Ancient viruses have left behind traces in our DNA. Researchers believe these contribute to neurological conditions. Could inhibiting our viral passengers pave the way for future treatments? Share on Pinterest What links neurological conditions and ancient viruses? Transposable elements, which scientists also call transposons or jumping genes, are stretches of DNA that harbor the ability to move around our genome. Scientists can trace back one type of transposon — human endogenous retroviruses (HERVs) — to ancient retroviruses that inserted themselves into the human genome millions of years ago. HERVs make up about 8% of our DNA. Some HERVs hold crucial functions during processes such as embryonic development. But most HERVs lie dormant, silenced by DNA modifications. Yet, in a recent review article in Frontiers in Genetics, researchers from Heinrich Heine University in Dusseldorf, Germany, detail how some HERVs may be reactivated and wreak havoc in our brain and central nervous system.

HERVs in neurological diseases Back in 1989, Hervé Perron, then at the University of Grenoble in France, was the first to identify the presence of viral particles in cell cultures isolated from the cerebrospinal fluid (CSF) of a person with multiple sclerosis (MS). He later discovered that these originated from a transposon called HERV-W. Activation of this dormant HERV results in an immune reaction. HERV-W envelope (ENV) RNA and protein are present at increasing levels in the serum and CFS of people with MS, but only rarely in those without the condition. “Linking this HERV reactivation to autoimmune attacks in MS, it was found that HERV proteins can trigger an immune response against myelin, which triggers MS-like disease in mouse models,” explains Patrick Kuery, a professor of neurodegeneration and senior review author. Several triggers can reactivate HERVs. One of them is infection with common viruses, such as the Epstein-Barr virus that causes infectious mononucleosis, and other members of the herpes virus family. Research also suggests that immune system mediators and environmental factors, such as diet and drugs, can switch HERVs back on, although there is limited evidence at this point. MS is not the only neurological disease where scientists suspect HERV involvement. A number of studies have implicated reactivation of HERV-K in amyotrophic lateral sclerosis (ALS), a form of motor neuron disease. When it comes to schizophrenia, the case is less clear. “HERV proteins have been reported to increase expression of schizophrenia-linked genes in cultured human brain cells,” explains Kuery. “However, studies on schizophrenia [patients] show inconsistent changes in HERV expression in blood, CSF, and postmortem brain tissue compared to healthy controls.”