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1. Treatment Options for Epstein-Barr Virus-Related Disorders of the Central Nervous System

Author

Andersen O, Ernberg I, and Hedström AK

Subjects
epstein-barr virus, infectious mononucleosis, central nervous system disease, multiple sclerosis, treatment, vaccination, Infectious and parasitic diseases, RC109-216
Abstract

Oluf Andersen,1 Ingemar Ernberg,2 Anna Karin Hedström3 1Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; 2Department of Microbiology, Tumor and Cell Biology, Biomedicum Q8C, Karolinska Institutet, Stockholm, 171 77, Sweden; 3Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, SwedenCorrespondence: Anna Karin Hedström, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, 171 76, Sweden, Tel +46762736426, Email anna.hedstrom@ki.seAbstract: Epstein-Barr virus (EBV), a causative agent for several types of lymphomas and mucosal cancers, is a human lymphotropic herpesvirus with the capacity to establish lifelong latent infection. More than 90% of the human population worldwide is infected. The primary infection is usually asymptomatic in childhood, whereas infectious mononucleosis (IM) is common when the infection occurs in adolescence. Primary EBV infection, with or without IM, or reactivation of latent infection in immunocompromised individuals have been associated with a wide range of neurologic conditions, such as encephalitis, meningitis, acute disseminated encephalomyelitis, and cerebellitis. EBV is also involved in malignant lymphomas in the brain. An increasing number of reports on EBV-related disorders of the central nervous system (CNS) including the convincing association with multiple sclerosis (MS) have put in focus EBV-related conditions beyond its established link to malignancies. In this review, we present the clinical manifestations of EBV-related CNS-disorders, put them in the context of known EBV biology and focus on available treatment options and future therapeutic approaches.Keywords: Epstein-Barr virus, infectious mononucleosis, central nervous system disease, multiple sclerosis, treatment, vaccination

Published
2023

5. Epstein-Barr Virus Latency and Activation in Vivo

Author

Ernberg, I., Compans, R. W., editor, Cooper, M., editor, Koprowski, H., editor, McConnell, I., editor, Melchers, F., editor, Nussenzweig, V., editor, Oldstone, M., editor, Olsnes, S., editor, Potter, M., editor, Saedler, H., editor, Vogt, P. K., editor, Wagner, H., editor, Wilson, I., editor, Potter, Michael, editor, and Melchers, Fritz, editor

Published
1990
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15. Epstein-Barr Virus Gene Expression During Primary B-Lymphocyte Infection, in Transformed and Burkitt Lymphoma-Derived Cell Lines

Author

Ernberg, I., Kallin, B., Dillner, J., Clarke, A., editor, Compans, R. W., editor, Cooper, M., editor, Eisen, H., editor, Goebel, W., editor, Koprowski, H., editor, Melchers, F., editor, Oldstone, M., editor, Vogt, P. K., editor, Wagner, H., editor, Wilson, I., editor, Melchers, Fritz, editor, and Potter, Michael, editor

Published
1986
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19. P11

Author

Tsidulko, A., primary, Matskova, L., additional, Astakhova, L., additional, Ernberg, I., additional, and Grigorieva, E., additional

Published
2015
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21. SYK interaction with ITGβ4 suppressed by Epstein-Barr virus LMP2A modulates migration and invasion of nasopharyngeal carcinoma cells

Author

Zhou, X, primary, Matskova, L, additional, Rathje, L-S Z, additional, Xiao, X, additional, Gish, G, additional, Werner, M, additional, Ignatyev, I, additional, Yu, N, additional, Zhao, W, additional, Tian, F, additional, Hou, B, additional, Zhang, Z, additional, Pawson, T, additional, Chen, F, additional, and Ernberg, I, additional

Published
2014
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23. Differences in the immunogenicity of latent membrane protein 1 (LMP1) encoded by Epstein-Barr virus genomes derived from LMP1-positive and -negative nasopharyngeal carcinoma

Author

L. F., Hu, Troyanovsky, B., Zhang, X. N., Trivedi, Pankaj, Ernberg, I., and Klein, G.

Subjects
Viral Matrix Proteins, B-Lymphocytes, Herpesvirus 4, Human, Mice, Mutation, Animals, Humans, Mammary Neoplasms, Experimental, Mice, Nude, Nasopharyngeal Neoplasms, Genome, Viral
Abstract

