From Ryan in Shimane, Japan:
Recently I have seen more and more atheists using an argument from retroviral insertion as proof that mankind evolved from a common ancestor.
The argument usually states that ERVs (endogenous retroviruses) are inserted randomly into the host’s DNA and that any two species sharing that ERV in the same location is proof that they share a common ancestor.
I wonder, is ERV and specifically HERV insertion random and is the 8% content in the human genome truly known to be retroviral since they are mostly single LTR (long terminal repeat) strands?
Ryan, you ask an important question. For many people (not only atheists, but even Christians who embrace evolutionary creationism), shared features in genomes of humans and great apes reflect common ancestry and compelling evidence for human evolution, even more so, if the shared sequence elements are nonfunctional. Why would a Creator intentionally introduce identical features in corresponding locations of genomes, if they lack function?
For quite some time, evolutionary biologists regarded ERVs (and sequence elements presumably derived from them, such as LTRs) as nonfunctional. According to the evolutionary paradigm, ERVs become instantiated in the genome as a consequence of a retroviral infection of germ line cells (which develop into sperm and egg cells). Because its genetic material is integrated into the gametes’ DNA, the retrovirus is passed on to offspring, becoming a permanent feature of the host genome. If the ERVs experience inactivating mutations, they lose the capacity to spawn new retroviral particles and, consequently, become nonfunctional features of the genome. Recombination events can fragment the ERV sequences and give rise to sequence elements such as LTRs.
For more details on the genesis of ERVs and their connection to human origins listen to the November 21, 2013, episode of Science News Flash: “Do Humans and Neanderthals Share a Common Ancestor?”
When evolutionary biologists present this type of argument, they make two interrelated assumptions: (1) the ERVs (and derived sequence elements) lack function and (2) the origin stems from rare, random events. As already noted, the question is, why would a Creator introduce nonfunctional ERVs and LTR sequences into an organism’s genome? And if the insertion of retroviruses into the host genome is random, then the only reasonable explanation for shared ERVs at corresponding locations is a common ancestor.
However, if these two assumptions are invalid, then we could legitimately interpret the shared ERVs and LTRs as either common design features (if these sequence elements display function) or the result of nonrandom, repeatable events that took place independently in separate organisms.
As discussed in Who Was Adam?, ERVs have been shown to possess an anti-retroviral function, serving to frustrate retroviral assembly via competitive inhibition. And LTRs are now recognized as critical elements in gene regulation. It also appears that retroviral insertion may not be random at all, but instead may take place at well-defined locations in the genome.1
Life scientists have become quite interested in the process of retroviral insertion in recent years because of the potential use of retroviruses in gene replacement therapy. A few years ago, researchers from Italy discovered that the Moloney Leukemia Virus (MLV) preferentially inserts near the start sites for active genes in a nonrandom manner. Though yet to be confirmed for HERVs (to my knowledge), this discovery suggests that nonrandom insertion may be a general feature of the retroviral integration into host genomes. If so, then the shared ERVs sequences in the human and chimpanzee genome may find explanation through the independent integration of retroviruses in their respective genomes.
For more on retroviral insertion and related topics, see these RTB resources: