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.
read more
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.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
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.
81
References
Viral suppression of the interferon system.
Friedemann Weber,Otto Haller +1 more
TL;DR: Here, a few well-characterized examples are described to illustrate the sophisticated and often multi-layered anti-IFN mechanisms employed by viruses.
81
Toll-like receptors in systemic lupus erythematosus; prospects for therapeutic intervention.
TL;DR: Pharmacologic modulation of TLR-directed pathways may offer new therapeutic approaches for the treatment of SLE.
80
The EBNA2-related resistance towards alpha interferon (IFN-alpha) in Burkitt's lymphoma cells effects induction of IFN-induced genes but not the activation of transcription factor ISGF-3.
TL;DR: The data suggest that the EBNA2-related IFN resistance in Burkitt's lymphoma cells acts downstream of the activation of ISGF-3, which previously has been shown to be required and sufficient for transcriptional activation of IFN-induced genes.
80
LMP1, a viral relative of the TNF receptor family, signals principally from intracellular compartments
Ngan Lam,Bill Sugden +1 more
TL;DR: The results imply that members of the TNF‐R family can signal from intracellular compartments containing lipid rafts and may do so when they act in autocrine loops, as demonstrated by a mutant of L MP1 which has significantly reduced localization at the plasma membrane yet signals as efficiently as does wild‐type LMP1.
Protection from Interferon-Induced Apoptosis by Epstein-Barr Virus Small RNAs Is Not Mediated by Inhibition of PKR
TL;DR: EBER inhibition of alpha-interferon-induced apoptosis, and potentially other PKR-mediated events, is unlikely to be mediated through direct inhibition of PKR, as previously thought.
75