Apoptotic effects of Human Herpesvirus-6A on glia and neurons as potential triggers for central nervous system autoimmunity

Human Herpesvirus type 6 (HHV-6A and/or HHV-6B) has been tentatively associated with multiple sclerosis (MS). However, there is currently no direct proof of pathogenicity. To determine whether exposure to HHV-6 variants is capable of inducing programmed cell death (apoptosis) in representative cell...

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Bibliographic Details
Published in:Journal of clinical virology 2006-12, Vol.37, p.S11-S16
Main Authors: Gardell, Jennifer L., Dazin, Paul, Islar, Janeen, Menge, Til, Genain, Claude P., Lalive, Patrice H.
Format: Article
Language:English
Subjects:
Apoptosis
Autoimmunity
Biological and medical sciences
Cell Line
Central Nervous System - pathology
Coculture Techniques
Flow Cytometry
Fundamental and applied biological sciences. Psychology
Herpesvirus 6, Human - pathogenicity
Human herpesvirus type 6
Human viral diseases
Humans
Infectious diseases
Medical sciences
Microbiology
Miscellaneous
Multiple sclerosis
Neuroglia - pathology
Neuroglia - virology
Neurons - pathology
Neurons - virology
T-Lymphocytes - virology
Time Factors
Viral diseases
Virology
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Summary:Human Herpesvirus type 6 (HHV-6A and/or HHV-6B) has been tentatively associated with multiple sclerosis (MS). However, there is currently no direct proof of pathogenicity. To determine whether exposure to HHV-6 variants is capable of inducing programmed cell death (apoptosis) in representative cell types of the central nervous system (CNS). HHV-6A and HHV-6B variants were grown on human T cell lines HSB2 and MOLT-3, respectively. Human neuronal (SK-N-SH), astrocytes (CRT), and oligodendrocytes (TC620) cell lines were exposed in vitro to infected T cells in a trans-well system for up to 4 days (5×10 4 cells target cells and 2×10 6 T cells). Apoptosis was measured by a FACS-based method. Exposure to HHV-6A induced apoptosis in a time-dependent manner, while exposure to HHV-6B did not. Three days after exposure, apoptosis was increased compared to normalized controls, by 239% in neurons, 321% in astrocytes, and 326% in oligodendrocytes, respectively. This study provides the demonstration that exposure to immune cells carrying replicating HHV-6A may injure glial cells and neurons by inducing apoptosis, and direct evidence for a causal association between HHV-6A with MS and related disorders.
ISSN:1386-6532
1873-5967
DOI:10.1016/S1386-6532(06)70005-1