Brigitte Huber

Brigitte Huber, PhD, is a Professor of Integrative Physiology & Pathobiology, at the Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts. She has studied the presence of retrovirus HERV K-18 as a potential biomarker for those who develop myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) after a case of infectious mononucleosis. HERV-K18 is one of many endogenous human retroviruses in the normal human genome. It can be activated in a variety of ways and affect the outcome of Epstein-Barr virus infection and influence autoimmune disease. Dr. Huber's research has shown that there are more HERV K-18 alleles in post-mononucleosis ME/CFS patients than in controls.

In 2011, Dr. Huber and her lab associates were one of the groups who were unable to duplicate Dr. Judy Mikovits's finding of the presence of XMRV in ME/CFS patients. In 2013, she and her lab associates were unable to show reactivation of human herpesvirus 6 (HHV-6) or human herpesvirus 7 (HHV-7) in chronic fatigue syndrome.

Education

 * BA, Biology, University of Zurich
 * MSc, Pharmacology, University of Basel
 * PhD, Immunogenetics, University of London
 * Postdoctoral Training, Harvard Medical School

Talks & interviews

 * 2010, Speaker at the 5th [[Invest in ME International ME Conference] on Presence of Retrovirus as a Biomarker for ME/CFS] DVD available

Studies

 * 2013, Human endogenous retrovirus-K18 superantigen expression and human herpesvirus-6 and human herpesvirus-7 viral loads in chronic fatigue patients."ABTRACT : METHODS : Blood and saliva were collected from 39 CFS cases and 9 healthy control subjects. Peripheral blood mononuclear cells (PBMCs) were tested for human endogenous retrovirus-K18 (HERV-K18) env transcripts using a TaqMan quantitative polymerase chain reaction (qPCR). In addition, viral copy number of human herpesvirus-6 (HHV-6) and human herpesvirus-7 (HHV-7) were measured in both saliva and PBMCs using TaqMan qPCRs. Transcript levels and viral copy number were compared to patient CFS symptom severity. RESULTS: HERV-K18 env transcripts were not significantly different between healthy control subjects and CFS patients. Also, HERV-K18 env transcripts did not correlate with HHV-6 viral copy number or HHV-7 viral copy number in either PBMCs or saliva. HHV-6 viral copy number and HHV-7 viral copy number in both PBMCs and saliva were not significantly different between healthy control subjects and CFS patients. HERV-K18 env transcripts, HHV-6 viral copy number, and HHV-7 viral copy number did not correlate with CFS symptom severity. CONCLUSIONS: We fail to demonstrate a difference in HERV-K18 env transcripts, HHV-6 viral copy number, and HHV-7 viral copy number between CFS patients and healthy controls. Our data do not support the hypothesis of reactivation of HHV-6 or HHV-7 in CFS."
 * 2011, Failure to Detect XMRV-Specific Antibodies in the Plasma of CFS Patients Using Highly Sensitive Chemiluminescence Immunoassays.
 * 2001, Epstein-Barr virus transactivates the human endogenous retrovirus HERV-K18 that encodes a superantigen.