Today, one of the most burning questions, still unanswered, has to do with the role of viral infections.
While schizophrenia is known to have at least some genetic component, a growing body of evidence has also linked this disorder to viral exposure, and this includes the Epstein-Barr virus (EBV), a herpes virus that causes infectious mononucleosis, also known as mono.
While past research has gone back and forth on this connection, a new study has pushed us a little closer to an answer.
Researchers at Johns Hopkins Medicine have now shown that people with schizophrenia have higher levels of antibodies against EBV, a potential new marker for this serious disorder.
“We found that individuals with schizophrenia had an unusual response to Epstein-Barr virus,” says senior author Robert Yolken, an expert in psychiatric disorders at Johns Hopkins.
“This indicated that the prevention and treatment of Epstein-Barr virus might represent an approach for the prevention and treatment of serious psychiatric disorders such as schizophrenia.”
The study gathered together 743 individuals, 432 of whom had received a schizophrenia diagnosis and 311 without a history of psychiatric disorders.
Most of the participants were found to have a low level of EBV-associated antibodies, which suggests that many had already been exposed to this common virus.
But when comparing the different levels of these antibodies, the researchers noticed a curious difference between the two groups. It appeared that those with schizophrenia were 1.7 to 2.3 times more likely to have increased levels of some specific types of EBV antibodies.
The research is buttressed by a recent study, which found that those with autoimmune disorders are around 40 percent more likely to develop psychotic disorders such as schizophrenia.
The reasons for this aberrant immune response are still unclear, although the researchers have proposed two suggestions: schizophrenia could be altering the immune system of these patients, making them more susceptible to EBV, or the EBV infection might somehow be increasing the risk of schizophrenia.
But there are still a lot of details to be combed out before we can start labelling the chicken and the egg. Strangely enough, for instance, the results did not extend to other herpes viruses.
When the study was repeated with related infections, like chicken pox and the virus that causes cold sores, the immune system of patients with schizophrenia appeared to be coping just fine.
Strangely enough, this suggests that EBV is the only herpes virus that can be linked to an increased risk of schizophrenia.
“The increased levels of antibodies to EBV virions found in the individuals are not reflective of a heightened immune response to human herpesvirus but is specific to EBV within this group of infectious agents,” the authors conclude.
Whatever the connection might be, it appears to be a powerful one. When the researchers began to delve into the genetics, they found that those with a higher genetic risk for schizophrenia as well as higher antibody levels to EBV, were more than eight times more likely to develop schizophrenia.
It’s a calculation that cannot be ignored, even if other studies have not found the same. The authors hope that with more research, some day we might be able to use this curious connection to create a new method for preventing and treating schizophrenia.
This study has been published in Schizophrenia Bulletin.