, immunofluoresence and western blot we show that B cells from subjects recently vaccinated against tick-borne encephalitis virus (TBEV) but not unvaccinated subjects respond to viral TBEV antigens with GrB secretion in a dosedependent manner. This response is direct and occurs only in the presence of co-activation with certain IL-2 family cytokines such as IL-21. Similar results were found with other viruses including hepatitis B and rabies. GrB production in B cells required activation of JAK1 and STAT3 and inhibition of JAK1 by pyridone 6 completely abrogated GrB induction by viral antigens or anti-BCR. Our findings suggest GrB secretion by B cells may be part of a novel, anti-viral immune response mechanism. Further studies will elucidate whether or not granzyme B-secreting B cells can act as cytotoxic cells towards virus-infected cells.

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22

Burwitz, Benjamin J., Patrick K. Hashiguchi, Mandana Mansouri, Christine Meyer, Roxanne M. Gilbride, Sreya Biswas, Jennie L. Womack, et al. "MHC-E–Restricted CD8+ T Cells Target Hepatitis B Virus–Infected Human Hepatocytes." Journal of Immunology 204, no. 8 (March 11, 2020): 2169–76. http://dx.doi.org/10.4049/jimmunol.1900795.

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23

Chen, H. Y., Z. X. Chen, R. F. Huang, N. Lin, and X. Z. Wang. "Hepatitis B virus X protein activates human hepatic stellate cells through upregulating TGFβ1." Genetics and Molecular Research 13, no. 4 (2014): 8645–56. http://dx.doi.org/10.4238/2014.october.27.4.

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24

Xun, Y. H., Y. J. Zhang, Q. C. Pan, R. C. Mao, Y. L. Qin, H. Y. Liu, Y. M. Zhang, et al. "Metformin inhibits hepatitis B virus protein production and replication in human hepatoma cells." Journal of Viral Hepatitis 21, no. 8 (October 24, 2013): 597–603. http://dx.doi.org/10.1111/jvh.12187.

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25

Chen, Mei-Fang, Hsing-Mei Lin, and Chen-Kung Chou. "Insulin Dominantly Suppresses Hepatitis B Virus Gene Expression in Cultured Human Hepatoma Cells." Journal of Biomedical Science 4, no. 6 (1997): 295–99. http://dx.doi.org/10.1159/000456992.

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26

Liang, T. J., W. J. Makdisi, S. Sun, K. Hasegawa, Y. Zhang, J. R. Wands, C. H. Wu, and G. Y. Wu. "Targeted transfection and expression of hepatitis B viral DNA in human hepatoma cells." Journal of Clinical Investigation 91, no. 3 (March 1, 1993): 1241–46. http://dx.doi.org/10.1172/jci116287.

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27

Chen, Mei-Fang, Hsing-Mei Lin, and Chen-Kung Chou. "Insulin dominantly suppresses hepatitis B virus gene expression in cultured human hepatoma cells." Journal of Biomedical Science 4, no. 6 (November 1997): 295–99. http://dx.doi.org/10.1007/bf02258353.

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28

Ning, Bo, and Chiaho Shih. "Nucleolar Localization of Human Hepatitis B Virus Capsid Protein." Journal of Virology 78, no. 24 (December 15, 2004): 13653–68. http://dx.doi.org/10.1128/jvi.78.24.13653-13668.2004.

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ABSTRACT Wild-type human hepatitis B virus (HBV) exhibits selective export of virions containing mature genomes. In contrast, changing an isoleucine to a leucine at amino acid 97 (I97L) of the HBV core antigen (HBcAg) causes it to release immature genomes. To elucidate the structure-function relationship of HBcAg at amino acid 97, we systematically replaced the isoleucine residue at this position with 18 other amino acids via mutagenesis. Twelve of the 18 mutants exhibited no significant phenotype, while five new mutants displayed strong phenotypes. The I97D mutant had a near lethal phenotype, the I97P mutant exhibited a significantly reduced level of virion secretion, and the I97G mutant lacked the full-length relaxed circular form of viral DNA. The tip of the spike of the capsid particle is known to contain a predominant B-cell epitope. However, the recognition of this exposed epitope by an anti-HBc antibody appeared to be affected by the I97E mutation or by histidine tagging at the C terminus of mutant HBcAg, which is presumably in the capsid interior. Surprisingly, the nuclear HBcAg of mutants I97E and I97W, produced from either a replicon or an expression vector, was found to be colocalized with nucleolin and B23 at a frequency of nearly 100% by confocal immunofluorescence microscopy. In contrast, this colocalization occurred with wild-type HBcAg only to a limited extent. We also noted that nucleolin-colocalizing cells were often binucleated or apoptotic, suggesting that the presence of HBcAg in the nucleolus may perturb cytokinesis. The mechanism of this phenomenon and its potential involvement in liver pathogenesis are discussed. To our knowledge, this is the first report of nucleolar HBcAg in culture.

