Pandemics can arise wherever animal or human populations are sufficiently large, and they are not confined to the modern age. Johan Jakobsson, Professor of Molecular Neurogenetics at Lund University, believes that the findings from the new study are highly relevant: they show that a virus can cause a DNA sequence to change across an entire population.
“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.
This, Jakobsson adds, helps our understanding of how gene regulation can protect or cause damage to, for example, the brain. In the new study, published in Science Advances , the researchers have discovered that an ancient viral remnant in the chimpanzee genome silences the LINC00662 gene. The same gene, meanwhile, is active in humans and plays an important role in our early brain development. The viral remnant belongs to a so-called endogenous retrovirus, PTERV1 – a virus that infected the chimpanzee population millions of years ago. The PTERV1 virus’s genetic material remained in the genome and has since been passed down through the generations.
The researchers observed that PTERV1 replicated itself in many locations within the chimpanzee’s DNA and that these viral sequences are systematically silenced through a process known as methylation – a mechanism that determines which genes are active or inactive.
To investigate how the viral remnant affects brain development, the researchers used human and chimpanzee stem cells to create brain organoids. These three-dimensional miniature organs resemble real brain tissue and can display certain characteristics of early brain development. A comparison of the organoids showed that the LINC00662 gene was active in the human models but completely silenced in the chimpanzee models.
“The gene was strongly expressed in the human organoids, but not at all in the chimpanzee organoids,” says Patricia Gerdes, postdoc in molecular neurogenetics at Lund University.
To test whether the viral remnant was responsible, the researchers used the CRISPR-Cas9 gene-editing tool to remove the viral DNA sequence from chimpanzee cells. Once the viral remnant had been removed, the gene was expressed 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.
The researchers also investigated the gene’s apparent function in humans. When they used CRISPR to silence LINC00662 in human brain organoids, this reduced the activity of genes involved in nerve-cell development and in the formation of connections between nerve cells.
The findings reinforce the view that humans and our closest relatives differ not only in which genes are present, but also in which genes are active. The researchers will next investigate whether other viral remnants may have had similar effects during the evolution of the brain and whether this type of DNA sequence is also linked to brain diseases.
Science Advances
Experimental study
Cells
Retroviral insertions contributed to the divergence of human and chimpanzee brains
23-Oct-2026