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Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host
Epstein-Barr virus (EBV) is a double-stranded DNA virus of the Herpesviridae family. This virus preferentially infects human primary B cells and persists in the human B cell compartment for a lifetime. Latent EBV infection can lead to the development of different types of lymphomas as well as carcin...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9355577/ https://www.ncbi.nlm.nih.gov/pubmed/35935191 http://dx.doi.org/10.3389/fmicb.2022.955603 |
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author | Albanese, Manuel Tagawa, Takanobu Hammerschmidt, Wolfgang |
author_facet | Albanese, Manuel Tagawa, Takanobu Hammerschmidt, Wolfgang |
author_sort | Albanese, Manuel |
collection | PubMed |
description | Epstein-Barr virus (EBV) is a double-stranded DNA virus of the Herpesviridae family. This virus preferentially infects human primary B cells and persists in the human B cell compartment for a lifetime. Latent EBV infection can lead to the development of different types of lymphomas as well as carcinomas such as nasopharyngeal and gastric carcinoma in immunocompetent and immunocompromised patients. The early phase of viral infection is crucial for EBV to establish latency, but different viral components are sensed by cellular sensors called pattern recognition receptors (PRRs) as the first line of host defense. The efficacy of innate immunity, in particular the interferon-mediated response, is critical to control viral infection initially and to trigger a broad spectrum of specific adaptive immune responses against EBV later. Despite these restrictions, the virus has developed various strategies to evade the immune reaction of its host and to establish its lifelong latency. In its different phases of infection, EBV expresses up to 44 different viral miRNAs. Some act as viral immunoevasins because they have been shown to counteract innate as well as adaptive immune responses. Similarly, certain virally encoded proteins also control antiviral immunity. In this review, we discuss how the virus governs innate immune responses of its host and exploits them to its advantage. |
format | Online Article Text |
id | pubmed-9355577 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93555772022-08-06 Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host Albanese, Manuel Tagawa, Takanobu Hammerschmidt, Wolfgang Front Microbiol Microbiology Epstein-Barr virus (EBV) is a double-stranded DNA virus of the Herpesviridae family. This virus preferentially infects human primary B cells and persists in the human B cell compartment for a lifetime. Latent EBV infection can lead to the development of different types of lymphomas as well as carcinomas such as nasopharyngeal and gastric carcinoma in immunocompetent and immunocompromised patients. The early phase of viral infection is crucial for EBV to establish latency, but different viral components are sensed by cellular sensors called pattern recognition receptors (PRRs) as the first line of host defense. The efficacy of innate immunity, in particular the interferon-mediated response, is critical to control viral infection initially and to trigger a broad spectrum of specific adaptive immune responses against EBV later. Despite these restrictions, the virus has developed various strategies to evade the immune reaction of its host and to establish its lifelong latency. In its different phases of infection, EBV expresses up to 44 different viral miRNAs. Some act as viral immunoevasins because they have been shown to counteract innate as well as adaptive immune responses. Similarly, certain virally encoded proteins also control antiviral immunity. In this review, we discuss how the virus governs innate immune responses of its host and exploits them to its advantage. Frontiers Media S.A. 2022-07-22 /pmc/articles/PMC9355577/ /pubmed/35935191 http://dx.doi.org/10.3389/fmicb.2022.955603 Text en Copyright © 2022 Albanese, Tagawa and Hammerschmidt. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Albanese, Manuel Tagawa, Takanobu Hammerschmidt, Wolfgang Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host |
title | Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host |
title_full | Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host |
title_fullStr | Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host |
title_full_unstemmed | Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host |
title_short | Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host |
title_sort | strategies of epstein-barr virus to evade innate antiviral immunity of its human host |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9355577/ https://www.ncbi.nlm.nih.gov/pubmed/35935191 http://dx.doi.org/10.3389/fmicb.2022.955603 |
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