Primate genetic element discovered to have transferred into human poxvirus

Scientists identified BC200, a gene exclusive to humans and primates, within the genome of a benign poxvirus that infects humans, suggesting at least two independent jumping events during modern human history. BC200 originated from a transposable element and was previously thought to have lost its ability to move when it was repurposed for cellular functions, particularly in neurons. The discovery reveals that this gene has retained its mobility despite serving an important biological role, challenging previous understanding of how domesticated genetic elements behave.

Nearly half of all human DNA originates from transposable elements—sequences capable of moving and copying themselves throughout genomes. BC200 emerged from one such element approximately 40 million years ago in primate ancestors, eventually becoming embedded in neurons where it likely helps regulate protein synthesis. Scientists long assumed that when jumping genes were repurposed for essential cellular functions, they would lose their capacity to move. This discovery contradicts that assumption, revealing BC200 remains mobile despite its role in neurological function.

The research identified BC200 sequences in molluscum contagiosum virus, a harmless human pathogen causing benign skin lesions. Two separate integration events during modern human history transferred BC200 into this virus's genome. Notably, BC200 insertions continue to occur in human germline cells and across primate species today, documented through genomic screening. Researchers now question whether the virus exploits these genetic sequences during human infection and how evolution maintains this unusual duality of function and mobility.