Weiss, a virologist then working at the University of Washington, wondered if the virus had become a permanent, harmless part of the chicken DNA. He and his colleagues treated cells from healthy chickens with mutation-triggering chemicals and radiation to see if they could flush the virus out from its hiding place. Just as they had suspected, the mutant cells started tochurn out the avian leukosis virus. In other words, these healthy chickens were not simply infected with avian leukosis virus in some of their cells; the genetic instructions for making the virus were implanted in all of their cells, and they passed those instructions down to their descendants.
These hidden viruses were not limited to just one oddball breed of chickens. Weiss and other scientists found avian leukosis virus embedded in many breeds, raising the possibility that the virus was an ancient component of chicken DNA. To see just how long ago avian leukosis viruses infected the ancestors of today’s chickens, Weiss and his colleagues travelled to the jungles of Malaysia. There they trapped red jungle fowl, the closest wild relatives of chickens. The red jungle fowl carried the same avian leukosis virus, Weiss found. On later expeditions, he found that other species of jungle fowl lacked the virus.
Out of the research on avian leukosis virus emerged a hypothesis for how it had merged with chickens. Thousands of years ago, the virus plagued the common ancestor of domesticated chickens and red jungle fowl. It invaded cells, made new copies of itself, and infected new birds, leaving tumors in its wake. But in at least one bird, something else happened. Instead of giving the bird cancer, the virus was kept in check by the bird’s immune system. As it spread harmlessly through the bird’s body, it infected the chicken’s sexual organs. When an infected bird mated, its fertilized egg also contained the virus’s DNA in its own genes.
As the infected embryo grew and divided, all of its cells also inherited the virus DNA. When the chick emerged from its shell, it was part chicken and part virus. And with the avian leukosis virus now part of its genome, it passed down the virus’s DNA to its own offspring. The virus remained a silent passenger from generation to generation for thousands of years. But under certain conditions, the virus could reactivate, create tumors, and spread to other birds.
Scientists recognized that this new virus was in a class of its own. They called it an endogenous retrovirus—endogenous meaning generated within . They soon found endogenous retroviruses in other animals. In fact, the viruses lurk in the genomes of justabout every major group of vertebrates, from fish to reptiles to mammals. Some of the new endogenous retroviruses turned out to cause cancer like avian leukosis virus, but many did not. Some seemed to be effectively muzzled by their host. Certain endogenous retroviruses carried by mice cannot infect mice cells, for example, but they can readily spread among rat cells.
Other endogenous retroviruses turned out to be crippled, carrying mutations that robbed them of the ability to make full-fledged viruses. They could still make new copies of their genes, however, which were then reinserted back into their host’s genome. And scientists also discovered some endogenous retroviruses that were so riddled with mutations that they could no longer do anything at all. They had become nothing more than baggage in their host’s genome.
Endogenous retroviruses can linger in their hosts for millions of years. In 2009, Aris Katzourakis, an evolutionary biologist at the University of Oxford, discovered hundreds of copies of endogenous retroviruses in the genome of the three-toed sloth. Their genes closely matched those of foamy viruses, free-living pathogens that infect primates and other mammals. Katzourakis concluded that foamy viruses infected the common ancestor of three-toed sloths and primates,