Innate immune modulation in EBV infection
TL;DR: Study of EBV-specific immune dysregulation is important for understanding EBV latency and oncogenesis, and will identify potential molecular targets for immunotherapeutic interventions.
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Abstract: Epstein-Barr Virus (EBV) belongs to the gammaherpesvirus family, members of which are oncogenic. Compared with other closely related herpesviruses, EBV has developed much more elaborate and sophisticated strategies for subverting host immune system, which may account for its high prevalence in immune competent hosts. Thus, study of EBV-specific immune dysregulation is important for understanding EBV latency and oncogenesis, and will identify potential molecular targets for immunotherapeutic interventions. Here I summarize the recent findings of individual EBV products in regulating host immune responses, with emphasis on the innate immune modulation.
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Citations
The interplay between Epstein-Barr virus and B lymphocytes: implications for infection, immunity, and disease
TL;DR: Mechanisms by which dysregulation of the host B cell and immune modulation by the virus can contribute to development of EBV+ B cell lymphomas are focused on.
The Incubation Period of Primary Epstein-Barr Virus Infection: Viral Dynamics and Immunologic Events.
Samantha K. Dunmire,Jennifer M. Grimm,David O. Schmeling,Henry H. Balfour,Kristin A. Hogquist +4 more
TL;DR: This study provides the first description of events during the incubation period of natural EBV infection in humans and definitive data upon which to formulate theories of viral control and disease pathogenesis.
Etiology of myasthenia gravis: Innate immunity signature in pathological thymus
Paola Cavalcante,Perrine Cufi,Renato Mantegazza,Sonia Berrih-Aknin,Pia Bernasconi,Rozen Le Panse +5 more
TL;DR: Growing evidence of chronic inflammation, TLR activation, and persistent viral infections in the thymus of MG patients, strongly supports the hypothesis that, in the context of a genetic susceptible background, the intrathymic innate immune responses to pathogen infections might contribute to MG etiology.
87
The Immune Response to Epstein Barr Virus and Implications for Posttransplant Lymphoproliferative Disorder.
TL;DR: The EBV life cycle is reviewed and the current understanding of the immune response to EBV in healthy, immunocompetent individuals, in transplant recipients, and in PTLD patients is discussed.
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Alan B. Rickinson
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TL;DR: There is strong serologic and epidemiologic evidence to suggest that previous exposure to Epstein–Barr virus markedly increases the risk of developing multiple sclerosis.
Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) induces the expression of the cellular microRNA miR-146a.
TL;DR: It is shown that the EBV-encoded latent membrane protein 1 (LMP1) induces the expression of miR-146a via NF-κB, which is involved in sequence-specific cleavage, translational repression or deadenylation of specific target mRNAs resulting in post-transcriptional gene silencing.
Is the Epstein-Barr virus EBNA-1 protein an oncogen?
Thomas F. Schulz,Susann Cordes +1 more
TL;DR: Observations that make an old acquaintance appear in a new light are reported that help understand how EBV causes cancer and why such a widely distributed carcinogen does so in only a comparatively small number of infected individuals.
Manipulation of the Toll-Like Receptor 7 Signaling Pathway by Epstein-Barr Virus
TL;DR: The interaction between EBV and TLR pathways was investigated in this article, where the authors found that EBV infection of primary B cells causes B-cell activation and proliferation, and that TLR activation requires binding of antigen to the B-cells receptor and a survival signal from ligand-bound CD40, signals provided by the EBV LMP1 and LMP2A latency proteins.