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29

Tong, Shuping, Jisu Li, and Jack R. Wands. "Carboxypeptidase D Is an Avian Hepatitis B Virus Receptor." Journal of Virology 73, no. 10 (October 1, 1999): 8696–702. http://dx.doi.org/10.1128/jvi.73.10.8696-8702.1999.

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ABSTRACT The receptor molecules for human and animal hepatitis B viruses have not been defined. Previous studies have described a 170 to 180 kDa molecule (p170 or gp180) that binds in vitro to the pre-S domain of the large envelope protein of duck hepatitis B virus (DHBV); cDNA cloning revealed the binding protein to be duck carboxypeptidase D (DCPD). In the present study, the DCPD cDNA was transfected into several nonpermissive human-, monkey-, and avian species-derived cell lines. Cells transfected with a plasmid encoding the full-length DCPD protein bound DHBV particles, whereas cells expressing truncated versions of DCPD protein that fail to bind the pre-S protein did not. The DHBV binding to DCPD-reconstituted cells was blocked by a monoclonal antibody that neutralizes DHBV infection of primary duck hepatocytes (PDH) and also by a pre-S peptide previously shown to inhibit DHBV infection of PDH. In addition to promoting virus binding, DCPD expression was associated with internalization of viral particles. The entry process was prevented by incubation of reconstituted cells with DHBV at 4°C and by the addition of energy-depleting agents known to block DHBV entry into PDH. These results demonstrated that DCPD is a DHBV receptor. However, the lack of complete viral replication in DCPD-reconstituted cells suggested that additional factors are required for postentry events in immortalized cell lines.

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30

Kotsianidis, Ioannis, Scott Patterson, Marianna Politou, Antonio Almeida, Despoina Pantelidou, Costas Tsatalas, George Bourikas, Irene Roberts, and Anastasios Karadimitris. "Evidence That Human NKT Cells Enhance Haemopoiesis through Recognition of CD1d Expressed in Haemopoietic Stem Cells with Long Term Clonogenic Capacity." Blood 104, no. 11 (November 16, 2004): 4129. http://dx.doi.org/10.1182/blood.v104.11.4129.4129.

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Abstract NKT cells, a novel class of regulatory T cells, secrete haemopoietic cytokines (GM-CSF, IL-3, IL-6) upon engagement of their TCR. Because of this property we hypothesized that NKT cells are involved in the regulation of haemopoiesis. NKT cells constitute <0.1% of T cells in blood, bone marrow and cord blood and are restricted by the glycolipid-presenting, non-polymorphic MHC-like molecule CD1d. CD1d is expressed in antigen presenting cells, thymocytes and in a variety of epithelial tissues including keratinocytes and enterocytes, but its expression in haematopoietic stem cells (HSC) has not been studied. Therefore we studied first the expression and function of CD1d in haemopoietic stem cells. Using multi-colour flow cytometry, we show that 1% of MACS-selected cord blood CD34+ cells are CD1d+ (n=6, range 0.4–1.67%). CD1d+CD34+ HSC express a variety of surface markers indicative of primitive HSC: CD7: 36.1% (35.6–36.4%), CD133: 68% (46.2–81.54%), CD117:74.2% (51–85.5%) and CD90 (Thy-1): 32.3% (26.7–39.1%); moreover, 6,2% (1.9–10.5%) and 12,8% (10.1–16%) of CD1d+CD34+ are CD1d+CD34+HLADR− and CD1d+CD34+CD38− respectively, consistent with an immature HSC phenotype. Expression of these markers by CD1d−CD34+ were identical to CD1d+CD34+ cells. Consistent with this, in long-term colony initiating cell (LTC-IC) assays (n=4), highly purified, flow-sorted, lineage-depleted (Stem Cell Technologies) Lin-CD1d+CD34+ HSC displayed a LTC-IC frequency of 1 in 35.7 cells (range 24.4–38) equivalent to those of CD1d−CD34+ HSC: LTC-IC frequency of 1 in 25.4 cells (range 20–30.3). Short term CFC activity of Lin−CD34+CD1d+ is slightly lower than their Lin−CD1d−CD34+ counterparts: 1 CFC per 15.3 cells (7.7–37.7) versus 1 CFC per 4.2 cells (3.8–5), respectively. To investigate the effect of cord blood NKT cells on the CFC activity of CD34+ cells, NKT were first activated ex vivo for 10 days in the presence of the CD1d-presented glycolipid a-galactosylceramide and subsequently were purified by flow-sorting using mAbs specific to their TCR a and b chains, i.e., anti-TCR Va24 and Vb11. Purified NKT were co-cultured in a ratio of 10:1 with CD34+ cells. In the absence of exogenous cytokines NKT enhanced the clonogenic capacity of CD34+ cells by 3-fold: 1 CFC per 14 cells (range 10.4–21) in the presence of NKT vs 1 per 43 cells (range 37–55.5) in the absence of NKT (n=4; p=0.024). By contrast, activated or resting autologous T cells co-cultured with CD34+ cells at the same ratio (10:1) had no effect on the CFC frequency, indicating that this enhancing effect on haemopoiesis is a unique property of NKT cells. The effect of NKT in the long-term clonogenic capacity is currently being evaluated. In summary, we have shown that a) CD1d is a novel marker expressed in HSC with long- and short -term clonogenic ability and b) CD1d-restricted NKT cells promote haemopoiesis These findings reveal a novel link between haemopoiesis and the CD1d-NKT axis of immune regulation and set the scene for the study of the role of NKT cells in the processes of engraftment and rejection in HSC transplantation.

