Epstein–Barr Virus-Specific Immune Control by Innate Lymphocytes

Münz, Christian

doi:10.3389/fimmu.2017.01658

Cited by 40 publications

(46 citation statements)

References 82 publications

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“…As reviewed in detail elsewhere, EBV infection induces innate immune responses (including an expansion of [CD56 dim CD16 neg ] NK cells) and adaptive immune responses. The above‐mentioned rapid expansion of mostly lytic‐antigen‐specific cytotoxic T cells is observed during acute infection.…”

Section: Immune Responses To Ebv Infectionmentioning

confidence: 99%

Signaling pathways involved in the T‐cell‐mediated immunity against Epstein‐Barr virus: Lessons from genetic diseases

Latour

Fischer

2019

Immunological Reviews

113

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Primary immunodeficiencies (PIDs) provide researchers with unique models to understand in vivo immune responses in general and immunity to infections in particular. In humans, impaired immune control of Epstein-Barr virus (EBV) infection is associated with the occurrence of several different immunopathologic conditions; these include non-malignant and malignant B-cell lymphoproliferative disorders, hemophagocytic lymphohistiocytosis (HLH), a severe inflammatory condition, and a chronic acute EBV infection of T cells. Studies of PIDs associated with a predisposition to develop severe, chronic EBV infections have led to the identification of key components of immunity to EBV -notably the central role of T-cell expansion and its regulation in the pathophysiology of EBV-associated diseases. On one hand, the defective expansion of EBV-specific CD8 T cells results from mutations in genes involved in T-cell activation (such as RASGRP1, MAGT1, and ITK), DNA metabolism (CTPS1) or co-stimulatory pathways (CD70, CD27, and TNFSFR9 (also known as CD137/4-1BB)) leads to impaired elimination of proliferating EBV-infected B cells and the occurrence of lymphoma. On the other hand, protracted T-cell expansion and activation after the defective killing of EBV-infected B cells is caused by genetic defects in the components of the lytic granule exocytosis pathway or in the small adapter protein SH2D1A (also known as SAP), a key activator of T-and NK cell-cytotoxicity. In this setting, the persistence of EBV-infected cells results in HLH, a condition characterized by unleashed T-cell and macrophage activation. Moreover, genetic defects causing selective vulnerability to EBV infection have highlighted the role of co-receptor molecules (CD27, CD137, and SLAM-R) selectively involved in immune responses against infected B cells via specific T-B cell interactions. K E Y W O R D S B-cell lymphoproliferation, cell-cytotoxicity, Epstein-Barr virus, hemophagocytic lymphohistiocytosis, primary immunodeficiency, T-cell proliferation | IMMUNE RE S P ON S E S TO EBV INFEC TI ONEpstein-Barr virus (EBV, also known as human herpesvirus 4) is a gamma herpes virus that only infects primates (primarily humans). 1,2 It is an encapsidated, double-stranded DNA virus with more than 100 genes. It is pandemic, since the great majority of human beings (>90%) have been infected by EBV. The main cell target is B lymphocytes that express CD21 -the membrane receptor for EBV entry through its 350 kDa major envelope glycoprotein. In immunocompetent adolescents and adults, EBV infection causes infectious mononucleosis (IM). Immunologically speaking, IM is characterized by a This article is part of a series of reviews covering Signaling and Signal Diversification in Immune

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Section: Immune Responses To Ebv Infectionmentioning

confidence: 99%

Signaling pathways involved in the T‐cell‐mediated immunity against Epstein‐Barr virus: Lessons from genetic diseases

Latour

Fischer

2019

Immunological Reviews

113

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“…*NKG2A+; when VACV is present, populations are expressed more strongly [19]. *NKG2A+KIR−; set a limit to lytic EBVreplication [28].…”

Section: Variety Of Nk-populations Typed By Receptor Lectinsmentioning

confidence: 99%

“…According to data provided by GLOBOCAN-2018 and IARC (International Agency for Research on Cancer) in 2018 Russia occupied the fifth place in the world as per number of death cases among oncologic patients. There are data on oncologic diseases in patients influenced by virus infec-tions and co-infections; for example, up to 2% neoplasms in the world are related to Epstein-Barr virus (EBV) [28]. Overall, risks related to tumor development against the background of occurring virus infections as well as factors that determine such risks or reduce them have not been studied to the extent they should be.…”

