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Article ; Online: Primary immunodeficiencies and the control of Epstein-Barr virus infection.

Palendira, Umaimainthan / Rickinson, Alan B

Annals of the New York Academy of Sciences

2015 Volume 1356, Page(s) 22–44

Abstract: Human primary immunodeficiency (PID) states, where mutations in single immune system genes predispose individuals to certain infectious agents and not others, are experiments of nature that hold important lessons for the immunologist. The number of ... ...

Abstract	Human primary immunodeficiency (PID) states, where mutations in single immune system genes predispose individuals to certain infectious agents and not others, are experiments of nature that hold important lessons for the immunologist. The number of genetically defined PIDs is rising rapidly, as is the opportunity to learn from them. Epstein-Barr virus (EBV), a human herpesvirus, has long been of interest because of its complex interaction with the immune system. Thus, it causes both infectious mononucleosis (IM), an immunopathologic disease associated with exaggerated host responses, and at least one malignancy, EBV-positive lymphoproliferative disease, when those responses are impaired. Here, we describe the full range of PIDs currently linked with an increased risk of EBV-associated disease. These provide examples where IM-like immunopathology is fatally exaggerated, and others where responses impaired at the stage of induction, expansion, or effector function predispose to malignancy. Current evidence from this rapidly moving field supports the view that lesions in both natural killer cell and T cell function can lead to EBV pathology.
MeSH term(s)	Animals ; Burkitt Lymphoma/genetics ; Burkitt Lymphoma/immunology ; Burkitt Lymphoma/pathology ; Genetic Diseases, Inborn/genetics ; Genetic Diseases, Inborn/immunology ; Genetic Diseases, Inborn/pathology ; Herpesvirus 4, Human/immunology ; Humans ; Immunity, Cellular ; Immunologic Deficiency Syndromes/genetics ; Immunologic Deficiency Syndromes/immunology ; Immunologic Deficiency Syndromes/pathology ; Infectious Mononucleosis/genetics ; Infectious Mononucleosis/immunology ; Infectious Mononucleosis/pathology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
Language	English
Publishing date	2015-09-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.12937
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Article ; Online: Emerging topics in human tumor virology.

Masucci, Maria G / Rickinson, Alan B

Seminars in cancer biology

2014 Volume 26, Page(s) 1–3

MeSH term(s)	Animals ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Humans ; Neoplasms/etiology ; Oncogenic Viruses/physiology ; Tumor Virus Infections/complications
Language	English
Publishing date	2014-06
Publishing country	England
Document type	Editorial ; Introductory Journal Article
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2014.04.006
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Article ; Online: Epstein-Barr virus-associated lymphomas.

Shannon-Lowe, Claire / Rickinson, Alan B / Bell, Andrew I

Philosophical transactions of the Royal Society of London. Series B, Biological sciences

2017 Volume 372, Issue 1732

Abstract: Epstein-Barr virus (EBV), originally discovered through its association with Burkitt lymphoma, is now aetiologically linked to a remarkably wide range of lymphoproliferative lesions and malignant lymphomas of B-, T- and NK-cell origin. Some occur as rare ...

Abstract	Epstein-Barr virus (EBV), originally discovered through its association with Burkitt lymphoma, is now aetiologically linked to a remarkably wide range of lymphoproliferative lesions and malignant lymphomas of B-, T- and NK-cell origin. Some occur as rare accidents of virus persistence in the B lymphoid system, while others arise as a result of viral entry into unnatural target cells. The early finding that EBV is a potent B-cell growth transforming agent hinted at a simple oncogenic mechanism by which this virus could promote lymphomagenesis. In reality, the pathogenesis of EBV-associated lymphomas involves a complex interplay between different patterns of viral gene expression and cellular genetic changes. Here we review recent developments in our understanding of EBV-associated lymphomagenesis in both the immunocompetent and immunocompromised host.This article is part of the themed issue 'Human oncogenic viruses'.
MeSH term(s)	Carcinogenesis ; Epstein-Barr Virus Infections/immunology ; Epstein-Barr Virus Infections/virology ; Herpesvirus 4, Human/physiology ; Humans ; Immunocompetence ; Immunocompromised Host ; Lymphoma/immunology ; Lymphoma/virology
Language	English
Publishing date	2017-09-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	208382-6
ISSN	1471-2970 ; 0080-4622 ; 0264-3839 ; 0962-8436
ISSN (online)	1471-2970
ISSN	0080-4622 ; 0264-3839 ; 0962-8436
DOI	10.1098/rstb.2016.0271
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Article ; Online: Proteome-wide analysis of CD8+ T cell responses to EBV reveals differences between primary and persistent infection.

