Fragments of a human brain-active gene turned up inside a poxvirus genome

BC200 is both a mobile element and a gene with a job in the cell. It began as a transposable element, one of the mobile sequences often called jumping genes, and a predecessor took hold in a common ancestor of monkeys and apes somewhere between 35 and 55 million years ago ^[5]. About 40 million years ago the cell put it to work, apparently helping regulate protein production in neurons ^[6]. Domestication like that usually costs an element its ability to move, but BC200 kept both ^[7]. "Somehow evolution hasn't been able to untangle these two things," said Cedric Feschotte of Cornell University's Department of Molecular Biology and Genetics in a university statement ^[8].

That retained mobility is what makes the viral finding credible. BC200 has no copying machinery of its own, so to move it borrows the enzymes of LINE-1, another mobile element that reverse-transcribes RNA into DNA and inserts it into a genome ^[15].

The team, which included scientists from Capital Normal University in China and the University of Texas at Arlington, went through the available poxvirus genomes looking for sequences that appeared mobile ^[9]. Two BC200-derived sequences stood out in molluscum contagiosum virus, one covering the gene's entire Alu-derived domain and the other shorter and broken at both ends ^[10]. Both are fragments, not an intact copy of the gene ^[11]. A few checks point to a human source: BC200 occurs in humans and related primates, and the virus is only known to infect people ^[12]. The researchers found no matching elements in the other poxviruses they examined, including a closely related virus that infects horses ^[13]. The signatures around the insertions fit two separate transfers, not one insertion that later copied itself inside the virus ^[14].

The transfers were reconstructed from DNA, so when and where they occurred stays open ^[16]. One clue sits in the skin, where BC200 turns up at low levels as well as in neurons, and human fibroblasts infected with the virus produced more of it ^[17]. That raises the possibility that infection creates conditions for a jump, though it does not establish where the historical transfers took place ^[18].

The same mobility is still at work in people. In sequencing data from 908 individuals, the team found eight BC200-derived insertions that differed from person to person ^[19]. Two were common across five continental groups, a sign of ancient origin; one was mostly African; the other five were rare, and four of those appeared in a single person each ^[20].

What the fragments do inside the viral genome, if anything, is unknown, and nothing here suggests the virus gained anything resembling brain function ^[21].