“Endogenous retroviruses (ERVs) and their expression in chronic fatigue syndrome”
PI: Dawei Li, PhD
University of Vermont
Dr. Dawei Li will use a novel algorithm developed by the University of Vermont Li Laboratory bioinformatics team to identify and type genome-wide endogenous retroviruses (ERVs). ERVs are viral elements in our genome that are derived from retroviruses. If successful, the study could identify genetic and viral causes of ME/CFS in severely ill patient cohorts identified by Drs. Alain Moreau (Université de Montréal), Ron Davis (Stanford University) & Wenzhong Xiao (Harvard University), and Alan Light (University of Utah). Dr. Li has set up a powerful collaboration that will leverage the collective knowledge and innovation across five laboratories.
Major Ramsay goals fulfilled:
✓ Bringing new researchers into the field. The Ramsay awards allowed Dr. Li, an innovative early career-stage researcher, to lead his first study on ME/CFS
“It is our hope that this project might lead to identification of endogenous retrovirus signatures that distinguish ME/CFS from a healthy condition. The long-term goal of our research is to establish genetic markers and, ultimately, a treatment for ME/CFS. Despite its prevalence and impact, ME/CFS receives little research funding from the NIH. I hope that this project will help demystify a devastating and understudied disease. I am fortunate to have been introduced into this fascinating field.”
Read a paper describing ERVcaller, a novel methodology to comprehensively analyze genome-wide ERVs, developed by Dr. Li’s lab here
Read the research team’s project summary below:
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe debilitating disease that affects approximately 1.3 million Americans. Currently, no molecular biomarkers or FDA-approved treatments are available. The causes of ME/CFS remain unknown; however, ME/CFS is known to be a chronic inflammatory disease. Endogenous retroviruses (ERVs), which comprise 8% of the human genome, are elements derived from ancient retroviruses. Most ERV elements normally remain silent; however, with certain biological triggers some ERVs can be activated to express viral proteins. Due to the viral nature, expression of ERVs may trigger response of the human immune system. We hypothesize that ERVs have significant impacts on the immune response and chronic inflammation features seen in ME/CFS patients.
In this project, we will carry out a comprehensive analysis of genome-wide ERVs and their gene expression to identify ERV signatures that are associated with proinflammatory cytokines and ME/CFS outcomes. If successful, findings from this project would prompt a new paradigm for thinking of ME/CFS as a disorder of ERV super-activation and suggest that anti-retroviral or anti-inflammatory drugs could be therapeutic for individual ME/CFS patients.