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Humanized mouse models for Epstein Barr virus infection

Münz, Christian (2017). Humanized mouse models for Epstein Barr virus infection. Current Opinion in Virology, 25:113-118.

Abstract

It is essential for the human immune system to control Epstein Barr virus (EBV), because this common human γ-herpesvirus efficiently spreads through the human population with more than 90% being persistently infected after 20 years of age even in developed countries. Moreover, it threatens each host with its potent growth transforming properties, readily immortalizing human B cells into persistently growing lymphoma cell lines. Since this virus only infects humans, mice with reconstituted human immune system components provide an informative in vivo model to study EBV infection, the associated tumor formation and immune control thereof. They recapitulate the different infection programs in human B cells, allow modeling EBV driven lymphoma formation and interrogation of the key cytotoxic lymphocyte responses that are also required to control this pathogen in humans. The respective lessons that were taught by these investigations will be discussed in this review as well as the challenges in the future to address the whole portfolio of EBV associated diseases and how they could be prevented by EBV specific immunotherapies.

Additional indexing

Item Type:Journal Article, not_refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Life Sciences > Virology
Uncontrolled Keywords:Virology
Language:English
Date:August 2017
Deposited On:22 Feb 2018 16:29
Last Modified:18 Jan 2025 02:37
Publisher:Elsevier
ISSN:1879-6257
OA Status:Green
Publisher DOI:https://doi.org/10.1016/j.coviro.2017.07.026
PubMed ID:28837889
Project Information:
  • Funder: SNSF
  • Grant ID: 310030_162560
  • Project Title: Role of autophagy proteins in endocytosis and exocytosis
  • Funder: SNSF
  • Grant ID: CRSII3_160708
  • Project Title: Identify new molecular mechanisms and cellular precursors to augment T cell function in chronic infections and tumors
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