mentioning

confidence: 99%

“…Viruses and tumors considered in relation to them. Viruses that are examined in the aspect under consideration include the following: arenaviruses (lymphocytic choriomeningitis virus, LCMV), herpes viruses (cytomegalovirus, CMV), in relation to acute leukemia and В-cell lymphomas; co-infections with other viruses; Epstein-Barr virus, EBV, in relation to mononucleosis, Burkitt lymphomas; vaginal herpes viruses [7,28,34]); papovaviruses (human papillomavirus, HPV, in relation to cervical cancer); pox viruses (cattle pox virus, mice pox virus, vaccinavirus or orthopoxvirus, VACV) [19,27]; retroviruses (human immunodeficiency virus, HIV, including co-infection with CMV; in relation to lymphomas); flaviviruses (hepatitis-С virus, HCV; in relation to hepatocellular carcinomas HCC); hepatitis-В virus [HBV] and hepatitis delta virus [HDV]) [25]; togaviruses (chikungunya virus; in relation to sarcomas) [24].…”

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confidence: 99%

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NK-cells that identify glycopatterns and their anti-tumor potential against a background of epidemically significant viral infections

Lakhtin¹,

Lakhtin²,

Алешкин³

et al. 2019

Health Risk Analysis

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Risks related to tumors development against a background of viral infections as well as factors that determine such risks or reduce them have not been examined profoundly so far. Our research goal was to accomplish a scientific review of research on a potential possessed by populations of lectin NK-cells (natural killers) in a body; such populations can have variable sets of lectin and other functionally significant cell surface receptors against tumors in a situation when viruses, including epidemically significant ones, penetrate a body. It is shown that cofunctioning of various receptors and their ligands that redistribute cytokines (glycopattern-identifying lectin (basis) receptors, Ig-similar receptors, cytotoxic receptors, and other effector (adjusting) receptors) plays a significant role in intercellular communications and effects produced by NK-populations. NK-populations network is a promising resource for body protection and it should be taken into account when developing new anti-tumor and anti-viralpreventive and medical strategies. When certain NK-populations with protective functions are absent in a body, it can be considered a new multi-factor risk of viral and oncologic diseases in an individual or a contingent living in a specific region. The reviewed data can be applied to develop new anti-tumor and anti-viral medications and vaccines as well as medical strategies. Probiotic lectins are promising ligands of intercellular communications associated with immune surveillance. Read online __________________________  Lakhtin M.V.

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“…Nevertheless, despite the fast mutation and evolution rates of particular viruses, a mutual adaptation between the host and the infectious agents takes place, including the reduced replication and expression of viral proteins, the modulation of the host response by viral-miRNAs, as well as the emergence of innate and adaptive immunity [ 4,5,6,7,8]. In addition to these mechanisms, cytokines produced by the host as a response to viral infections induce the expression of AID/APOBEC (Activation-Induced cytidine Deaminase/Apolipoprotein B Editing Complex) family genes, which are important for antibody maturation and inhibition of viral infections through mutagenic and non-mutagenic mechanisms.…”

Section: Introductionmentioning

confidence: 99%

APOBEC-mediated DNA alterations: a possible new mechanism of carcinogenesis in EBV-positive gastric cancer

Bobrovnitchaia

Valieris

Drummond

et al. 2018

Preprint

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Mechanisms of viral oncogenesis are diverse and include the off-target activity of enzymes expressed by the infected cells, which evolved to target viral genomes for controlling their infection. Among these enzymes, the single-strand DNA editing capability of APOBECs represent a well-conserved viral infection response that can also cause untoward mutations in host DNA. Here we show , after evaluating somatic single-nucleotide variations and transcriptome data in 240 gastric cancer samples, a positive correlation between APOBEC3s mRNA-expression and the APOBEC-mutation signature, both increased in EBV+ tumors. The correlation was reinforced by the observation of APOBEC-mutations preferentially occuring in transcriptionally-active loci. The EBV-infection and APOBEC3 mutation-signature axis was confirmed in a validation cohort of 112 gastric cancer patients. Our findings suggest that APOBEC3 upregulation in EBV+ cancer may boost the mutation load, providing further clues to the mechanisms of EBV-induced gastric carcinogenesis. After further validation, this EBV-APOBEC axis may prove to be a secondary driving force in the mutational evolution of EBV+ gastric tumors, whose consequences in terms of prognosis and treatment implications should be vetted.

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Epstein–Barr Virus-Specific Immune Control by Innate Lymphocytes

Cited by 40 publications

References 82 publications

Signaling pathways involved in the T‐cell‐mediated immunity against Epstein‐Barr virus: Lessons from genetic diseases

Signaling pathways involved in the T‐cell‐mediated immunity against Epstein‐Barr virus: Lessons from genetic diseases

NK-cells that identify glycopatterns and their anti-tumor potential against a background of epidemically significant viral infections

APOBEC-mediated DNA alterations: a possible new mechanism of carcinogenesis in EBV-positive gastric cancer

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