There are many kinds of viruses that border our perception of what constitutes living versus non-living. One group of viruses, the retroviruses, infect organisms like us humans by invading our cells and eventually integrating themselves into our genetic material, collectively called the genome. The Human Immunodeficiency Virus (HIV), which causes AIDS, is an example of a retrovirus.
Most retroviruses infect cells in different parts of animals, whereas some retroviruses infect germline cells. In the latter case, the viral genetic information may be occasionally passed on by an animal to its offspring along with the animal's genetic information. Often the virus may "come alive" in the offspring and cause further infection. However, sometimes this viral genetic information may be disrupted in the offspring by random modifications. This viral genetic information then becomes useless as it codes for a dysfunctional retrovirus, but it may continue to persist and be passed on from parent to offspring, generation after generation, during the course of evolution.
Today about eight percent of the human genome comprises such relics of viral infection that occurred in our ancestors over millions of years. There are thousands of such remnants of viral infection in our genome, called Endogenous Retroviruses (ERVs). The grand Human Genome Project, completed in 2003, identified these relics in our DNA. Most of these relics are believed to be useless, and are part of what biologists call "junk DNA." However, a few of these viral elements have actually evolved to play important roles in our own body, like providing resistance to infection by other retroviruses.
Often one can find multiple copies of similar viral genetic information in our genome, each slightly different from the other. The supposition therefore is that the same, or a series of genetically similar retroviruses, inserted their genetic information into human beings multiple times during our evolution. Each piece of information must have undergone slightly different modifications.
Heidmann and his colleagues studied one such family of retroviral elements in the genome, dubbed HERV-K (HML2), that supposedly came from a single virus that infected us millions of years ago. Since all of these elements are slightly different from one another, the scientists compared the genetic information contained in all these elements to conjure a common sequence that they believed best resembled the ancient virus that infected our ancestors. Once they used this common genetic information to make a virus, they found that it infects human cells just like a "real" virus would, albeit very weakly.
After scientists recreated the Phoenix virus, they studied its life cycle and mode of infection. Such studies can provide valuable information about how the virus might have disseminated itself in the human genome millions of years ago. The groups' finding is the first instance where researchers have actually created a complete functional retrovirus using retroviral elements found in the human genome. Professor of Biology Dick Goldsby said of this research, "[It] is yet another demonstration of the power of knowing the complete human genome. Not only do you get to see what is there, but by playing this kind of molecular scrabble you can learn something about what was there."
Many scientists are very excited about such work. Professor of Biology David Ratner said, "The work [is] interesting, as folks have long discussed the evolutionary relationship between transposable elements and viruses." Assistant Professor of Biology Michael Hood concurred, saying, "[It is] very interesting (well worth publishing), and illustrates how the simplest evolving things are little more than their DNA sequences, [though it is] not terribly surprising that their approach worked."
In their study, the scientists also addressed the possibility of such a virus spontaneously arising in humans by recombination of genetic information. Based on preliminary work done using such retroviral elements, the authors show human cells to still have the potential to produce infectious retroviruses. Such a finding is indeed frightening. "One thing [they] found interesting and slightly scary was how some of these deactivated HERVs can be reactivated through splicing mechanisms naturally done in our cell. Sounds like a movie just waiting to happen," said Alex S. Zaman '08.
However, biologists from our own college assure us that there is no reason to panic, and we can continue sleeping soundly for the time being. Hood noted that, "Although it may be true that human cells still have the potential to produce infectious retroviruses, (the published research) does not say how likely such an event is to happen." Ratner, too, believes such findings are not cause for concern yet. He explained, "For one thing, these elements [that] have been around for millions of years, previously as infectious viruses, more recently as inherited bits of DNA-haven't killed us off yet, [such research is] unlikely to be [dangerous]."
One important reason humans are now resistant to viruses like Phoenix is that over the course of our evolution, we have become suited to counteract the effect of multiplication of such retroviral elements i.e. ERVs. However, scientists often worry that retroviral elements found in the genome of other species like pigs may be introduced into our own species by, say, organ transplants.
Ratner explained, "Researchers have been concerned about ERVs in other species that are being considered as a source of organ transplants. Pigs likely carry ERVs. Conceivably, the implantation of a pig heart into a human patient would introduce PERV (Pig ERV) containing cells into a person. Down the line, the PERV might recombine with the patients own (Human) ERVs, and then what? No one knows. Some folks worry about this, others think the scenario a) unlikely, and b) not likely to generate anything dangerous that wouldn't have arisen by other means. Pigs and people have coexisted for a long time before organ transplants."