Herpes viruses in the CNS including EBV. What do we know.

[frodo]

This review is centered in herpes simplex virus 1 and human herpesvirus 6, but they deal with all the family, including EBV. Recently it was found that EBV infects several kind of the cells in the brain and also the B-cells of the immune system (http://journals.plos.org/plosone/articl ... ne.0192109)

To put it in context, the whole family of Herpes viruses HV known to produce diseases are: HSV-1, HHV-6A, HHV-6B, herpes simplex virus 2 (HSV-2), varicella-zoster virus (VZV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus-7 (HHV-7), and human herpesvirus-8 (HHV-8 or Kaposi's sarcoma-associated herpesvirus)

Contributions of neurotropic human herpesviruses herpes simplex virus 1 and human herpesvirus 6 to neurodegenerative disease pathology

http://www.nrronline.org/article.asp?is ... t=Hogestyn

Abstract

Human herpesviruses (HVs) have developed ingenious mechanisms that enable them to traverse the defenses of the central nervous system (CNS).

The ability of HVs to enter a state of latency, a defining characteristic of this viral family, allows them to persist in the human host indefinitely. As such, HVs represent the most frequently detected pathogens in the brain. Under constant immune pressure, these infections are largely asymptomatic in healthy hosts.

However, many neurotropic HVs have been directly connected with CNS pathology in the context of other stressors and genetic risk factors. In this review, we discuss the potential mechanisms by which neurotropic HVs contribute to neurodegenerative disease (NDD) pathology by highlighting two prominent members of the HV family, herpes simplex virus 1 (HSV-1) and human herpesvirus 6 (HHV-6).

We (i) introduce the infectious pathways and replicative cycles of HSV-1 and HHV-6 and then (ii) review the clinical evidence supporting associations between these viruses and the NDDs Alzheimer's disease (AD) and multiple sclerosis (MS), respectively. We then (iii) highlight and discuss potential mechanisms by which these viruses exert negative effects on neurons and glia. Finally, we (iv) discuss how these viruses could interact with other disease-modifying factors to contribute to the initiation and/or progression of NDDs.