AUTHOR=Kerr Jonathan R. 

TITLE=Epstein-Barr Virus Induced Gene-2 Upregulation Identifies a Particular Subtype of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

JOURNAL=Frontiers in Pediatrics

VOLUME=7

YEAR=2019

URL=https://www.frontiersin.org/journals/pediatrics/articles/10.3389/fped.2019.00059

DOI=10.3389/fped.2019.00059

ISSN=2296-2360

ABSTRACT=<p>Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is a chronic multisystem disease characterized by a variety of symptoms, and exhibits various features of an autoimmune-like disease. Subtypes are well recognized but to date are difficult to identify objectively. The disease may be triggered by infection with a variety of micro-organisms, including Epstein-Barr virus (EBV). A subset of CFS/ME patients exhibit up regulation of EBV virus induced gene 2 (<italic>EBI2</italic>) mRNA in peripheral blood mononuclear cells (PBMC), and these patients appear to have a more severe disease phenotype and lower levels of EBNA1 IgG. <italic>EBI2</italic> is induced by EBV infection and has been found to be upregulated in a variety of autoimmune diseases. <italic>EBI2</italic> is a critical gene in immunity and central nervous system function; it is a negative regulator of the innate immune response in monocytes. Its heterogeneous expression in CFS/ME could explain the variable occurrence of a variety of immune and neurological abnormalities which are encountered in patients with CFS/ME. The <italic>EBI2</italic> subtype occurred in 38–55% CFS/ME patients in our studies. Further work is required to confirm the role of EBV and of <italic>EBI2</italic> and its oxysterol ligands in CFS/ME, and to identify the most practical means to identify patients of the EBI subtype. There are two <italic>EBI2</italic> antagonists currently in development, and these may hold promise in the treatment of CFS/ME patients of the EBI subtype.</p>