Literature DB >> 23812328

Innate immune responses against Epstein Barr virus infection.

Obinna Chijioke1, Tarik Azzi, David Nadal, Christian Münz.   

Abstract

EBV persists life-long in >95% of the human adult population. Whereas it is perfectly immune-controlled in most infected individuals, a minority develops EBV-associated diseases, primarily malignancies of B cell and epithelial cell origin. In recent years, it has become apparent that the course of primary infection determines part of the risk to develop EBV-associated diseases. Particularly, the primary symptomatic EBV infection or IM, which is caused by exaggerated T cell responses, resulting in EBV-induced lymphocytosis, predisposes for EBV-associated diseases. The role of innate immunity in the development of IM remains unknown. Therefore, it is important to understand how the innate immune response to this virus differs between symptomatic and asymptomatic primary EBV infection. Furthermore, the efficiency of innate immune compartments might determine the outcome of primary infection and could explain why some individuals are susceptible to IM. We will discuss these aspects in this review with a focus on intrinsic immunity in EBV-infected B cells, as well as innate immune responses by DCs and NK cells, which constitute promising immune compartments for the understanding of early immune control against EBV and potential targets for EBV-specific immunotherapies.

Entities:  

Keywords:  B cells; Toll-like receptor; dendritic cells; infectious mononucleosis; natural killer cells

Mesh:

Year:  2013        PMID: 23812328      PMCID: PMC3828602          DOI: 10.1189/jlb.0313173

Source DB:  PubMed          Journal:  J Leukoc Biol        ISSN: 0741-5400            Impact factor:   4.962


  69 in total

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  17 in total

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Review 2.  Malaria - how this parasitic infection aids and abets EBV-associated Burkitt lymphomagenesis.

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3.  BZLF1 Attenuates Transmission of Inflammatory Paracrine Senescence in Epstein-Barr Virus-Infected Cells by Downregulating Tumor Necrosis Factor Alpha.

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5.  γ-Herpesvirus load as surrogate marker of early death in HIV-1 lymphoma patients submitted to high dose chemotherapy and autologous peripheral blood stem cell transplantation.

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6.  EBV BART MicroRNAs Target Multiple Pro-apoptotic Cellular Genes to Promote Epithelial Cell Survival.

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Review 7.  Study of viral pathogenesis in humanized mice.

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Review 8.  Interference with the Autophagic Process as a Viral Strategy to Escape from the Immune Control: Lesson from Gamma Herpesviruses.

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9.  Cooperation between Epstein-Barr virus immune evasion proteins spreads protection from CD8+ T cell recognition across all three phases of the lytic cycle.

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Review 10.  Recognition of human oncogenic viruses by host pattern-recognition receptors.

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