Discovery of PathoGENEIC ViRAL MOLECULAR mimicries

VIRUSES CAN ESCAPE THE IMMUNE SYSTEM BY PRODUCING PROTEINS that ARE SIMILAR TO thE HUMAN ONES. WE AIMED AT DISCOVERING THESE VIRAL PROTEINS in order to link them TO HUMAN PRotEINs related to THE CIRCADIAN RHYTHM that is disrupted in ME/CFS patients

Viral proteins can be similar in structure and sequence to the human ones

Background

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) has been widely reported as a post-infection sequela by survivors of Ebola, Chikungunya, Dengue, and Severe Acute Respiratory Syndrome (SARS) outbreaks. Similar debilitating sequela is expected in the aftermath of the ongoing pandemic of COVID-19 caused by SARS-like coronavirus 2 (SARS-CoV2). Pathologically speaking, ME/CFS has been hypothesized as an aberrant immune response against viral and human proteins sharing similar molecular characteristics - the so-called molecular mimicry. However, the precise causal proteins of ME/CFS remain to be identified. In this project, an integrative bioinformatic analysis will be conducted to discover candidate molecular mimicries between human proteins from the circadian rhythm and different human viruses including SARS-CoV2. To achieve this goal, available human genetic data coupled with computational and statistical techniques from bioinformatics, immunogenetics, and population genetics will be used.

Impact

Dr. Nuno Sepúlveda has been invited to present the results of this project at the 2nd International Meeting of the Chronic Fatigue Center (Charité Berlin, 11-12 May 2023).