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Some pieces of our DNA can copy themselves into new locations. Copies derived from one gene active in human brain cells appear to have taken that journey further: into a virus.

Researchers found two such sequences, derived from a gene called BC200, inside molluscum contagiosum virus, which infects our skin and causessmall, raised lesions.

The discovery reveals an unusual genetic double life. BC200 acquired a cellular role millions of years ago, yet retained the ability to produce copies that insert themselves elsewhere.

A study published in Science suggests this movement has continued throughout primate evolution, contributed to differences among human genomes, and carried BC200-derived sequences across the boundary between humans and a virus.

But the virus didn’t simply take a gene from a brain cell, and nothing suggests it gained anything resembling brain function. What these sequences actually do inside the virus is still unknown.

BC200 works differently from most genes: it skips the step of coding for a protein altogether, producing a short RNA molecule instead – one that’s especially abundant in neurons.

Laboratory experiments suggest this RNA helps regulate protein production. Its precise physiological role, however, remains poorly understood.

A gene being especially active in one tissue does not mean its DNA exists only there. Most cells with a nucleus carry essentially the same genetic information. What differs is which genes they use, and how much.

Calling BC200 a “brain gene” describes its activity in neurons.

Its origins lie in a transposable element, one of the mobile DNA sequences often called “jumping genes”. Some make copies of themselves that enter new locations while the original stays put.

A predecessor of BC200 became established in a common ancestor of monkeys and apes roughly 35 to 55 million years ago. Around 40 million years ago, it was recruited for a cellular role, apparently in regulating protein production in neurons.

Such recruitment typically accompanies a loss of mobility. BC200 appears to have retained both abilities.

“Somehow evolution hasn’t been able to untangle these two things,” Cedric Feschotte, in Cornell University’s Department of Molecular Biology and Genetics, says in auniversity statement.

The team, including researchers at Capital Normal University in China and the University of Texas at Arlington, screened available poxvirus genomes for sequences resembling mobile genetic elements.

Two BC200-derived sequences stood out in molluscum contagiosum virus. One covered the human gene’s entire Alu-derived domain, a region inherited from its mobile ancestor. The other was shorter and incomplete at both ends.

So what turned up in the virus are fragments derived from BC200 – not a complete, intact copy of the gene itself.

Several clues pointed to a human origin. BC200 occurs in humans and related primates, while molluscum contagiosum virus is only known to infect humans in nature.

The researchers found no corresponding elements in other poxvirus genomes they examined, including a closely related virus infecting horses.

The analysis pointed to two separate transfer events, not a single insertion that later duplicated itself inside the virus.

The likely mechanism involves LINE-1, another mobile genetic element capable of producing the molecular machinery to copy RNA into DNA and insert it into a genome.

BC200 has no transport machinery of its own, so it hitches a ride on LINE-1’s – borrowing another element’s equipment to make the jump.

Genetic signatures surrounding the viral insertion supported this explanation. However, the team reconstructed the transfer from DNA evidence, rather than watching it happen.

Although BC200 RNA is abundant in neurons, it is also expressed at low levels in skin. The researchers found increased BC200 expression in cultured human fibroblasts infected with the virus.

That suggests infection might help create conditions for transfer, without directly establishing where the historical events occurred.

The team then examined sequencing data from 908 people, identifying eight BC200-derived insertions that varied among individuals.

Two were widespread across five continental population groups, suggesting ancient origins. Another was largely restricted to African individuals. The remaining five were rarer: one occurred in just two people, while four were each detected in a single individual.

These rare insertions suggest very recent activity. Being detected in one person, however, does not establish that an insertion arose during that person’s lifetime.

Across anthropoid primates, the researchers also identified hundreds of lineage-specific insertions, placing the viral discovery within millions of years of continued movement.

Whether the virus benefits remains uncertain. The team found evidence that its BC200-derived sequences are transcribed into RNA. Such RNA might help manipulate protein production in infected cells, but that possibility still needs testing.

The study does not demonstrate that the virus has become more dangerous. Instead, it shows that acquiring a cellular function need not end a genetic element’s mobility.

BC200’s combination of function and movement makes the boundary between genes and jumping DNA appear more flexible than expected.

The research has been published in Science.