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A groundbreaking study has revealed that ancient viral DNA, embedded in the human genome for millions of years, plays a critical role in the brain’s susceptibility to psychiatric disorders such as schizophrenia, bipolar disorder, and depression. Published today in Nature Communications, the research identifies specific “fossilized” viral sequences—known as human endogenous retroviruses (HERVs)—that are actively expressed in the brain and influence neurological function, offering a potential new avenue for targeted therapies.
The Viral Remnants Inside Us
Around 8% of the human genome is composed of these ancient viral remnants, left behind by infections that occurred in our primate ancestors. For decades, scientists dismissed most of this DNA as “junk,” silent relics with no biological purpose. However, a team led by Dr. Timothy Powell at King’s College London and Dr. Rodrigo Duarte at the Broad Institute of MIT and Harvard has now demonstrated that certain HERVs are far from inert.
Using post-mortem brain tissue samples from nearly 800 individuals—some with diagnosed mental health conditions and some without—the researchers mapped where and when these viral genes were turned on. They identified two specific HERV families, HERV-K and HERV-H, that are more active in the brains of people with schizophrenia and bipolar disorder compared to healthy controls.
“We found that these ancient viruses are not just sitting there quietly,” said Dr. Duarte in a statement. “They can be reactivated and influence the expression of nearby human genes, particularly those involved in immunity and synaptic function.”
How Ghost Genes Affect the Brain
The study found that HERVs can act as “enhancers” —DNA sequences that amplify the activity of other genes. When a specific HERV sequence became active, it boosted the expression of a gene linked to inflammation in the brain, a known factor in multiple psychiatric conditions.
Conversely, other HERVs appeared to suppress genes crucial for forming connections between neurons. This dual mechanism—both promoting inflammation and hindering neural communication—could explain the complex, overlapping symptoms seen in mood and psychotic disorders.
“It is a bit like having hidden switches in our genetic wiring,” explained Dr. Powell. “Depending on the environment and other genetic factors, these switches can flick on or off, altering the risk of mental illness.”
Implications for Treatment
These findings represent a paradigm shift. Most current psychiatric medications target neurotransmitter systems like dopamine or serotonin, often with limited efficacy and significant side effects. Because HERVs are unique to the human genome and differ between individuals, they present an entirely new class of drug targets.
For example, antiretroviral drugs, similar to those used to treat HIV, are already being tested in early clinical trials to see if they can dampen HERV activity in the brain. Additionally, CRISPR-based gene editing could theoretically silence specific harmful viral sequences.
“Imagine being able to ‘turn off’ a genetic risk factor that has been lying dormant since the Stone Age,” said Dr. Duarte. “That is the promise of this research, though we are years away from clinical application.”
Broader Impact and Next Steps
The discovery also reshapes our understanding of human evolution. It suggests that ancient viral pandemics did not just leave scars on our ancestors’ immune systems—they left permanent marks on our mental health. This interplay between infection, evolution, and brain function may help explain why mental illness persists in the population despite its serious disadvantages.
The research team is now expanding the study to include larger, more diverse populations and investigating whether lifestyle factors—such as stress, infection, or diet—trigger HERV reactivation.
“We are only scratching the surface,” said Dr. Powell. “This is not junk DNA. It is a hidden archive of our evolutionary past that continues to shape our present health.”
Related Reading:
- How ancient viruses influence cancer and autoimmune diseases
- The role of inflammation in treatment-resistant depression
