Abstract
Human herpesvirus 6A (HHV-6A) is a common virus with a worldwide distribution that has been associated with multiple sclerosis. Whether HHV-6A can replicate in dendritic cells (DC) and how the infection might modulate the functional properties of the cell are currently not well known and need further investigations. Here, we show that a non-productive infection of HHV-6A in DC leads to the up-regulation of HLA-ABC, via autocrine IFN-α signaling, as well as the up-regulation of HLA-DR and CD86. However, HHV-6A exposure reduces IL-8 secretion by DC and their capacity to stimulate allogenic T cell proliferation. The ability to suppress DC functions important for activation of innate and adaptive immune responses might be one successful strategy by which HHV-6A avoids the induction of appropriate host defense mechanisms, and thus facilitating persistent infection.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptive Immunity
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CD4-Positive T-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / immunology
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Cytokines / biosynthesis
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Dendritic Cells / immunology*
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Dendritic Cells / virology*
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HLA Antigens / metabolism
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Herpesvirus 6, Human / immunology*
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Herpesvirus 6, Human / pathogenicity*
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Herpesvirus 6, Human / physiology
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Host-Pathogen Interactions / immunology
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Humans
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Immune Tolerance
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Immunity, Innate
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Inflammation Mediators / metabolism
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Interferon-alpha / metabolism
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Interleukin-4 / biosynthesis
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Virus Replication
Substances
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Cytokines
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HLA Antigens
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IL4 protein, human
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Inflammation Mediators
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Interferon-alpha
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Interleukin-4
Grants and funding
This work was supported from grant 4769/07-225 from faculty funds from the Board of Doctoral Education at Karolinska Institutet and a grant from the Swedish Association for Persons with Neurological Disabilities; grant from the Swedish Dental Society; unrestricted grant from BiogenIdec, Merck Serono and Sanofi-Aventis; grant from The Swedish Research Council; grants from KI Funds; grant 2008Fobi0783 from KI funds; IMI-grant (ABIRISK project); and unrestricted grant from BiogenIdec, Merck Serono and Sanofi-Aventis. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.