Wednesday, January 20, 2010
With the current interest in the retrovirus XMRV, the Patient Advocate came across the name of Brigette Huber again. In the excitement of XMRV we tend to forget about other important research.
The Patient Advocate notices that Dr. Huber is speaking at the upcoming CFS/ME conference in London in May 2010. Here is what the conference brochure says:
"Professor Huber studied immunogenetics at University of London and is currently Professor of Pathology at Tufts University, Boston, USA. Dr. Huber joined the faculty of Tufts Medical School in 1977, and her laboratory has investigated the cellular and molecular mechanisms involved in the immune response since that time. She has studied the presence of retrovirus HERV K-18 as a marker for those who might develop ME/CFS after an acute infection such as mononucleosis. Her research shows that EBV induces the HERV K-18 envelope gene to trigger the expression of a specific superantigen and that there are more HERV K-18 alleles in post-mono ME/CFS patients than in controls. She hopes to identify other subsets among CFS patients."
Dr. Huber is studying an endogenous retrovirus - HERV K-18 and its relation to infectious mononucleosis induced CFS/ME patients. IM is connected to EBV. Dr. Huber's work is both serious and exciting and now is a good time to remember that there is other serious research going on in CFS, research that might bring some answers.
Dr. Huber does important research on a potential subset of CFS/ME, funded by the NIH with a five year grant. Dr. Huber gave a talk at the Viral conference in Baltimore, MD in June 2008. In the Patient Advocate's report on that conference, the PA did not even take note of her talk, which shows how much he knows. Two years later the PA begins to register what she is doing. Her talk can be seen here: www.scivee.tv/node/6864
Here is some further information on her work:
"Brigitte Huber, PhD, of the Tufts University School of Medicine, presented evidence at a medical conference that suggested that a reactivated ancient retrovirus embedded in the human genome may be active in chronic fatigue syndrome (CFS) and multiple sclerosis (MS) patients. Danish scientists at the same conference suggested that the activation of this retrovirus, dormant in healthy individuals, could be the reason why autoimmune conditions worsen with viral infections.
Chronic Fatigue Syndrome and Multiple Sclerosis Patients at Increased Risk From the Effects of HERV-K18 Activation
"Patients with profoundly fatiguing diseases such as MS and CFS may be particularly susceptible to HERV-K18 activation," said Dr. Huber. The announcement was made at the International Symposium on Viruses in CFS and Post-Viral Fatigue, a satellite conference of the 6th International Conference on HHV-6 & 7. Using an SNP-based genotyping method, Dr. Huber found that both MS and CFS patients (whose illness had been triggered by infectious mononucleosis) were at a higher relative risk for containing HERV-K18 variants known to induce superantigen activity. Superantigens are proteins that are able to induce a strong undifferentiated T-cell response believed to impair the immune system over time.
Viral activity and/or immune activation has been shown to trigger HERV-K18 activity. Both Epstein-Barr virus infection (infectious mononucleosis) and interferon-alpha administration are associated with HERV-K18 activity. "HHV-6 activates HERV-K18 as well," said Danish investigator Per Hollsberg, MD and professor from the University of Aarhus In Denmark. His PhD student Vanda Lauridsen Turcanova presented this data at the same conference. "Furthermore, this retrovirus activation may have important consequences for autoimmunity," he added.
HERV-K18 activation may be the endpoint of an HHV6/EBV interferon pathway operating in both MS and CFS. HHV-6 is being investigated as a co-factor in both diseases. Other retroviruses, HERV-H and HERV-W, have been implicated in MS by other researchers. Over 75% of MS patients meet the criteria for CFS. Fatigue is often the most disabling symptom for MS patients. The two diseases also share characteristics such as grey matter atrophy, impaired cerebral glucose metabolism, autonomic nervous system activity and altered patterns of brain activity.
Dr. Huber's study suggests that endogenous retroviral activation in CFS and MS could produce some of the symptoms associated with both diseases. She has received a National Institutes of Health (NIH) grant to study these issues. Per Hollsberg has done extensive research on the role of EBV and HHV-6 in multiple sclerosis."