Could a virus that infected chimpanzees millions of years ago help explain how the human brain became different?
Researchers at Lund University have discovered that ancient viral DNA embedded in the chimpanzee genome silences a gene involved in early human brain development. Their study, published in Science Advances, found that the gene, LINC00662, remains active in human brain organoids, where it helps support the development of nerve cells and the connections between them.
The finding offers a way to explore how humans and chimpanzees developed different biological traits despite sharing much of their genetic makeup. Evolution can change how existing genes are used, as well as which genes a species carries.
“The virus we investigated specifically affected chimpanzees. Yet humans and chimpanzees have largely the same genetic makeup. That is why it is important to understand the differences in how genes are regulated. Our findings suggest that one gene, LINC00662, plays a significant role in early human brain development,” says Johan Jakobsson, professor of molecular neurogenetics at Lund University.
How Viral DNA Silences A Gene
The genetic remnant belongs to PTERV1, an endogenous retrovirus. Its DNA became embedded in the chimpanzee genome during an ancient infection and has been inherited ever since. The researchers found copies of the viral sequence at numerous locations throughout chimpanzee DNA.
Those sequences are systematically shut down through methylation, a chemical process that helps regulate gene activity. At the LINC00662 location, the inherited viral insertion also keeps the neighboring gene silent.
To examine this difference during brain development, the team grew brain organoids from human and chimpanzee stem cells. These miniature, three-dimensional structures resemble brain tissue and reproduce some features of its early development.
“The gene was strongly expressed in the human organoids, but not at all in the chimpanzee organoids,” says Patricia Gerdes, a postdoctoral researcher in molecular neurogenetics at Lund University.
Removing the Virus Restores Gene Activity
The researchers then tested whether the viral sequence caused the shutdown. Using the CRISPR-Cas9 gene-editing tool, they removed it from chimpanzee cells. LINC00662 became active again.
“This shows that it is in fact the viral insertion that is responsible for the gene being switched off in chimpanzees,” says Patricia Gerdes.
A separate experiment explored the gene’s role in humans. When the team used CRISPR to silence LINC00662 in human brain organoids, genes involved in nerve cell development and the formation of connections between those cells became less active.
For Jakobsson, the results show how an infection can leave a lasting genetic change across a population, while helping explain how gene regulation can protect the brain or contribute to damage. The team will next investigate whether other viral remnants influenced brain evolution and whether such sequences are linked to brain diseases.
Reference: “Retroviral insertions contributed to the divergence of human and chimpanzee brains” by Patricia Gerdes, Ofelia Karlsson, Raquel Garza, Diahann A. M. Atacho, PingHsun Hsieh, Bharat Prajapati, DongAhn Yoo, Chandramouli Muralidharan, Anita Adami, Carrie Davis-Hansson, Emily M. Johansson, Yogita Sharma, Laura Castilla-Vallmanya, Wiktor West, Meghna Vinod, Lucian Domitrovic, Pia A. Johansson, Jenny Johansson, Christopher H. Douse, Chandrasekhar Kanduri, Patric Jern, Evan E. Eichler and Johan Jakobsson, 23 October 2026, Science Advances.
DOI: 10.1126/sciadv.aeg5791
This study was funded by the Swedish Research Council; the Swedish Brain Foundation; Cancerfonden; Barncancerfonden; the Swedish Government Initiative for Strategic Research Areas (MultiPark & StemTherapy); and the European Union’s Horizon Europe research and innovation program.
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