Forrest, Calum / Hislop, Andrew D / Rickinson, Alan B / Zuo, Jianmin

PLoS pathogens

2018 Volume 14, Issue 9, Page(s) e1007110

Abstract: Human herpesviruses are antigenically rich agents that induce strong CD8+T cell responses in primary infection yet persist for life, continually challenging T cell memory through recurrent lytic replication and potentially influencing the spectrum of ... ...

Abstract	Human herpesviruses are antigenically rich agents that induce strong CD8+T cell responses in primary infection yet persist for life, continually challenging T cell memory through recurrent lytic replication and potentially influencing the spectrum of antigen-specific responses. Here we describe the first lytic proteome-wide analysis of CD8+ T cell responses to a gamma1-herpesvirus, Epstein-Barr virus (EBV), and the first such proteome-wide analysis of primary versus memory CD8+ T cell responses to any human herpesvirus. Primary effector preparations were generated directly from activated CD8+ T cells in the blood of infectious mononucleosis (IM) patients by in vitro mitogenic expansion. For memory preparations, EBV-specific cells in the blood of long-term virus carriers were first re-stimulated in vitro by autologous dendritic cells loaded with a lysate of lytically-infected cells, then expanded as for IM cells. Preparations from 7 donors of each type were screened against each of 70 EBV lytic cycle proteins in combination with the donor's individual HLA class I alleles. Multiple reactivities against immediate early (IE), early (E) and late (L) lytic cycle proteins, including many hitherto unrecognised targets, were detected in both contexts. Interestingly however, the two donor cohorts showed a different balance between IE, E and L reactivities. Primary responses targeted IE and a small group of E proteins preferentially, seemingly in line with their better presentation on the infected cell surface before later-expressed viral evasins take full hold. By contrast, target choice equilibrates in virus carriage with responses to key IE and E antigens still present but with responses to a select subset of L proteins now often prominent. We infer that, for EBV at least, long-term virus carriage with its low level virus replication and lytic antigen release is associated with a re-shaping of the virus-specific response.
MeSH term(s)	Antigens, Viral/immunology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/virology ; Carrier State/immunology ; Carrier State/virology ; Gene Expression/genetics ; Genes, Viral ; HLA Antigens/immunology ; Herpesvirus 4, Human/genetics ; Herpesvirus 4, Human/immunology ; Herpesvirus 4, Human/pathogenicity ; Host-Pathogen Interactions/immunology ; Humans ; Infectious Mononucleosis/immunology ; Infectious Mononucleosis/metabolism ; Infectious Mononucleosis/virology ; Proteome/immunology ; Proteome/metabolism
Chemical Substances	Antigens, Viral ; HLA Antigens ; Proteome
Language	English
Publishing date	2018-09-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1007110
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Article ; Online: Epstein-Barr virus and infectious mononucleosis: what students can teach us.

Rickinson, Alan B / Fox, Christopher P

The Journal of infectious diseases

2013 Volume 207, Issue 1, Page(s) 6–8

MeSH term(s)	Antibodies, Viral/blood ; Female ; Herpesvirus 4, Human/immunology ; Humans ; Infectious Mononucleosis/epidemiology ; Male
Chemical Substances	Antibodies, Viral
Language	English
Publishing date	2013-01-01
Publishing country	United States
Document type	Comment ; Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jis647
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Article ; Online: EBV meets its match.

