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D’Addario, M., Libermann, T.A., Xu, J., Ahmad, A. and Menezes, J. (2001) Epstein-Barr Virus and Its Glycoprotein-350 Upregulate IL-6 in Human B-Lymphocytes via CD21, Involving Activation of NF-κB and Different Signaling Pathways. Journal of Molecular Biology, 308, 501-514.
https://doi.org/10.1006/jmbi.2001.4589

has been cited by the following article:

• TITLE: The Role of Epstein-Barr Virus in the Pathogenesis of Multiple Sclerosis

  AUTHORS: Bandana Pandey

  KEYWORDS: Epstein-Barr Virus, Multiple Sclerosis, Latent, Pathogenesis, Immune System

  JOURNAL NAME: Open Access Library Journal, Vol.11 No.11, November 26, 2024

  ABSTRACT: Epstein Barr Virus (EBV) is a ubiquitous human lymphotropic herpesvirus which is also called Gamma herpesvirus and has been involved in several cancers. EBV is the first human tumor virus identified. There has been much epidemiological and mechanistic evidence to prove the causal role of EBV in multiple sclerosis (MS). Multiple Sclerosis is a chronic autoimmune disease of the central nervous system characterized by demyelination and neuroinflammation. For this paper, I aim to provide answers to questions like how a virus, which leads to benign latent infection, can promote cancers and autoimmune disease, how EBV plays an important role in the development of multiple sclerosis, how EBV is involved in the pathogenesis of multiple sclerosis and how this study will help to find the way for future MS treatments. Scientists have long suspected but failed to prove the link between viruses and multiple sclerosis (autoimmune disease). A study led by Stanford Medicine researchers proves that EBV triggers multiple sclerosis by priming the immune system to attack the body’s nervous system. This research paper aims to provide an overview of the current understanding of the role of Epstein Barr Virus in the pathogenesis of multiple sclerosis.