[Note: This study indicates HHV-6A, a neurotropic virus associated with MS, appears to activate the HERV-K18 retrovirus. Dr. Huber is conducting another study, funded by the CFIDS Association’s Campaign to Accelerate CFS Research – “HERV-K18 as a risk factor for CFS.”]
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 78 h.
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.
Source: Journal of Clinical Virology, online Jun 6, 2009. PMID: 19505843, by Tai AK, Luka J, Ablashi D, Huber BT. Department of Pathology, Tufts University School of Medicine, Boston; b-Bioworld Consulting Laboratories, Mt. Airy, Maryland; HHV-6 Foundation, Santa Barbara, California, USA. [E-mail: Brigitte.firstname.lastname@example.org]