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J Clin Virol. 2009 Sep;46(1):47-8. doi: 10.1016/j.jcv.2009.05.019. Epub 2009 Jun 7.

HHV-6A infection induces expression of HERV-K18-encoded superantigen.

Author information

1
Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, United States.

Abstract

BACKGROUND:

The human endogenous retrovirus K-18 (HERV-K18) encodes a superantigen that causes deregulation of the immune system. This provirus is transcriptionally silent, but can be induced by Epstein-Barr virus (EBV) infection and IFN-alpha treatment.

OBJECTIVES:

Since the herpesvirus EBV induces HERV-K18 expression in human B cells, it was of interest to determine if other herpesviruses would have similar HERV-K18 transactivation properties. Human herpesvirus (HHV)-6A, a neurotropic virus associated with multiple sclerosis, was a logical candidate for these studies.

STUDY DESIGN:

HSB2 cells (HHV-6-negative control), HSB2-ML cells (containing latent HHV-6A genome) and HSB2/HHV-6A cells (HSB-2 cells productively infected with HHV-6A) were compared for their level of HERV-K18 transcription, using quantitative RT-PCR.

RESULTS:

Latently infected HSB2-ML cells showed a significant increase in HERV-K18 RNA compared to the control cells. HERV-K18 expression was even greater in HSB2 cells productively infected with HHV-6A for 78h.

CONCLUSION:

These results imply that HHV-6A, either in latent form or during acute infection, directly transactivates HERV-K18. This HERV-K18 induction may be mediated through IFN-alpha that is produced by the HHV-6A-infected cells. The functional implications of superantigen expression are discussed.

PMID:
19505843
DOI:
10.1016/j.jcv.2009.05.019
[Indexed for MEDLINE]

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