Fox, Christopher P / Rickinson, Alan B

Blood

2010 Volume 115, Issue 5, Page(s) 920–921

Language	English
Publishing date	2010-02-04
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2009-11-252437
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Article: Burkitt lymphoma: revisiting the pathogenesis of a virus-associated malignancy.

Kelly, Gemma L / Rickinson, Alan B

Hematology. American Society of Hematology. Education Program

2007 , Page(s) 277–284

Abstract: Burkitt lymphoma (BL), a tumor occurring in endemic, sporadic and AIDS-associated forms, is the classic example of a human malignancy whose pathogenesis involves a specific cellular genetic change, namely, a chromosomal translocation deregulating ... ...

Abstract	Burkitt lymphoma (BL), a tumor occurring in endemic, sporadic and AIDS-associated forms, is the classic example of a human malignancy whose pathogenesis involves a specific cellular genetic change, namely, a chromosomal translocation deregulating expression of the c-myc oncogene, complemented in many cases by the action of an oncogenic virus, the Epstein-Barr virus (EBV). Here we review recent work in two complementary areas of research: (1) on cellular genetic changes that occur in addition to the c-myc translocation in BL, in particular the capacity of p53/ ARF pathway breakage or of c-myc mutation to decouple the pro-proliferative effects of c-myc deregulation from its pro-apoptotic effects; and (2) on a postulated role for EBV in BL pathogenesis, through adopting restricted forms of virus latent gene expression that remain compatible with the c-myc-driven growth program but offer the tumor additional protection from apoptosis. We stress the many fundamental questions that remain to be resolved and, in that regard, highlight the general lessons that might be learned through understanding how two other infectious agents, malaria and HIV, dramatically enhance BL incidence.
MeSH term(s)	Burkitt Lymphoma/complications ; Burkitt Lymphoma/genetics ; Burkitt Lymphoma/pathology ; Burkitt Lymphoma/virology ; HIV Infections/complications ; Herpesvirus 4, Human/pathogenicity ; Humans ; Malaria/complications
Language	English
Publishing date	2007
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1520-4391
ISSN	1520-4391
DOI	10.1182/asheducation-2007.1.277
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Article: Antigens and autophagy: the path less travelled?

Taylor, Graham S / Rickinson, Alan B

Autophagy

2007 Volume 3, Issue 1, Page(s) 60–62

Abstract: The Epstein-Barr virus (EBV)-coded nuclear antigen (EBNA) 1, a latent cycle protein endogenously expressed in EBV-transformed B lymphoblastoid cell lines (LCLs), is reported to be processed for CD4(+) T cell recognition by an intracellular route ... ...

Abstract	The Epstein-Barr virus (EBV)-coded nuclear antigen (EBNA) 1, a latent cycle protein endogenously expressed in EBV-transformed B lymphoblastoid cell lines (LCLs), is reported to be processed for CD4(+) T cell recognition by an intracellular route involving antigen delivery to the endosome/lyosome (MHC class II loading) compartment via macroautophagy. In contrast we find that, in the same cell type, two other virus-coded nuclear proteins of the latent cycle, EBNA2 and EBNA3C, are processed by a different route that is unaffected by autophagy inhibition. This involves the intercellular transfer of an antigenic moiety, detectable in cell-free culture supernatants, and its uptake and processing as exogenous antigen by neighboring cells. The process is cumulative and leads over several days of LCL culture to high levels of CD4+ T cell epitope display. The presentation of certain EBV lytic cycle proteins to CD4+ T cells has also recently been found to involve a similar intercellular antigen transfer. It becomes important to know why, even in the same cell type, some antigens but not others appear to access the MHC class II presentation pathway by autophagy.
MeSH term(s)	Antigen Presentation/physiology ; Antigens/physiology ; Antigens, Viral/immunology ; Autophagy/immunology ; CD4-Positive T-Lymphocytes/physiology ; Epstein-Barr Virus Nuclear Antigens/immunology ; Genes, MHC Class II/physiology ; Herpesvirus 4, Human/immunology ; Humans ; Viral Proteins/immunology
Chemical Substances	Antigens ; Antigens, Viral ; EBNA-2 protein, Human herpesvirus 4 ; EBNA-3C, epstein-barr virus ; Epstein-Barr Virus Nuclear Antigens ; Viral Proteins ; EBV-encoded nuclear antigen 1 (O5GA75RST7)
Language	English
Publishing date	2007-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.3425
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Article ; Online: Immune defence against EBV and EBV-associated disease.

