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Epstein-Barr virus infections, cause of infectious mononucleosis, have been badociated with the subsequent development of systemic lupus erythematosus and other chronic autoimmune diseases, but the mechanisms at the The origin of this badociation has not been clearly established. Now, a new computer method shows that a viral protein found in human cells infected with the Epstein-Barr virus could activate genes badociated with an increased risk of autoimmunity.
Epstein-Barr virus infection is very common in the world's human population. Most people acquire it at the beginning of their childhood, they feel no symptoms or only a brief and light condition similar to a cold, and they remain infected throughout their lives but remain asymptomatic. When the infection occurs for the first time in adolescence or early in adulthood, the Epstein-Barr virus can lead to an infectious syndrome of mononucleosis, also known as the name of "sickness of the kiss", which usually resolves itself with rest. rarely causes serious complications.
When the Epstein-Barr virus infects human immune cells, a protein produced by the virus (Ebna2) recruits human proteins called transcription factors to bind to both regions of the virus genome and the cell's own genome. Together, Ebna2 and human transcription factors alter the expression of adjacent viral genes.
In the new study, the team of Dr. John B. Harley, director of the Center for Autoimmune Genomics and Etiology at the Cincinnati Children's Hospital Medical Center in the United States United, has shown that Ebna2 and its transcription factors activate some of the human genes badociated with the risk of suffering from lupus and other autoimmune diseases, including multiple sclerosis, rheumatoid arthritis and intestinal diseases. inflammation, type 1 diabetes, juvenile idiopathic arthritis and celiac disease.
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