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31

Park, Sung Gyoo, and Guhung Jung. "Human Hepatitis B Virus Polymerase Interacts with the Molecular Chaperonin Hsp60." Journal of Virology 75, no. 15 (August 1, 2001): 6962–68. http://dx.doi.org/10.1128/jvi.75.15.6962-6968.2001.

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ABSTRACT Previous studies showed that hepatitis B virus polymerase (HBV Pol) interacts with host factors such as the Hsp90 complex, which is a critical step in viral genome replication. In this report, we propose that another chaperone, Hsp60, interacts with human HBV Pol and that this is a very important step for maturation of human HBV Pol into the active state. In the immunoprecipitation of recombinant human HBV Pol expressed in insect cells with the recombinant baculovirus expression system, the 60-kDa protein was coimmunoprecipitated with Pol and the protein was identified as Hsp60 through peptide sequencing and immunogenic analysis with an anti-Hsp60 antibody. In vitro experiments showed that Hsp60 strongly affected human HBV Pol activity in that (i) blocking of Hsp60 by the protein-specific antibody reduced human HBV Pol activity, (ii) the activity was increased by addition of Hsp60 in the presence of ATP, and (iii) ATP synergistically activated human HBV Pol with Hsp60. In vivo experiments showed that inhibition of Hsp60 in cells by a mutant Hsp60, CΔ540, resulted in the reduction of human HBV Pol activity. In summary, our results indicate that the interaction is significant for conversion of human HBV Pol into the active state.

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Lou, XiaoLi, YanQiang Hou, and DongYu Liang. "Effects of hepatitis B virus X protein on human T cell cytokines." Canadian Journal of Microbiology 59, no. 9 (September 2013): 620–26. http://dx.doi.org/10.1139/cjm-2013-0259.

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Chronic infection with hepatitis B virus (HBV) plays a significant role in hepatocellular carcinoma development. To investigate the effect of hepatitis B virus X protein (HBx) on inflammatory cytokines of human T cell, a eukaryotic expression vector, HBx-pEGFP-C1, was constructed and transfected into the Jurkat human T-cell line. Jurkat cells were transfected transiently using Lipofectamine 2000 and activated by phytohemagglutinin (PHA). Interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), IL-4, IL-10, IL-13, and IL-14 mRNA was measured. The results showed that the vector HBx-pEGFP-C1 was successfully constructed, and HBx was expressed in Jurkat cells. Compared with a control group, mRNA of IL-1β and TNF-α was significantly elevated in the HBx-pEGFP-C1 group (p < 0.05), while IL-4, IL-10, IL-13, and IL-14 mRNA was decreased (p < 0.05). Therefore, transient overexpression of HBx promoted PHA-induced pro-inflammatory cytokine secretion and repressed anti-inflammatory cytokine secretion in human T cells.

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Jameel, S., and A. Siddiqui. "The human hepatitis B virus enhancer requires trans-acting cellular factor(s) for activity." Molecular and Cellular Biology 6, no. 2 (February 1986): 710–15. http://dx.doi.org/10.1128/mcb.6.2.710-715.1986.

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The activity of the hepatitis B viral enhancer element was studied in various cell lines. This enhancer shows strict host and tissue specificity in that it is functional only in liver cells of human origin. Further, it requires trans-acting factor(s) present in liver cells for activity, and this activity is independent of hepatitis B virus gene products in the cell lines tested.

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Jameel, S., and A. Siddiqui. "The human hepatitis B virus enhancer requires trans-acting cellular factor(s) for activity." Molecular and Cellular Biology 6, no. 2 (February 1986): 710–15. http://dx.doi.org/10.1128/mcb.6.2.710.

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The activity of the hepatitis B viral enhancer element was studied in various cell lines. This enhancer shows strict host and tissue specificity in that it is functional only in liver cells of human origin. Further, it requires trans-acting factor(s) present in liver cells for activity, and this activity is independent of hepatitis B virus gene products in the cell lines tested.

