Researchers at Lund University in Sweden report that a viral pandemic millions of years ago left a lasting mark on chimpanzee DNA — and possibly on how our brains diverged.

The retrovirus, named PTERV1 (Pan troglodytes endogenous retrovirus 1), infected chimpanzees and other African apes but not humans. One of its insertions sits inside the LINC00662 gene and silences it in chimpanzee cells, while the same gene is strongly active during early human brain development.

The team, led by professor Johan Jakobsson and postdoc Patricia Gerdes, published the findings in Science Advances, combining genome comparisons, stem-cell models and CRISPR gene editing.

Humans and chimpanzees differ in only about 1.2 percent of their DNA after 5–6 million years of separate evolution, yet our brains are roughly three times larger. The idea that a virus — not a protein-coding mutation — could help drive that gap is a striking twist.

According to ScienceAlert, Gerdes said ancient viruses can leave DNA behind in the genome and those remnants can affect nearby genes, making PTERV1 a particularly interesting candidate because it is found in chimpanzees and other African apes but not in humans.

phys.org notes Jakobsson's view that the findings show a virus can cause a DNA sequence to change across an entire population.

The researchers grew brain organoids from human and chimpanzee stem cells and found LINC00662 was strongly expressed in the human models but undetectable in the chimpanzee ones.

Using CRISPR-Cas9, they removed the roughly 7,000-letter viral insertion from chimpanzee stem cells — and the gene switched back on, confirming the insertion is responsible for the silencing.

The Brighter Side of News reports that the viral sequence is suppressed by methylation, which spread into surrounding gene regulatory regions, and that the human gene's RNA peaked in fetal brain tissue around 10 to 12 weeks after conception.

When the team suppressed LINC00662 in human organoids, markers of nerve-cell extension development declined by day 30.

The work reframes retroviral insertions as active participants in brain evolution, not just genomic junk. It reinforces the view that humans and chimpanzees differ not only in which genes they carry but in which genes are switched on.

Gerdes told ScienceAlert that if humans had the same insertion it probably would have switched off LINC00662 and altered brain-cell development, though she cautioned it cannot be predicted this would produce a particular brain shape or ability.

The Brighter Side of News stresses the study identifies one molecular mechanism of divergence without establishing effects on intelligence, overall brain size or disease — and there is no Planet of the Apes scenario looming from removing the insertion in adult brains.

The Lund team plans to investigate whether other viral remnants had similar effects on brain evolution and whether this type of DNA sequence is linked to brain diseases.

Open questions remain: The Brighter Side of News notes researchers have not yet identified the DNA-binding repressor that targets PTERV1, and it is unclear why humans escaped infection — theories include protection by a unique antiviral protein, TRIM5α, or simply different habitats when the pandemic hit.

Future work will test additional remnants to learn whether LINC00662 is an unusual case or one of many inherited consequences of ancient infections.