There are currently a few cellular and genetic studies being conducted on Chronic Fatigue Syndrome:
The Tufts University School of Medicine in Boston is currently studying the presence of human endogenous retrovirus k18 (HERV-K18) as a risk factor for Chronic Fatigue Syndrome. A pilot study has shown that there is a strong correlation between infectious agents and Chronic Fatigue Syndrome. The study also identified the presence of a specific HERV-K18 allele superantigen from within the cells that may prove to be a predictor for postinfectious CFS.
The University of Miami is currently studying possible mechanisms of immune system dysfunction and working to match those findings with CFS symptom clusters and severity. The 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.
The Ohio State University is studying 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.