The CFIDS Association commonly reports on research that has been completed and published, but we recognize that readers are also interested in learning about studies that are upcoming or under way. Here’s a summary of three of the five Association-funded studies under way.
Brigitte T. Huber, PhD, of Tufts University School of Medicine in Boston is exploring the presence of human endogenous retrovirus k18 (HERV-K18) as a risk factor for CFS. Results from Huber’s pilot study have shown a strong correlation between infectious agents and CFS. The study also identified the presence of a specific HERV-K18 allele—a superantigen from within the cell—that may prove to be a predictor for postinfectious CFS.
Superantigens constitute a class of proteins capable of deregulating the immune system. Huber has expanded the size of the patient group to examine this relationship, furthering the collective understanding of the diverse interactions that take place between an infectious virus and the immune system of its host. She also hopes to confirm whether a correlation exists between the presence of a particular HERV-K18 allele and the development of CFS. If so, this could provide a viable diagnostic biomarker for the illness in at least a subset of patients.
Nancy Klimas, MD, of the University of Miami is investigating possible mechanisms of immune system dysfunction and working to match those findings with CFS symptom clusters and severity. Her research team is focusing on a key neuropeptide (neuropeptide Y) and a membrane associated with converting peptides to amino acids (known as CD26) and how these two elements may relate to cell damage in CFS. Elevated levels of neuropeptide Y have been demonstrated to cause defects in the function of immune system cells like natural killer (NK) cells and T cells. It also plays a role in the inflammatory process, cardiorespiratory system, nervous system and endocrine system. Preliminary data indicates that CD26 is depleted in CFS, most likely through chronic cellular activation, resulting in immune dysfunction and, ultimately, the symptoms of CFS.
Lastly, a study led by Ronald Glaser, PhD, of Ohio State University is just beginning with support from the CFIDS Association. Dr. Glaser and his team, including three clinical collaborators—Dr. Nancy Klimas, Dr. Dedra Buchwald and Dr. Gailen Marshall—will provide patient samples that will be tested for the presence of incomplete viral proteins that may be responsible for increasing the production of certain cytokines capable of inducing some of the characteristic CFS symptoms. This research is particularly timely given the renewed interest in the role of various viruses in CFS.
As these research teams each focus on their individual investigations of the underlying mechanisms of CFS, the Association will continue to keep you posted on the results.
The CFIDS Association, through your donations, provides the largest source of CFS research money aside from the federal government. We’ve funded nearly $4.7 million in research, but we can do more with your help.
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