Long, Heather M / Taylor, Graham S / Rickinson, Alan B

Current opinion in immunology

2011 Volume 23, Issue 2, Page(s) 258–264

Abstract: Epstein-Barr virus (EBV), a B-lymphotropic herpesvirus widespread in the human population and normally contained as an asymptomatic infection by T cell surveillance, nevertheless causes infectious mononucleosis and is strongly linked to several types of ... ...

Abstract	Epstein-Barr virus (EBV), a B-lymphotropic herpesvirus widespread in the human population and normally contained as an asymptomatic infection by T cell surveillance, nevertheless causes infectious mononucleosis and is strongly linked to several types of human cancer. Here we describe new findings on the range of cellular immune responses induced by EBV infection, on viral strategies to evade those responses and on the links between HLA gene loci and EBV-induced disease. The success of adoptive T cell therapy for EBV-driven post-transplant lymphoproliferative disease is stimulating efforts to target other EBV-associated tumours by immunotherapeutic means, and has reawakened interest in the ultimate intervention strategy, a prophylactic EBV vaccine.
MeSH term(s)	Animals ; Epstein-Barr Virus Infections/immunology ; Herpesvirus 4, Human/immunology ; Histocompatibility Antigens/genetics ; Histocompatibility Antigens/immunology ; Humans ; Neoplasms/immunology ; Neoplasms/therapy ; T-Lymphocytes/immunology ; Virus Internalization
Chemical Substances	Histocompatibility Antigens
Language	English
Publishing date	2011-01-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2010.12.014
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Article ; Online: The immunology of Epstein-Barr virus-induced disease.

Taylor, Graham S / Long, Heather M / Brooks, Jill M / Rickinson, Alan B / Hislop, Andrew D

Annual review of immunology

2015 Volume 33, Page(s) 787–821

Abstract: Epstein-Barr virus (EBV) is usually acquired silently early in life and carried thereafter as an asymptomatic infection of the B lymphoid system. However, many circumstances disturb the delicate EBV-host balance and cause the virus to display its ... ...

Abstract	Epstein-Barr virus (EBV) is usually acquired silently early in life and carried thereafter as an asymptomatic infection of the B lymphoid system. However, many circumstances disturb the delicate EBV-host balance and cause the virus to display its pathogenic potential. Thus, primary infection in adolescence can manifest as infectious mononucleosis (IM), as a fatal illness that magnifies the immunopathology of IM in boys with the X-linked lymphoproliferative disease trait, and as a chronic active disease leading to life-threatening hemophagocytosis in rare cases of T or natural killer (NK) cell infection. Patients with primary immunodeficiencies affecting the NK and/or T cell systems, as well as immunosuppressed transplant recipients, handle EBV infections poorly, and many are at increased risk of virus-driven B-lymphoproliferative disease. By contrast, a range of other EBV-positive malignancies of lymphoid or epithelial origin arise in individuals with seemingly intact immune systems through mechanisms that remain to be understood.
MeSH term(s)	Adaptive Immunity ; Animals ; Carrier State ; Epstein-Barr Virus Infections/complications ; Epstein-Barr Virus Infections/diagnosis ; Epstein-Barr Virus Infections/immunology ; Epstein-Barr Virus Infections/virology ; Herpesvirus 4, Human/immunology ; Herpesvirus 4, Human/physiology ; Humans ; Immunity, Innate ; Immunocompromised Host ; Immunologic Deficiency Syndromes/etiology ; Lymphoproliferative Disorders/etiology
Language	English
Publishing date	2015-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev-immunol-032414-112326
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