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Schilling, Ralf, Samreen Ijaz, Michail Davidoff, Jia Yee Lee, Stephen Locarnini, Roger Williams, and Nikolai V. Naoumov. "Endocytosis of Hepatitis B Immune Globulin into Hepatocytes Inhibits the Secretion of Hepatitis B Virus Surface Antigen and Virions." Journal of Virology 77, no. 16 (August 15, 2003): 8882–92. http://dx.doi.org/10.1128/jvi.77.16.8882-8892.2003.

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ABSTRACT Hepatitis B immunoglobulin is used for prophylaxis against hepatitis B virus (HBV) and is thought to act by neutralization of virions and hepatitis B virus surface antigen (HBsAg)-containing particles in circulation. Using a panel of hepatocyte-derived cell lines, the present study investigated in vitro whether HBs-specific immunoglobulin G (IgG) is internalized in hepatocytes and whether it interacts with HBsAg in the cells. By immunoelectron microscopy and immunoblotting, human IgG and FcRn receptor for IgG were demonstrated on cellular membranes and in cytoplasmic extracts, irrespective of the HBsAg status of the cells. Furthermore, HBsAg and anti-HBs were shown to be colocalized in the same cellular compartment by two-color confocal microscopy. Endocytosis of HBs-specific IgG caused intracellular accumulation of HBsAg in a dose-dependent manner and inhibited the secretion of HBsAg and HBV virions from the cells. These effects were not observed with F(ab)2 fragments or nonimmune IgG as controls. The specificity of intracellular HBsAg- anti-HBs interaction was further investigated in cells transfected with HBV genomes expressing wild-type HBsAg or immune escape HBsAg (with a G145R mutation). Monoclonal anti-HBs markedly reduced the secretion of wild-type HBsAg, while the secretion of mutant HBsAg was not affected. These results suggest that HBs-specific IgG binds to hepatocytes and interacts with HBsAg within the cells. This may be relevant for the selection of surface antibody escape mutations.

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Baldus, Stephan E., Thomas K. Zirbes, Ion-Corin Weidner, Uta Flucke, Elke Dittmar, Juergen Thiele, and Hans P. Dienes. "Comparative Quantitative Analysis of Macrophage Populations Defined by CD68 and Carbohydrate Antigens in Normal and Pathologically Altered Human Liver Tissue." Analytical Cellular Pathology 16, no. 3 (1998): 141–50. http://dx.doi.org/10.1155/1998/192975.

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Liver macrophages, which are involved in the different types of hepatitis, may indirectly induce hepatic fibrogenesis, since they have the possibility to activate hepatic stellate cells and fibroblasts by secretion of TGF-β , TNF-α and IL-1. To evaluate variations of the number of liver macrophages and their subpopulations, a quantification was carried out in normal human liver tissue, fatty liver, fatty liver hepatitis and hepatitis B. Identification was performed by the mab PG-M1 (anti-CD68) and, comparatively, four lectins,Griffonia simplicifoliaagglutinin I (GSA-I),Erythrina cristagalliagglutinin (ECA), peanut agglutinin (PNA) and soybean agglutinin (SBA). A slight decrease in the frequency of macrophages in pericentral fields was observable in fatty liver and fatty liver hepatitis as compared to normal liver tissue. On the other hand, the number of CD68+cells was significantly enhanced in hepatitis B with moderate and severe inflammatory activity. The highest incidence of macrophages was found in portal tracts of liver with fatty liver hepatitis and, particularly, hepatitis B. The fraction of cells stained by ECA, PNA or SBA did not increase significantly under pathological conditions. In contrast, the percentage of GSA-I binding macrophages was higher in liver parenchyma of hepatitis B and in portal tract macrophages in fatty liver hepatitis and also hepatitis B. In conclusion, our results indicate that GSA-I may aid in the detection of the subpopulation of activated macrophages which are assumed to play a pivotal role in liver pathology.

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Urata, Noboru, Tsunamasa Watanabe, Noboru Hirashima, Yoshiyuki Yokomaku, Junji Imamura, Yasumasa Iwatani, Masaaki Shimada, and Yasuhito Tanaka. "Cytokines and Chemokines Involved in Hepatitis B Surface Antigen Loss in Human Immunodeficiency Virus/Hepatitis B Virus Coinfected Patients." Journal of Clinical Medicine 10, no. 4 (February 18, 2021): 833. http://dx.doi.org/10.3390/jcm10040833.

