Molecular Evidence 5: Endogenous Retroviruses
The fifth and final piece of evidence is from endogenous retroviruses.
First, I want to get something straight- I know that the plural of virus is virii. But I’ve heard plenty of scientists use the word viruses, so I’m going to use it here. If I was writing a paper, I’d use virii, but this is just a podcast, targeted toward non-science people, so I think viruses is fine. If any of you want to try to talk about this subject with your friends or family, you’ll look a lot less crazy if you don’t insist on calling them virii, at any rate.
I’m sure most of you have experienced some kind of illness from a virus, but what is it, exactly? A virus is about as low as you can go on the complexity scale of life and still have people arguing about whether is actually qualifies as something that’s actually alive. If you remember me talking about transposons from two weeks ago, you remember that a transposon is basically just mobile DNA that has to stay within a cell. Well, a virus is just a little more complex than that- it’s mobile DNA that can leave a cell. Structurally, a virus is a shell made of protein or membrane filled with genetic information. That’s it. A virus can’t reproduce on its own, doesn’t take in energy, doesn’t have a metabolism, doesn’t grow, doesn’t respond to stimuli, and isn’t made out of cells. It violates almost all criteria for life, and yet… it is organized, it is composed of the same macromolecules that all other life forms are composed of, and it can reproduce. It might be a little disconcerting to think that you’ve suffered through an infection by something that isn’t technically alive- at least with a bacterial infection, the little bugs are growing, eating, and reproducing- if they’re alive, they can be killed, and that’s what antibiotics are for. You can’t technically kill a virus, since it’s technically not alive.
Depending on the type of virus, they can be spread in different ways and affect different cells in your body. Some viruses don’t last if they’re exposed to air, some do very well as airborne particles. Some viruses target liver cells, like hepatitis C, and some viruses target immune cells, like HIV. All viruses follow the same basic infection cycle. First, they attach somehow to a host cell. Then, either the viral genome itself or the entire virion moves into the host cell. Once the genome is exposed to the host genetic replication machinery, it begins to transcribe viral genes that code for proteins which are necessary to make more virus particles. The viral genome is also replicated during this time, and these copies are packaged into full virus particles, and this process continues until the cell explodes or until it dies from metabolic drain. At this point, the newly replicated virus particles are free to infect more cells, move around the body, and even venture outside the body where they can come in contact with other potential hosts.
Viruses carry their genome either as DNA or as RNA. For the viruses that use DNA, it’s treated just as the DNA from the host cell. The DNA is transcribed into RNA, which is then translated into protein. Some of the viruses use RNA sequences to store their genetic information, however. These viruses use RNA as their template and make more RNA copies from that template, which are then translated into protein. But there’s another variety of RNA viruses that is a little more complicated. It uses the same proteins that I told you were used by retrotransposons to replicate- reverse transcriptase and integrase. These viruses use reverse transcriptase to reverse transcribe their RNA genome into a DNA sequence, which is then integrated into the host genome. Because of this process, these viruses are called retroviruses. The most well-known retrovirus is human immunodeficiency virus, or HIV, which is the virus that causes AIDS by targeting specific immune cells. Any of you that have cats are probably aware of the Feline Leukemia virus, which is also a retrovirus.
Some of you may be thinking- hey, these retroviruses sound awfully similar to the retrotransposons you talked about before- and they are, certainly. It seems very likely that that retroviruses and retrotransposons share common ancestry way back in the past, but trying to establish which one came first is more than a little difficult at this point.
So, now everyone knows what a retrovirus is, I hope, but what is an endogenous retrovirus? Well, you know that a retrovirus functions by inserting its DNA into the genome of its host cell. Once that happens, the DNA is there for the entire life of the cell. But what if that cell has an exceptionally long life? What if it’s, for lack of a better word, immortal? Germ cells are kind of immortal- the cells that are passed on to descendents during procreation. In males, these would be spermatocytes, and in females, these would be oocytes. Let’s say that a retrovirus infected a germ cell which produced spermatocytes that fertilized and egg and resulted in a new organism. What would happen? Well, since that germ cell has a copy of the viral DNA, and all the cells in the progeny were derived from that germ cell, every single cell in the body of the progeny would also have the viral DNA. At this point, the virus is endogenous- that is, it exists natively in the organisms own’s genome from birth because of an infection that occurred one or more generations previous to it. The virus can still be actively transcribed, and continue to be infectious, but it will continue to be passed on to further progeny. Since the endogenous retrovirus, or ERV, is not necessary for reproduction, there is no selective pressure to keep it free from mutations, and so ERVs will acquire mutations at about the same rate as other non-essential non-coding DNA. Eventually, ERVs are rendered inactive because of these mutations, and they sit quietly in the host genome, a testament to an infection that occurred generations in the past.
The evolutionary hypothesis would posit that for any two given organisms, finding common ERV sequences in their respective genomes would be a confirmation of common heredity between them, since the only mechanism to explain common ERV sequences would be a shared ancestry. There is no conceivable reason, outside of common descent, why any two unrelated organisms would have the same ERV insertions. So let’s look at the evidence.
ERVs make up as much as 8% of the human genome, comprising close to 30,000 separate insertions. There have been seven common insertions characterized so far between humans and chimpanzees, with more expected as the published genomes of both are analyzed more closely. A Russian study looked at the insertions of the Human Endogernous Retrovirus, or HERV-K, and compared insertions of HERV among different primates to see which insertions are held in common by which species of primate. Figure 4.4.1 at the Talk.Origins website that I’ve been referencing comes from this study- I’ve included it also in the mp3 that you’re listening to- if you open it in iTunes, you should be able to see it as attached artwork just after the logo. This figure shows all of the HERV insertions that were found, and a cladogram was constructed to indicate phylogenetic relationships. Individual arrows mark specific insertions, and all branch points to the right of an arrow have that insertion in common. The cladistic relationship predicted by ERV evidence is exactly what is predicted by evolutionary theory- humans and chimpanzees are more closely related, with gorillas as the next most related species, followed by orangutans, gibbons, Old World monkeys, and New World monkeys. This takes into account evidence from 14 separate insertions. Again, there is no reason for insertions to be held in common without common ancestry. The evidence from ERVs is devasating to the null hypothesis, and exceptionally strongly supports evolutionary theory.