A protein made by the Epstein-Barr virus binds to areas of the human genome linked to an increased risk of certain autoimmune diseases.

Many college students know it as the virus that causes the “kissing disease,” or “mono” (mononucleosis.)

But the Epstein-Barr virus (EBV) may also increase the risk of lupus and six other autoimmune diseases by changing how certain human genes are expressed, a new study suggests.

The immune system protects the body from infections and diseases. With autoimmune diseases, the immune system mistakenly attacks the body’s own cells.

Scientists think these conditions likely result from a combination of genetic and environmental factors.

Autoimmune diseases are difficult to treat — no cure is available — and can lead to a lifetime of debilitating symptoms.

The National Institute of Environmental Health Sciences estimates that autoimmune diseases affect more than 23.5 million Americans.

Previous research has linked EBV infection to an increased risk of developing autoimmune diseases, such as multiple sclerosis and systemic lupus erythematosus.

The new study, published on April 16 in Nature Genetics, offers a potential mechanism for how environmental factors and genes interact to make some people more likely to develop these diseases.

In the study, the researchers used data sets to look for associations between EBV infection and autoimmune diseases.

A team led by researchers at Cincinnati Children’s Hospital Medical Center found that a virus protein present in EBV-infected human cells may turn on genes that are associated with an increased risk of lupus and other autoimmune diseases.

They looked at genes activated in immune cells called B lymphocytes that are involved in fighting viral infections.

Researchers found that the virus protein binds to several locations along the human genome that are linked to an increased risk of autoimmune diseases.

This includes lupus, celiac disease, inflammatory bowel disease, juvenile idiopathic arthritis, multiple sclerosis, rheumatoid arthritis, and type 1 diabetes.

The researchers reported that they also found hints of how the virus takes control of the immune system via proteins that can turn a gene “on or off.”

Human cells contain proteins called transcription factors that are responsible for turning on and off certain genes. Using these proteins to turn genes on and off at the right time helps them carry out their individual functions and respond to their environment.

When the virus infects cells, it makes its own proteins or transcription factors. These proteins can change how the B cells function. And as a result, it can lead to the development of autoimmune disease.

The researchers found that the seven autoimmune diseases shared a common set of abnormal transcription factors or proteins.

Binding of these abnormal transcription factors to a certain part of the genetic code increases the risk of lupus or the other autoimmune diseases.

The study still doesn’t answer the question of why almost everyone has an EBV infection at some point in their life, but only a much smaller number develop an autoimmune disease.

EBV is one of the most widespread viruses. Between 90 and 95 percent of adults worldwide are eventually infected with the virus during their lifetime, according to medical reference UpToDate.

Many people become infected with the virus when they are children. They usually don’t have any symptoms at this time, or have only a mild, cold-like illness.

Teens or adults who are infected may develop more severe symptoms, including fever, sore throat, swollen lymph nodes, and fatigue. Symptoms last for weeks and sometime months, but rarely are there serious complications.

After infection, the virus remains in the body, although most people only get sick once.

Having mono as a teen or adult, or EBV infection earlier, doesn’t mean you will definitely develop lupus.

That means other factors are involved.

There are also dozens of gene variants that increase a person’s risk of developing autoimmune diseases.

The researchers found that the virus protein did not interact with many of these genes. And some people whose genes were activated by the protein did not develop an autoimmune disease.

More research is needed to understand why only some people infected with EBV go on to develop an autoimmune disease. Understanding why that happens could help researchers develop new treatments or create a vaccine against EBV.

An EBV vaccine might prevent not only mono, but also autoimmune diseases in some people, similar to how the HPV vaccine reduces the risk of cervical cancer.

While more work needs to be done, the discovery that a virus is involved in the development of autoimmune disease is a promising step forward.