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It has been reported that hepatic flare (HF), attributable to the development of immune reconstitution inflammatory syndrome (IRIS) in human immunodeficiency virus (HIV)/hepatitis B virus (HBV) coinfected patients, occurs frequently after the start of anti-retroviral therapy (ART). We have observed several cases of hepatitis B surface antigen (HBsAg) loss after IRIS. However, the factors leading to HBsAg clearance remain unknown. We measured CD4+ and CD8+ T cells, cytokines and chemokines in 16 patients coinfected HIV-1 and HBV with IRIS, and analyzed the factors leading to HBsAg clearance after IRIS. There was no significant difference in the CD4+ and CD8+ T cell counts between the HBsAg clearance and non-clearance groups, while the serum concentrations of almost all cytokines and chemokines in the HBsAg clearance group were higher than in the HBsAg non-clearance group at any time of observation. In particular, IP-10 at the ALT peak, GM-CSF and IL-12 one month after the ALT peak and TNF-α and GM-CSF after the ALT concentrations fell to within normal limits, were significantly higher in the HBsAg clearance group. It seems that HBsAg loss after IRIS requires continued immune responses against HBV, involving Th1 cytokines.

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Iser, David M., Nadia Warner, Peter A. Revill, Ajantha Solomon, Fiona Wightman, Suha Saleh, Megan Crane, et al. "Coinfection of Hepatic Cell Lines with Human Immunodeficiency Virus and Hepatitis B Virus Leads to an Increase in Intracellular Hepatitis B Surface Antigen." Journal of Virology 84, no. 12 (March 31, 2010): 5860–67. http://dx.doi.org/10.1128/jvi.02594-09.

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ABSTRACT Liver-related mortality is increased in the setting of HIV-hepatitis B virus (HBV) coinfection. However, interactions between HIV and HBV to explain this observation have not been described. We hypothesized that HIV infection of hepatocytes directly affects the life cycle of HBV. We infected human hepatic cell lines expressing HBV (Hep3B and AD38 cells) or not expressing HBV (Huh7, HepG2, and AD43 cells) with laboratory strains of HIV (NL4-3 and AD8), as well as a vesicular stomatitis virus (VSV)-pseudotyped HIV expressing enhanced green fluorescent protein (EGFP). Following HIV infection with NL4-3 or AD8 in hepatic cell lines, we observed a significant increase in HIV reverse transcriptase activity which was infectious. Despite no detection of surface CD4, CCR5, and CXCR4 by flow cytometry, AD8 infection of AD38 cells was inhibited by maraviroc and NL4-3 was inhibited by AMD3100, demonstrating that HIV enters AD38 hepatic cell lines via CCR5 or CXCR4. High-level infection of AD38 cells (50%) was achieved using VSV-pseudotyped HIV. Coinfection of the AD38 cell line with HIV did not alter the HBV DNA amount or species as determined by Southern blotting or nucleic acid signal amplification. However, coinfection with HIV was associated with a significant increase in intracellular HBsAg when measured by Western blotting, quantitative HBsAg, and fluorescence microscopy. We conclude that HIV infection of HBV-infected hepatic cell lines significantly increased intracellular HBsAg but not HBV DNA synthesis and that increased intrahepatic HBsAg secondary to direct infection by HIV may contribute to accelerated liver disease in HIV-HBV-coinfected individuals.

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Li, Yao, Yuchen Xia, Xiaoming Cheng, David E. Kleiner, Stephen M. Hewitt, Julia Sproch, Tong Li, Hui Zhuang, and T. Jake Liang. "Hepatitis B Surface Antigen Activates Unfolded Protein Response in Forming Ground Glass Hepatocytes of Chronic Hepatitis B." Viruses 11, no. 4 (April 25, 2019): 386. http://dx.doi.org/10.3390/v11040386.

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Ground glass hepatocytes (GGHs), a histological hallmark of chronic hepatitis B virus (HBV) infection, contain excessive hepatitis surface antigen (HBsAg) in the endoplasmic reticulum (ER), which is linked to unfolded protein response (UPR). The mechanism by which HBV activates UPR has not been fully defined. To investigate this, HepG2-NTCP cells and primary human hepatocytes (PHHs) were either infected with HBV or transduced with adenoviral vectors expressing replication-competent HBV genome or individual HBV genes. UPR markers were evaluated by qPCR, Western blotting, and immunofluorescence. Apoptosis and cell viability were measured by Caspase-3/7 and ATPlite assay respectively. We found that UPR markers were induced by the overexpression of HBsAg in HepG2-NTCP cells and PHHs. Elevation of UPR-induced genes showed a dose-dependent correlation with HBsAg levels. In HBV-infected livers, GGHs also demonstrated excessive accumulation of HBsAg associated with increased BIP/GRP78 staining, a marker of UPR. Prolonged activation of UPR by HBsAg overexpression induced signs of apoptosis. Overexpression of HBsAg can induce ER stress through protein kinase RNA-like endoplasmic reticulum kinase (PERK) pathway in vitro, and may be linked to the appearance of GGHs. The activation of UPR by HBsAg may sensitize hepatocytes to cell death and result in possible subsequent cellular changes leading to a premalignant phenotype.

