Viruses may play a part in schizophrenia

Researchers often investigate genetic and brain disturbances for causes of schizophrenia, a severe mental disorder of unknown origin. A new angle on schizophrenia comes from a study suggesting that a virus causes or triggers some cases of this often-debilitating condition.

Certain retroviruses, which carry genetic information in RNA instead of DNA, display elevated activity in the central nervous systems of nearly 30 percent of young adults hospitalized for the first time with schizophrenia, according to a report in the April 10 Proceedings of the National Academy of Sciences.

“While a low level of retrovirus expression occurs in most human tissues, we found an unexpectedly high level of expression in the cerebrospinal fluids from individuals who’d had a recent onset of schizophrenia,” says neurovirologist Robert H. Yolken of Johns Hopkins School of Medicine in Baltimore, a coauthor of the new report.

Some retroviruses, such as the AIDS virus, HIV, enter the body from external sources. Others, called endogenous retroviruses, inserted themselves into the human genome at various times during the course of evolution.

Yolken’s group detected DNA sequences produced by endogenous retroviruses in the cerebrospinal fluid of 10 of 35 individuals within 6 weeks of their initial hospitalization for schizophrenia. The most common sequence, found in seven participants, is known from prior research to be activated in multiple sclerosis. That retroviral sequence also appeared in 1 of 20 people with chronic schizophrenia who had been ill for periods ranging from 1 to 37 years, the researchers say.

In contrast, no retroviral footprints appeared in the cerebrospinal fluid of 22 individuals with other brain disorders and 30 volunteers who were free of neurological and psychiatric ailments.

Reasons for this retroviral activation in some instances of schizophrenia remain unknown, Yolken says. He and his colleagues plan to examine whether using drugs that block retroviral activity helps to dampen any of schizophrenia’s symptoms. Those include hallucinations, delusions, social withdrawal, and difficulty in interpreting everyday sights, sounds, and feelings.

Little direct evidence exists for a viral influence on schizophrenia, cautions psychiatrist Daniel R. Weinberger of the National Institute of Mental Health in Bethesda, Md. “These new results have to be independently replicated,” he says.

Nonetheless, the new data raise intriguing issues, remarks psychiatrist David A. Lewis of the University of Pittsburgh in a commentary published with the new study. For example, the clustering of retroviral sequences in people with recent-onset schizophrenia suggests that the activation of certain retroviruses contributes to the disorder’s initial progression, Lewis says. However, the appearance of retroviruses in only a minority of patients supports the view that schizophrenia arises through several different causal pathways, he adds.