In Our Genes, Old Fossils Take On New Roles

HERVs, however, go one better.

HERVs attack the "germline" cells that make sperm and eggs. HERVs become a part of the host's inherited genome. Unlike HIV, they outlive the organism they infect, because they are passed on to the host's offspring and the offspring's offspring. (This is what makes them endogenous, or "born-within.")

All of the thousands of endogenous retroviruses in the human genome appear to be crippled and inactivated by mutations that occurred after their initial, successful invasion. They aren't able to be transcribed from the host DNA to replicate and infect another cell. Many are mere fragments. Most reside in stretches of chromosomes between genes where they aren't disturbing anything.

But parts of a few HERVs have been incorporated into human genes, taking on new roles.

For example, a protein called syncytin, which helps cells fuse together in the placenta, is actually the envelope gene from a HERV. A study published in January found that tissue from women with preeclampsia or intrauterine growth restriction -- two conditions that threaten fetal health -- had abnormally low amounts of syncytin.

Other studies have found that proteins derived from HERV genes -- or antibodies against the proteins -- are common in testicular tumors, breast cancer tissue and melanomas.

Whether the HERVs' reawakening there causes cancer, or is an effect of it, or is neither, isn't known. Nevertheless, "there is quite a bit that suggests there is some clinical significance to these HERVs," said Ravi Subramanian, a molecular biologist at Tufts University who is studying them in breast tumors.

In other species, endogenous retroviruses have evolved into tools for self-defense against their cousins, the retroviruses prowling the outside world (exogenous retroviruses).

For example, mice and chickens make proteins for the envelope, or outer shell, of several remnant retroviruses in their genomes. Once made, those proteins migrate to the surface of the animal cells and attach to receptors that are used by invading retroviruses as initial docking sites. With the receptors occupied, infection can't occur.

In sheep, researchers are discovering an especially interesting story.

Sheep today sometimes develop lung or nasal tumors caused by circulating retroviruses. Ancestors of those viruses began creeping into the genome even before sheep and goats diverged from each other more than 5 million years ago.

A team led by Massimo Palmarini of the University of Glasgow Veterinary School studied two of those endogenous retroviruses. They found that wild species (such as bighorn and Dall sheep) had versions of the two retroviruses that differed slightly from the versions carried by domesticated species. The retroviral genes in those animals contained a mutation that impeded infection by the cancer-causing viruses.

In a paper published in November, the researchers argued that when people began rounding up wild sheep 9,000 years ago, the newly confined herds probably suffered epidemics of the cancer-causing viruses. Only those animals whose endogenous viruses had by chance mutated into the protective form survived.

Today, thanks to natural selection and intentional breeding, all domesticated sheep carry the "updated" versions.