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Chen, Hua-Chien, Chen-Kung Chou, Chang-Ming Sun, and Sheau Farn Yeh. "Suppressive effects of destruxin B on hepatitis B virus surface antigen gene expression in human hepatoma cells." Antiviral Research 34, no. 3 (May 1997): 137–44. http://dx.doi.org/10.1016/s0166-3542(97)01031-0.

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41

Biasco, Luca, Cristina Baricordi, Stefania Merella, Cynthia Bartholomae, Alessandro Ambrosi, Danilo Pellin, Clelia Di Serio, Christof Von Kalle, Manfred Schmidt, and Alessandro Aiuti. "Uncovering Haematopoietic System Dynamics and Single Multipotent Progenitors Activity In Vivo In Humans by Retroviral Tagging." Blood 116, no. 21 (November 19, 2010): 2611. http://dx.doi.org/10.1182/blood.v116.21.2611.2611.

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Abstract Abstract 2611 The long-standing model of human haematopoiesis postulates that myeloid and lymphoid lineages branch separately at very early stages, producing myeloid or erythroid cells and T or B cells, respectively. Conversely, a revised scheme of haematopoietic hierarchy was recently proposed, in which myeloid cells represent a prototype of blood cells, while erythroid, T and B cells are specialized cell types. The validity of these models has been mainly tested in vivo in the mouse, and in vitro through clonal assays on human haemopoietic stem cells (HSC). However, a clear definitive elucidation of the real nature of human haemopoiesis should ideally involve the ability to track the dynamics, survival and differentiation potential of haemopoietic progenitor clones for a long period of time directly in vivo in humans. Upon retroviral gene transfer, transduced cells are univocally tagged by vector insertions allowing them to be distinguished and tracked in vivo by integration profiling. We previously showed that gene therapy (GT) for adenosine deaminase (ADA) deficient SCID based on infusion of transduced CD34+ cells and reduced intensity conditioning, resulted in full multilineage engraftment, in the absence of aberrant expansions. Therefore, long-term studies in these patients provide a unique human model to study in depth haemopoietic clonal dynamics by retroviral tagging. For this reason, we performed a comprehensive multilineage longitudinal insertion profile of bone marrow (BM) (CD34+, CD15+, CD19+, Glycophorin+) and peripheral blood (PB) (CD15+, CD19+, CD4+, CD8+ cells, naïve and memory T cell subpopulations) cells in 4 patients 3–6 years after GT, retrieving to date 1055 and 1999 insertions from BM and PB cell lineages respectively. We could shape the insertional landscape of each lineage through a tri-factorial analysis based on the number of integrations retrieved, the percentage of vector positive cells and the number of insertion shared with other lineages. We were able to uncover the effects of selective advantages of gene-corrected cells in periphery and the frequency of identical integrants in different haematopoietic compartments. BM cells displayed the highest proportion of shared integrants (up to 58.1%), reflecting the real-time repopulating activity of gene-corrected progenitors. On the other hand, PB samples carried in general a higher frequency of vector positive cells, with the exception of PB CD15+ cells showing insertional landscapes very similar to the one of BM lineages. Interestingly, the detection of exclusively shared myeloid-T\B or myeloid-erythroid integrants may be supportive of a myeloid-based haemopoiesis model. We also uncovered “core integrants”, shared between CD34+ cells and both lymphoid and myeloid lineages, stably tagging active long-term multipotent progenitors overtime. Strikingly, one of these progenitor clones carried an insertion inside one of the two fragile sites of MLLT3 gene, involved by translocation events in mixed lineage leukemia. We were able to track this and another integrant (downstream the LRRC30 gene) by specific PCRs, confirming the multilineage contribution to haematopoiesis of the relative progenitor clones and their fluctuating lineage outputs over 4 years, without showing aberrant expansions. We also retrieved 170 and 174 integrations from 4 T cell subtypes (Naive, TEMRA, Central and Effector memory) in two patients under PBL-GT and HSC-GT respectively. We found evidences that single naive T cell clones may survive in patients for up to 10 years after last infusion while maintaining their differentiation capacity into different T cell subpopulations. Interestingly, a cluster of 4 insertions (one of them shared among all T cell subtypes) was found in proximity of the interferon regulatory factor 2 binding protein 2 (IRF2BP2) gene in naive T cells from PBL-GT patient, thus suggesting an influence of transcriptional activity of this region on selective advantage of gene-corrected lymphocytes. In conclusion, through retroviral tagging, we can uniquely track single transduced haemopoietic cells directly in vivo in humans. The application of mathematical models to our insertion datasets is allowing to uncover new information on the fate and activity of haematopoietic progenitors and their differentiated progeny years after transplantation in GT patients. Disclosures: No relevant conflicts of interest to declare.

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Köck, Josef, and Hubert E. Blum. "Hypermutation of hepatitis B virus genomes by APOBEC3G, APOBEC3C and APOBEC3H." Journal of General Virology 89, no. 5 (May 1, 2008): 1184–91. http://dx.doi.org/10.1099/vir.0.83507-0.

