Epstein-Barr virus may cause disruption of the blood brain barrier, with macrophage invasion of brain parenchyma and development of MS plaques
Steven R.Brenner, Neurologist, St. Louis University Dept. of Neurology and PsychiatrySBren20979@aol.com
None
Submitted February 17, 2012
Tzartos et al. discuss innate immune activation by Epstein-Barr virus (EBV). [1] This is particularly interesting because active EBV infection may not be characteristic of multiple sclerosis (MS) brain, although EBV encoded RNA macrophages were detected in areas overexpressing IFN-alpha in active MS lesions. The recent description of a gamma virus infection causing a spontaneous MS- like disease in nonhuman primates may be of interest, since the virus causing the disease is a simian herpesvirus with some similarities to EBV, a gamma-2 herpesvirus being isolated from active encephalomyelitis lesions. [2] Plaques were typically centered on venules and small veins.
EBV can infect the endothelial cells making up the blood brain barrier, possibly disrupting the blood brain barrier and permitting entry of auto-reactive T cells into the brain, causing active MS lesions in the brain parenchyma. [3]
EBV may infect the vascular endothelium causing rupture of the blood brain barrier, permitting macrophage entry into the brain parenchyma, activation of the innate immune system and MS plaque formation.
1. Tzartos JS, Phil D, Khan G, Meager A, et al. Association of innate immune activation with latent Epstein-Barr virus in active MS lesions. Neurology 2012; 78:15-23.
2. Axthelm M, Bourdette DN, Marracci G H, et al. Japanese macaque encephalomyelitis: A spontaneous multiple sclerosis like disease in a nonhuman primate.
Annals of Neurology 2011; 70:362-373.
3. Casiraghi C, Dorovini-Zis K, Horwitz MS. Epstein-Barr virus infection of human brain microvessel endothelial cells: a novel role in multiple sclerosis. J Neuroimmunol 2011; 230: 173-177.
For disclosures, contact the editorial office at journal@neurology.org.
Tzartos et al. discuss innate immune activation by Epstein-Barr virus (EBV). [1] This is particularly interesting because active EBV infection may not be characteristic of multiple sclerosis (MS) brain, although EBV encoded RNA macrophages were detected in areas overexpressing IFN-alpha in active MS lesions. The recent description of a gamma virus infection causing a spontaneous MS- like disease in nonhuman primates may be of interest, since the virus causing the disease is a simian herpesvirus with some similarities to EBV, a gamma-2 herpesvirus being isolated from active encephalomyelitis lesions. [2] Plaques were typically centered on venules and small veins. EBV can infect the endothelial cells making up the blood brain barrier, possibly disrupting the blood brain barrier and permitting entry of auto-reactive T cells into the brain, causing active MS lesions in the brain parenchyma. [3] EBV may infect the vascular endothelium causing rupture of the blood brain barrier, permitting macrophage entry into the brain parenchyma, activation of the innate immune system and MS plaque formation.
1. Tzartos JS, Phil D, Khan G, Meager A, et al. Association of innate immune activation with latent Epstein-Barr virus in active MS lesions. Neurology 2012; 78:15-23.
2. Axthelm M, Bourdette DN, Marracci G H, et al. Japanese macaque encephalomyelitis: A spontaneous multiple sclerosis like disease in a nonhuman primate. Annals of Neurology 2011; 70:362-373.
3. Casiraghi C, Dorovini-Zis K, Horwitz MS. Epstein-Barr virus infection of human brain microvessel endothelial cells: a novel role in multiple sclerosis. J Neuroimmunol 2011; 230: 173-177.
For disclosures, contact the editorial office at journal@neurology.org.