Journal of Clinical Virology
Volume 46, Issue 1 , Pages 47-48, September 2009

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

  • Albert K. Tai

      Affiliations

    • Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, United States
  • ,
  • Janos Luka

      Affiliations

    • Bioworld Consulting Laboratories, Mt. Airy, MD 21771, United States
  • ,
  • Dharam Ablashi

      Affiliations

    • HHV-6 Foundation, Santa Barbara, CA 93108, United States
  • ,
  • Brigitte T. Huber

      Affiliations

    • Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, United States
    • Corresponding Author InformationCorresponding author. Tel.: +1 617 636 3989; fax: +1 617 636 0449.

published online 08 June 2009.

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-α 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-α that is produced by the HHV-6A-infected cells. The functional implications of superantigen expression are discussed.

Abbreviations: EBV, Epstein–Barr virus, HERV, human endogenous retrovirus, HHV-6, human herpesvirus 6, MS, multiple sclerosis

Keywords: HHV-6A, HERV-K18, Superantigen, MS

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PII: S1386-6532(09)00194-2

doi:10.1016/j.jcv.2009.05.019

Journal of Clinical Virology
Volume 46, Issue 1 , Pages 47-48, September 2009