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Hepatitis B virus (HBV) is a DNA virus that causes liver disease and replicates by reverse transcription of an RNA template. Previous studies have reported that HBV genomes bearing G→A hypermutation are present at low frequency in human serum. These mutations are most likely due to the activity of apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like (APOBEC) cytosine deaminases, cellular proteins known to confer innate immunity against retroviruses by generating lethal hypermutations in viral genomes. This study assessed APOBEC3G, APOBEC3C and APOBEC3H, three members of this protein family present in human liver, for their ability to edit HBV genomes. Transfection of human HepG2 hepatoma cells with a plasmid encoding the APOBEC3C protein resulted in abundant G→A mutations in the majority of newly formed HBV genomes. By contrast, transfection of APOBEC3G- and APOBEC3H-encoding plasmids only marginally increased hypermutation rates above the level caused by the cytosine deaminases naturally present in HepG2 cells. APOBEC3G- and APOBEC3H-mediated hypermutation, however, was clearly revealed by transfection of chicken LMH hepatoma cells, which lack endogenous cytosine deaminases. These results indicate that APOBEC3G, APOBEC3C and APOBEC3H have the ability to edit HBV DNA and that each protein is likely to contribute to various degrees to the generation of modified genomes in human liver cells.

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Uchida, Takuro, Nobuhiko Hiraga, Michio Imamura, Masataka Tsuge, Hiromi Abe, C. Nelson Hayes, Hiroshi Aikata, et al. "Human Cytotoxic T Lymphocyte-Mediated Acute Liver Failure and Rescue by Immunoglobulin in Human Hepatocyte Transplant TK-NOG Mice." Journal of Virology 89, no. 19 (August 5, 2015): 10087–96. http://dx.doi.org/10.1128/jvi.01126-15.

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ABSTRACTHepatitis B virus (HBV)-specific cytotoxic T lymphocytes (CTLs) are critical in eliminating infection. We developed an animal model in which HBV-infected human hepatocytes are targeted by HBV-specific CTLs. After HBV inoculation in human hepatocyte-transplanted herpes simplex virus type-1 thymidine kinase-NOG mice, human peripheral blood mononuclear cells (PBMCs) were administered, and albumin, HBV DNA, alanine aminotransferase (ALT), and cytokine levels were analyzed. Histopathological and flow-cytometric analysis of infiltrating human immune cells were performed, and the efficacy of CTL-associated antigen-4 immunoglobulin (CTLA4Ig) against liver damage was evaluated. PBMC treatment resulted in massive hepatocyte damage with elevation of ALT, granzyme A, and gamma interferon and decrease in albumin and HBV DNA. The number of liver-infiltrating human lymphocytes and CD8-positive cells was significantly higher in HBV-infected mice. HBV-specific CTLs were detected by core and polymerase peptide-major histocompatibility complex-tetramer, and the population of regulatory T cells was significantly decreased in HBV-infected mice. Serum hepatitis B surface (HBs) antigen became negative, and HBs antibody appeared. CTLA4Ig treatment strongly inhibited infiltration of mononuclear cells. CTLA4Ig treatment will be used to treat patients who develop severe acute hepatitis B to prevent liver transplantation or lethality. This animal model is useful for virological and immunological analysis of HBV infection and to develop new therapies for severe acute hepatitis B.IMPORTANCEWithout liver transplantation, some HBV-infected patients will die from severe liver damage due to acute overreaction of the immune system. No effective treatment exists, due in part to the lack of a suitable animal model. An animal model is necessary to investigate the mechanism of hepatitis and to develop therapeutic strategies to prevent acute liver failure in HBV infection. We developed an animal model in which HBV-infected human hepatocytes are targeted by human HBV-specific CTLs. In this model, HBV-infected human hepatocytes were transplanted into severely immunodeficient NOG mice in order to reconstruct elements of the human immune system. Using this model, we found that CTL-associated antigen-4 immunoglobulin was able to suppress damage to HBV-infected hepatocytes, suggesting an approach to treatment. This animal model is useful for virological and immunological analysis of HBV infection and to develop new therapies for severe acute hepatitis B.

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Evripioti, Antonia Alexandra, Ana Maria Ortega-Prieto, Jessica Katy Skelton, Quentin Bazot, and Marcus Dorner. "Phosphodiesterase-induced cAMP degradation restricts hepatitis B virus infection." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1773 (April 8, 2019): 20180292. http://dx.doi.org/10.1098/rstb.2018.0292.

