virus--a short sequence of DNA (or possibly RNA) encased in a protective protein shell--approaches the bumpy surface of a human cell. Surface features of the virus have evolved shapes that are complementary to features on the cell's outer membrane, so that when the two come together, they attach like the hooks and loops of Velcro, forming a tough bond. This sets off additional mechanisms in the virus, analogous to the trigger hairs inside a venus flytrap. The triggers signal the protein shell to inject its nucleic acid cargo through the membrane and into the cell, where it will commandeer the machineries of reproduction, and begin producing copies of itself by the millions of millions.
If the virus is of a special type known as a retrovirus, then it has an additional trick up its sleeve: the DNA comes bundled with additional wetware that, by a process not completely understood, transports it directly to the cell's nucleus and splices it directly into the genome of the cell--a safe and comfortable home where no immune mechanism can touch it. Unfortunately for the virus, though, cell nuclei do have a habit of switching genes on and off. If this happens to the genes left in place by the virus, then the interloper can be permanently deactivated, a short segment of "junk DNA" in the long, long sequence of the cell's genome. And if the infected cell is a germline cell responsible for the production of sperm or eggs, this junk, which produces nothing, may become a part of the genetic legacy passed along to the host's children.
We are made of virus
Now, animals that live in large, dense groups are far more vulnerable to "colonization" by viruses. Large mammal herds, migratory bird flocks and nesting sites, rodent warrens and similar sites provide the ideal breeding ground for diseases to spread. Moreover, evolution drives these viruses in very particular ways: virulent ones that spread quickly can easily kill off an entire herd, leaving the virus with no new hosts to jump to, while viruses with low infection rates, very long incubation periods, and/or low rates of immune-foiling mutation may be unable to spread quickly enough to keep from dying out themselves. The most effective viruses mutate rapidly and are easy to catch, but tend to have mild, nonlethal symptoms. Particularly successful examples include rhinoviruses (a.k.a. "the common cold"), influenza and, yes, retroviruses.
In fact, these viruses are so successful that many animal populations support standing viral nation-states of their own. And human beings are, unfortunately, the perfect ambassadors. Not only do we live in extremely large, dense populations, we also keep large mammal herds and bird flocks as food stock, and unwittingly support a variety of rodents and other vermin in our cities and homes. Each of these species is in a perfect position to pass its diseases along to us. When it comes to catching viruses, humans are the hands-down gold medallists of the animal kingdom.
This is highly inconvenient, as it lands most of us in bed several times each year, fighting off duck and pig and rat viruses our bodies would rather not have to deal with. But as our technology progresses and we begin, slowly, to take control of our evolution, this viral legacy presents an altogether different sort of grief: the more closely we examine our genome, the more we realize we are mostly made of virus.
A grandmother's attic
Yucky? Well, yeah. Current estimates show the 46 chromosomes of the human genome, like a grandmother's attic, contain about 97 percent junk DNA, and analysis of the junk shows millions of years of retroviral accumulation. (Whether the junk is all retroviral is not clear, but retroviruses are at least a leading source.) This accumulation isn't harmful--most of it is broken up and mutated almost beyond recognition--but it isn't helpful either, it isn't "human" in any meaningful sense, and it surely does take up space.
Despite all the hullabaloo about the "completion" of the human genome project, simply mapping out the chromosomes is only the first small step of a much larger endeavor. The second step, which has already begun, is figuring out where, in the 1.5-gigabyte haystack of our chromosomes, the actual human genes are, and what they are, and what their functions are in the complex machinery of our bodies.
Here we can gain some insight by examining much simpler genomes, such as those of lower animals and even bacteria. In fact, this may be the only way to trace the origin and application of many genes. There does appear to be a minimal "core genome" of the 300-odd genes required for the basic housekeeping functions of DNA replication, repair and metabolism that are common to all organisms. Many of the genes we find in our gut bacteria (e. coli, otherwise known as "yogurt") are essentially identical in form and function to genes we find in ourselves, in the most primitive archaea and cryptobacteria, and even in plants and fungi. As compared with others, these genes are easily identified and their purposes categorized.
A puffer fish shortcut
Moving up the evolutionary ladder a bit, we have tubeworms and other primitive invertebrates, which do not possess advanced organs such as eyes or nervous systems, but are at least multicellular organisms with the basics of tissue differentiation figured out. As their genomes are studied and contrasted against the simpler ones of single-celled creatures, the extra genes required to support these functions will gradually emerge. Still, there is (almost literally) a world of difference between a tubeworm and a human being. To get a handle on the genetics of really advanced features such as the skeleton, spinal column, high-bandwidth sensory organs, jointed limbs and digits, and of course the brain, most research is directed toward other primates, and toward rodents. These avenues are fruitful, because except for a few superficial features like size and intelligence, there is surprisingly little difference between these creatures and ourselves.
Unfortunately, one of the similarities is that mice and monkeys also have a lot of junk DNA, which hampers the identification and study of functional genes. As with humans, we don't even know how many genes these lesser mammals possess, much less where they are or what they do. But Sydney Brenner of Berkeley's Molecular Science Institute has found a shortcut of sorts, in the genes of the puffer fish Rugu rubripes. This antisocial marine creature concentrates tetrodotoxin, an algal poison that Haitian sorcerers use to place enemies into a deathlike coma, to rise again as "zombies," and that thrill-seeking sushi-eaters consume in small doses as a kind of recreational drug. The puffer fish also, for some reason, has a lot less junk DNA than other animals--virtually none, in fact. So while the study of puffer fish DNA receives very little funding, it is so much easier than research on humans or mice that it may in fact lead the race to the right answers.
Humans: more complicated than fish
Brenner has already found, for example, that puffer fish have about 50,000 genes, a few hundred of which are ancient "core" DNA, and 20,000 more of which are similar to genes found in tubeworms and their kin. The rest, somewhere around 30,000 genes, are the ones responsible, one way or another, for constructing a complex multicellular organism, with advanced eyes, limbs, skeleton and nervous system. Now, humans are more complicated than fish, and probably require more genes. But not a huge amount more. Not twice as many, probably not even 10% more. So when the final human gene count rolls in, probably sometime next year, we will already have a very good idea how many of those genes are responsible for the human-ness and mammal-ness that set us apart from the puffer fish.
Next, of course, we'll have to figure out which genes make us different, and why and how they do it. Then we'll have to classify the SNPs, or single-nucleotide polymorphisms (the replacement of one DNA "letter" with another), that make one human-not-fish different from another human-not-fish, and then discern which SNPs are responsible for the various genetic diseases that plague us, and which are merely cosmetic or behavioral. Then we'll need to learn just how much change or mutation, beyond mere SNPs, these genes can tolerate before they cease to function, or function so differently that the results cannot properly be called "human" any longer.
Is there a race of superhuman beings in our future, waiting to take over from us? The usual caveats of God-playing aside, all I can say is I hope so. Shouldn't we wish for our children to be better than ourselves? In any case, as with a grandmother's attic, the first step in cleaning up the place is the very thing we're doing right now: sorting the treasures from the junk.
Wil McCarthy is a rocket guidance engineer, robot designer, science fiction author and occasional aquanaut. He has contributed to three interplanetary spacecraft, five communication and weather satellites, a line of landmine-clearing robots, and some other "really cool stuff" he can't tell us about. His short fiction has graced the pages of Analog,
Asimov's, SF Age and other major publications, and his
novel-length works include Aggressor Six, the New York Times Notable
Bloom, and The Collapsium.