We have previously shown that an EBV-encoded latent membrane protein 1 (LMP1) gene derived from a nude mouse-propagated nasopharyngeal carcinoma (NPC) tumor and expressed in nonimmunogenic murine mammary carcinoma S6C cells failed to convey immunogenicity (rejectability) in syngeneic mice, whereas the corresponding B-cell derived LMP1 gene made the mice highly immunogenic. This raised the question of whether LMPL-expressing NPCs have been selected for low immunogenicity at the viral gene expression level. If so, LMP1-negative tumors that carry highly methylated LMP1 regulatory sequences may not have been exposed to a similar immunoselection. In the present study, we have compared LMP1 genes derived from two LMP1-positive NPCs and two LMP1-negative NPCs. All four genes were expressed in S6C cells in parallel with the previously tested isolates from a B-cell (B95-8)-derived and a nude mouse-propagated NPC (Cao)-derived gene. As in the previous study, we have found that the B-cell-derived LMP1 isolate was highly immunogenic. LMP1-positive tumor-derived isolates were poorly immunogenic, whereas the isolates from the LMP1-negative NPC tumor had intermediate immunogenicity. Sequence data revealed that LMP1 genes from LMP1-expressing NPC had 16 amino acid substitutions, whereas LMP1 from non-LMP1-expressing NPC had only 9 amino acid changes in the coding region. Three of the changes were at shared sites, but with different modifications. The fact that the gene from non-LMP1-expressing NPC mutated at a low frequency but was more immunogenic than the LMP1 gene derived from LMP1-expressing NPC, which was highly mutated but less immunogenic, favors the idea that LMP1-positive tumors escape immunosurveillance in immunocompetent hosts by either a selective down-regulation of LMP1 expression, methylation in the LMP1 promoter sequence, or mutation of LMP1 in LMP1-expressing samples.

Published
2000

27. Expression of Epstein-Barr-virus-related nuclear antigens and B-cell markers in lymphomas of SIV-immunosuppressed monkeys

Author

Li, Sl, Feichtinger, H, Kaaya, E, Migliorini, Paola, Putkonen, P, Biberfeld, G, Middeldorp, Jm, Biberfeld, P, Ernberg, I., Pathology, CCA - Cancer immunology, CCA - Target Discovery & Preclinial Therapy Development, CCA - Biomarkers, CCA - Evaluation of Cancer Care, AII - Infectious diseases, and AII - Cancer immunology

Subjects
hemic and lymphatic diseases
Abstract

Simian-immunodeficiency-virus(SIV)-infected cynomolgus monkeys develop B-cell lymphomas in approximately one third of the cases. We have now studied the expression of cynomolgus-Epstein-Barr-virus(cyno-EBV) nuclear antigens in 13 cyno-EBV-carrying SIVsm-associated monkey lymphomas and established cell lines from 3 of these tumors. Immunoblots of cell lysates were probed with polyspecific and monospecific reagents directed against human EB-virus EBNAI-6, and against the membrane protein LMPI. An EBNA2-cross-reacting protein was demonstrated in 8 lymphoma tissues (8/13) and in the 3 cell lines derived from the tumors. All tumors expressed a polypeptide with 50 to 55 kDa molecular weight, which cross-reacted with some antibodies to EBNAI. Absorption experiments with normal monkey tissue showed that this polypeptide was specific for the cyno-EBV-carrying lymphoma cells. Equivalents of EBNA3-6 and LMPI could not be detected. Immunophenotypical characterization showed that the monkey lymphomas were similar to human HIV-associated B-cell lymphomas. Malignant B-cell lymphomas in experimentally SIVsm-infected cynomolgus monkeys can be a model for EBV-associated lymphomagenesis in immunodeficiency states.

Published
1993

31. NotI subtraction and NotI-specific microarrays to detect copy number and methylation changes in whole genomes

Author

Li, J., primary, Protopopov, A., additional, Wang, F., additional, Senchenko, V., additional, Petushkov, V., additional, Vorontsova, O., additional, Petrenko, L., additional, Zabarovska, V., additional, Muravenko, O., additional, Braga, E., additional, Kisselev, L., additional, Lerman, M. I., additional, Kashuba, V., additional, Klein, G., additional, Ernberg, I., additional, Wahlestedt, C., additional, and Zabarovsky, E. R., additional

Published
2002
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50. Blastogenic response of purified human T-lymphocyte populations to Epstein-Barr virus (EBV).

Author

Gergely, P., Ernberg, I., Klein, G., and Steinitz, M.

Subjects
*T cells, *LEUCOCYTES, *CELL proliferation, *EPSTEIN-Barr virus diseases, *CORD blood, *B cells
Abstract

The blastogenic response of T-cell populations to infectious EBV (B95-8 strain) was studied. The addition of virus increased the [3H]thymidine uptake of unfractionated lymphocytes from seropositive and seronegative subjects, and from cord blood, but not from patients with infectious mononucleosis. The same amount of virus evoked a small response in purified T cells from seropositive donors, but not in T cells from the other sources. The addition of autologous B lymphocytes with EBV adsorbed on their surfaces caused a more significant blastogenic response, which was even more pronounced in the presence of mercaptoethanol. [ABSTRACT FROM AUTHOR]

Published
1977

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