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Hepatitis B virus (HBV) entry into hepatocytes is mediated via a high-affinity interaction between the preS1 glycoprotein and sodium/bile acid cotransporting polypeptide (NTCP). To date, in vitro model systems rely on high multiplicities of infection to achieve infection of cell lines overexpressing human NTCP. This study investigates a novel regulatory pathway for NTCP trafficking to the cell surface, induced by DMSO-mediated cellular differentiation. DMSO rapidly induces high cell surface expression of NTCP and results in increased susceptibility of cells to HBV infection. Additionally, DMSO treatment induces actin, as well as Tubulin reshaping within the cells. We show that direct disruption of the actin and Tubulin network directly enhances NTCP expression and the subsequent susceptibility of cells to HBV infection. DMSO induces these changes via alterations in the levels of cyclic (c)AMP, which participates in the observed actin rearrangements. Blocking of phosphodiesterases (PDEs), which degrade accumulated cAMP, had the same effect as DMSO differentiation and demonstrates that DMSO prevents phosphodiesterase-mediated cAMP degradation. This identifies adenylate cyclase as a novel target for blocking the entry of HBV via targeting the cell surface accumulation of NTCP. This article is part of the theme issue ‘Silent cancer agents: multi-disciplinary modelling of human DNA oncoviruses’.

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Mancini-Bourgine, Maryline, Florence Bayard, Patrick Soussan, Qiang Deng, Yu-Chun Lone, Dina Kremsdorf, and Marie-Louise Michel. "Hepatitis B Virus Splice-Generated Protein Induces T-Cell Responses in HLA-Transgenic Mice and Hepatitis B Virus-Infected Patients." Journal of Virology 81, no. 10 (March 14, 2007): 4963–72. http://dx.doi.org/10.1128/jvi.02619-06.

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ABSTRACT Hepatitis B virus splice-generated protein (HBSP), encoded by a spliced hepatitis B virus RNA, was recently identified in liver biopsy specimens from patients with chronic active hepatitis B. We investigated the possible generation of immunogenic peptides by the processing of this protein in vivo. We identified a panel of potential epitopes in HBSP by using predictive computational algorithms for peptide binding to HLA molecules. We used transgenic mice devoid of murine major histocompatibility complex (MHC) class I molecules and positive for human MHC class I molecules to characterize immune responses specific for HBSP. Two HLA-A2-restricted peptides and one immunodominant HLA-B7-restricted epitope were identified following the immunization of mice with DNA vectors encoding HBSP. Most importantly, a set of overlapping peptides covering the HBSP sequence induced significant HBSP-specific T-cell responses in peripheral blood mononuclear cells from patients with chronic hepatitis B. The response was multispecific, as several epitopes were recognized by CD8+ and CD4+ human T cells. This study provides the first evidence that this protein generated in vivo from an alternative reading frame of the hepatitis B virus genome activates T-cell responses in hepatitis B virus-infected patients. Given that hepatitis B is an immune response-mediated disease, the detection of T-cell responses directed against HBSP in patients with chronic hepatitis B suggests a potential role for this protein in liver disease progression.

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WEI, JINGCHEN, LIANKU LIN, XIAOJIAN SU, SHAOYAN QIN, QING XU, ZUNIAN TANG, YAN DENG, YUEHAN ZHOU, and SONGQING HE. "Anti-hepatitis B virus activity of Boehmeria nivea leaf extracts in human HepG2.2.15 cells." Biomedical Reports 2, no. 1 (November 22, 2013): 147–51. http://dx.doi.org/10.3892/br.2013.205.

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Lee, Jiahong, Yusi Zhou, Mingxuan Wang, and Wei Ning Chen. "Inhibitory Effect of Bovine Lactoferrin on Human Hepatitis B Virus Replication in HepG2.2.15 Cells." BIO 1, no. 1 (May 12, 2011): 64–66. http://dx.doi.org/10.5618/bio.2011.v1.n1.3.

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Ho, Li-Kang, Ming-Jaw Don, Hua-Chien Chen, Sheau-Farn Yeh, and Jau-Ming Chen. "Inhibition of Hepatitis B Surface Antigen Secretion on Human Hepatoma Cells. Components fromRubia cordifolia." Journal of Natural Products 59, no. 3 (January 1996): 330–33. http://dx.doi.org/10.1021/np960200h.

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Zhang, Wei-ying, Fu-qing Xu, Chang-liang Shan, Rong Xiang, Li-hong Ye, and Xiao-dong Zhang. "Gene expression profiles of human liver cells mediated by hepatitis B virus X protein." Acta Pharmacologica Sinica 30, no. 4 (April 2009): 424–34. http://dx.doi.org/10.1038/aps.2009.22.

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Hong, Seung-Ho, Okki Cho, Koyngmin Kim, Ho-Joon Shin, Sergei V. Kotenko, and Sun Park. "Effect of interferon-lambda on replication of hepatitis B virus in human hepatoma cells." Virus Research 126, no. 1-2 (June 2007): 245–49. http://dx.doi.org/10.1016/j.virusres.2007.03.006.

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