The virus that causes Mono can activate genes associated with autoimmune diseases

The virus that causes mononucleosis, called Epstein-Barr virus (EBV), is surprisingly common in the human population with more than 90% of people contracting the virus by the age of 20. Most of the time, infections are not symptomatic and people don’t know they have the virus. In 35-50% of people however, the infection causes mononucleosis which is characterized by extreme fatigue, cough, and fever. There has been a number of studies over the years that link EBV infection to a variety of autoimmune disorders including: multiple sclerosis and Hodgkin’s Lymphoma. For the most part these studies have only been able to show correlation and not causation in part due to the ubiquitous nature of the virus in human populations. In a recent paper published by a team from Cincinnati, researchers discovered that a viral protein is able to bind to human DNA and turn on genes that are associated with lupus, multiple sclerosis,  rheumatoid arthritis, inflammatory bowel disease, and type-1 diabetes.

Inside our cells, genes within the DNA are turned on (transcribed) when specific proteins, called transcription factors, bind to them. These genes can then be made into proteins and the cell can use them to perform whatever function it needs. We thought that only human transcription factors can bind to our DNA to turn on genes but this doesn’t appear to be true. Using a variety of cells known with EBV infections, the researchers saw that a protein made by the virus, called EBNA2, binds to our DNA in coordination with our own transcription factors. Interestingly, the genes that EBNA2 bind to seem to be enriched for genes known to be associated with different autoimmune diseases. That is to say, these genes are known to be mutated in people with autoimmune diseases (like lupus) and it appears the EBNA2 interacts with these genes to turn them on. This is a striking finding and adds information about the causative nature of EBV in these autoimmune diseases.

So what does this mean? Since 90% of people in the world have EBV why isn’t there more lupus, multiple sclerosis, or diabetes? This paper highlights the importance of understanding the interactions between our genes and our environment as it relates to human disease. Not everyone has the mutations increase their risk for lupus or multiple sclerosis and not all those with the mutations will encounter EBV. Those who have the mutations and encounter EBV may go on to develop the disease or they may not. We don’t have the full picture yet and there may be other environmental factors that contribute to the disease. There is however growing evidence that EBV may play a pivotal role in many of our autoimmune diseases and a vaccine towards it may be an efficient way to lower our risk for these diseases. Just as a vaccine against HPV should reduce the incidence of cervical cancer in women, a EBV vaccine may reduce the incidence of a number of serous diseases.

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