[Note: The full text PDF of this NIH study is available at http://www.ajtr.org/files/AJTR1208006.pdf. Techies can view a video that steps through antibody profiling by LIPS (the process developed by Dr. Peter Burbelo and his team, used in this study). The CFS subjects were selected based on the 1994 Fukuda definition.]
Human herpesvirus 6A (HHV-6A) and human herpesvirus 6B (HHV-6B) are associated with a variety of conditions including rash, fever, and encephalitis and may play a role in several neurological diseases.
Here luciferase immunoprecipitation systems (LIPS) was used to develop HHV-6 serologic diagnostic tests using antigens encoded by the U11 gene from HHV-6A (p100) and HHV-6B (p101). Analysis of the antibody responses against Renilla luciferase fusions with different HHV-6B p101 fragments identified an antigenic fragment (amino acids 389 to 858) that demonstrated about 86% seropositivity in serum samples from healthy US blood donors.
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Additional experiments detected a HHV-6A antigenic fragment (amino acids 751-870) that showed about 48% antibody seropositivity in samples from Mali, Africa, a known HHV-6A endemic region.
In contrast to the high levels of HHV-6A immunoreactivity seen in the African samples, testing of US blood donors with the HHV-6A p100 antigenic fragment revealed little immunoreactivity. To potentially explore the role of HHV-6 infection in human disease, a blinded cohort of controls (n=59) and chronic fatigue syndrome (CFS) patients (n=72) from the US was examined for serum antibodies.
While only a few of the controls and CFS patients showed high level immunoreactivity with HHV-6A, a majority of both the controls and CFS patients showed significant immunoreactivity with HHV-6B.
However, no statistically significant differences in antibody levels or frequency of HHV-6A or HHV-6B infection were detected between the controls and CFS patients. These findings highlight the utility of LIPS for exploring the seroepidemiology of HHV-6A and HHV-6B infection, but suggest that these viruses are unlikely to play a role in the pathogenesis of CFS.
Source: American Journal of Translational Research, Oct 30, 2012. by Burbelo PD, Bayat A, Wagner J, Nutman TB, Baraniuk JN, Iadarola MJ. Neurobiology and Pain Therapeutics Section, Laboratory of Sensory Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD; The Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD; Division of Rheumatology, Immunology and Allergy, Georgetown University, Washington, D.C. [Email: burbelop@.nidcr.nih.gov]