A human brain gene can still jump through DNA, and turned up inside a poxvirus

Molluscum contagiosum virus, the poxvirus behind a common childhood skin infection, carries two copies of a human gene that is still capable of moving around the genome. The gene is BC200, a stretch of DNA active mainly in neurons, and its presence in the virus points to an act of genetic theft from infected human skin cells. Cornell University molecular biologist Cedric Feschotte led the work, published in Science on September 24, 2026, with Cheng Sun of Capital Normal University in Beijing and Ellen Pritham of the University of Texas at Arlington as fellow lead researchers.

BC200, a neuronal RNA built from a jumping gene

The gene does not make a protein. It makes a short non-coding RNA, and the question the Science paper answers is whether the DNA behind that RNA is still capable of copying itself into new places in the genome, as its ancestors once did.

According to Cornell’s release, BC200 originated from an ancient transposon, a mobile genetic element, roughly 40 million years ago in a primate ancestor. It codes for a non-coding RNA believed to regulate how neuronal messenger RNAs are translated into proteins, and it is expressed primarily in neurons. The team also reports low levels in germ cells, and elevated levels in the brains of Alzheimer’s patients, along with abnormal expression in certain tumors.

Transposons make up about half of human DNA, but few of them can still move. The unusual feature, as Feschotte put it, is that genes repurposed from transposable elements usually stop moving, while BC200 appears to have kept that capacity while taking on a cellular role. Cornell describes it as the first documented human gene that is both still mobile and clearly serving a cellular function, a combination that evolution had not been known to leave intact in a human gene.

Two insertions in molluscum contagiosum virus

The researchers found two independent insertions of human BC200 in the genome of molluscum contagiosum virus, a poxvirus that infects only humans. The CDC describes the infection as one that causes raised lesions on the skin, mostly in children aged 1 to 10, which typically clear within six months to a year.

The timing of the two events is reported differently by different outlets. An abstract of the paper, reproduced on Lifeboat, says the insertions were likely acquired within the last 160,000 years through LINE-1 retrotransposition activity, the same copy-and-paste machinery that mobilizes many human transposons. Cornell puts the transfers at roughly 100,000 years ago. IFLScience reports minimum ages of at least 25,000 years for one copy and 31,000 years for the other, so the two events were separated by thousands of years.

Evidence that the gene is still moving

The claim that BC200 can still jump rests on more than the viral copies. The abstract describes hundreds of lineage-specific insertions across primate evolution, plus individual-specific variants in human populations, which suggests that transposition continues today. A copy that is present in one person’s genome and absent in another’s is the signature of a recent insertion, and the abstract treats those individual-specific variants as the sign that the process is ongoing rather than finished millions of years ago.

Why the virus kept the copies is one of the open puzzles. Poxviruses have a high deletion rate that should quickly purge nonessential sequences, the authors note, so the persistence of these ancient copies suggests the virus found them valuable. The authors say this blurs the line between gene and transposon.

First author Pu Gao and the lead researchers are now asking whether the virus uses BC200 to manipulate host cells. They also plan to test whether the gene’s mobility in cancer cells produces mutations, according to Finger Lakes 1.

Estimated insertion dates in a genomic record

The poxvirus finding is a genomic observation: the gene sits in the viral genome in a pattern that fits transfer from infected skin cells into the virus, and the ScienceBlogs write-up says BC200 likely jumped in skin cells during infection. The data cannot be replayed in real time, since the insertions happened tens of thousands of years ago, which is why the dating ranges are estimates and not measurements, and why the three outlets quoted above can differ without contradicting the paper itself. The same record also leaves the cancer and Alzheimer’s links as associations: BC200 is abnormally expressed in certain tumors and elevated in Alzheimer’s brains, according to Cornell, and the team has not yet shown that its mobility causes mutations in either setting.

Funding came from the National Natural Science Foundation of China, the University of Texas at Arlington and Cornell University. The questions left for the follow-up work are whether BC200 jumps in cancer cells, and whether germ-cell activity at the low levels reported could lead to heritable insertions.

This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.

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