New data on mononucleosis
Harmless "kissing disease" increases the risk of lupus
A group of researchers from the Cincinnati Children's Hospital Medical Center (Cincinnati Children's Hospital Medical Center) established a link between the infection of patients with the Epstein–Barr virus and an increased risk of a dangerous autoimmune disease – systemic lupus erythematosus.
The virus, discovered in 1964 by English scientists Michael Epstein and Yvonne Barr, is one of the most common among people. In the USA, up to 95% of the adult population is infected with it. The most common manifestation of this virus is infectious mononucleosis, or "kissing disease". It is transmitted by airborne droplets, not only when kissing, but also, for example, when sharing dishes.
The incubation period is quite long, up to three weeks, and all this time the infected person can transmit the virus to others. Symptoms of the disease are weakness, fever, sore throat, enlarged lymph nodes. Patients have enlarged liver and spleen, often when pressed in the area of the right hypochondrium, pain is felt. A blood test reveals cells of a special kind – atypical mononuclears.
Most often, people suffer from mononuleosis at a young age, up to 30 years. After the symptoms disappear, a person remains a carrier of the virus for life, but usually the body's immune system keeps the virus under control.
However, doctors have long noticed that the Epstein–Barr virus is not always so harmless. In particular, they drew attention to the connection of this virus with several autoimmune disorders, including multiple sclerosis and rheumatoid arthritis. It was also found that children infected with the virus are 50 times more likely to have lupus.
To determine the reasons for this, a team of researchers led by John Harley examined five proteins of the Epstein–Barr virus. It was found that one of them (EBNA-2), when the virus enters human B-lymphocytes, interacts with several genome loci associated with an increased risk of lupus. A similar interaction is observed with variants of genes that entail a high risk of several other autoimmune diseases. The study was the first indication of a possible mechanism for how environmental factors, such as infections, alter genetic risk and make some people more vulnerable to autoimmune inflammatory diseases. It also points to a possible therapy pathway using EBNA2 inhibitors or other proteins that bind to DNA at the same loci.
The work was published in the journal Nature Genetics.
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