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FBNSV is one of several “multipartite viruses” that split their genes among different capsules. These oddballs were first discovered in the 1940s, and though they account for about 20 percent of known viral species, they’re still rather obscure. Blanc thinks that’s because they almost always infect plants and fungi, and only two have been found in animals—one in a moth and one in a mosquito. “I lecture on several virology courses, and even people in Ph.D. programs haven’t heard of them,” he laments. “They’re everywhere, but because they’re mainly on plants, no one cares.”
These viruses have always been baffling, even to virologists who knew about them. Everyone assumed that they could only reproduce if all the segments infected the same host cell. But the risk of losing a piece, and so dooming the others, skyrockets as the number of pieces goes up. In 2012, two researchers calculated that the odds of successfully getting every segment in the same cell become too low with anything more than three or four segments. FBNSV, with its eight segments, “should never have evolved,” Blanc says. Its mere existence suggests “that something must be wrong in the conceptual framework of virology.”
Perhaps, he realized, these viruses don’t actually need to unite their segments in the same host cell. “If theory was saying that this is impossible, maybe the viruses just don’t do it,” he says. “And once we had this stupid idea, testing it was very easy.”
His colleagues Anne Sicard and Elodie Pirolles labeled pairs of FBNSV’s genes with molecules that glowed in different colors—red for one segment, for example, and green for another. Then, they simply looked down a microscope to see whether the colors overlapped in the same cells. They almost never did. When the team first saw that, “we were jumping and running around the lab,” Blanc says. “But we were also scared about it being a [mistake]. We took six years to verify it.”
For example, they showed that the levels of one segment aren’t tied to the levels of another, as you would expect if they were replicating in the same host cell. Instead, in any one infected plant, the different segments seem to accumulate at different rates.
But that discovery raised another problem. Each of the eight segments carries a gene with its own vital role. One makes the proteins that copy the virus’s DNA once it gets inside its hosts. Another creates the proteins that form the virus’s capsules. See the problem? If these segments end up in different cells, the DNA-copying one shouldn’t be able to make capsules, the capsule-making gene shouldn’t be able to copy itself, and both of them would be stuck.
That doesn’t happen, the team discovered, because the virus’s genes might be stuck in neighboring cells, but the proteins created by those genes can move. The capsule-making protein can get into a cell with the DNA-copying gene, and cover it. The DNA-making protein can get into a cell with the capsule-making gene, and copy it. Think of the eight segments as factories in different cities, shipping assembly robots to one another so that each site can manufacture its own separate product. It is within this expansive trade network that the distributed virus truly exists.