Harmit Malik described the relationship between organisms and viruses as an “evolutionary arms race” that “never ends.” Darwin did not foresee this particular “arms race,” or the tremendous role that viruses, nonliving infectious agents, would have regarding evolution. His theories for evolution acknowledged diversity based on heritable change, overproduction, competition for limited resources, reproductive potential, and time, but never considered how viruses can act as selective forces. While his premises buttress science’s understanding of viruses, Darwin likely envisioned only competition between living organisms.
I think his surprise would have also been toward comparing molecular homologies to infer evolutionary relationships. In his time, he had no understanding of genetics or how they could provide evidence for evolution. Biogeography and comparative anatomy have become irrelevant compared to more reliable and numerical measures of molecular homology. Biologists have investigated lineages and lineage relationships of many organisms through molecular analyses of retrovirus fragments in their genome.
Something that surprised me is that retrovirus gene fragments compose 8% of our genetic information. Considering how retroviruses function by incorporating within cell genomes, this shouldn’t have been a total surprise. Nevertheless, I was under the impression that when active viruses are recognized by the immune system, the host cell would be destroyed and viral DNA eliminated. This assumption of course ignored latency periods and germ line propagation of viruses. Ancestral viruses must have infected the germ line cells of our ancestors to be permanently incorporated within the genome (and perhaps recombination in meiosis created the fragments). The miraculous part is how our cells manage to function normally with the interruption of virus fragments in our genome; I previously had thought that locus was a determinant in protein synthesis and if a virus replaced the position of where a coding gene would normally be, the mRNA produced from that locus would instead transcribe the viral gene, preventing indefinite latency. But with further understanding of the complex regulation behind transcription and genome organization (ex. transposable elements), a cell can in fact carry out regular function and still code for that displaced gene, ignoring the dormant viral genes. The virus fragments reiterate how the functions of cell regulation are absolutely amazing.
The article suggests that viruses have essentially driven evolution. Its conclusion, which addresses the premises of Luis P. Villarreal’s 2004 essay, arrives at the source for divergence from the common ancestor of humans and chimpanzees: viruses. Research by Harmit Malik and Michael Emerman provide support for divergence from the common ancestor due to variations in the TRIM5α gene that either resisted (humans) or was susceptible (chimpanzees and gorillas) to the endogenous PtERV virus.
Additionally, paleovirological research shows that viruses may have also had a role in the evolution of mammals, as the mechanism for placental cells to fuse together “employs the exact mechanism that enables retroviruses to latch on to the cells they infect.” In other words, mammals evolved the ability to give birth through infection of endogenous retroviruses.
The possibility that viruses have shaped evolution through competition makes a great deal of sense to me. These nonliving capsules of protein and nucleic acids have a remarkable aptitude for evolution, and can therefore drive the evolution of living organisms. This perspective on viruses adds a component to Darwin’s theory of natural selection, because viruses, too, act as a selective force. The article more so expands my understanding of viruses; they not only cause disease but propel evolution.
Beside the one mention of reviving polio as being “pointless,” the goals of reviving extinct viruses seem reasonable and attainable. More data surrounding virology, HIV, human evolution, and mammalian evolution can be uncovered through researching these extinct viruses because viruses were and continue to be instrumental in evolution. Moreover, different groups are jumping to recreate viruses to draw connections to today’s scourges. The federal government revived the 1918 flu virus to create vaccines, for example. Another interesting development was HIV’s connection to the TRIM5α and PtERV gene, which may offer some mechanisms for combatting HIV.
Additionally, the teams that are bringing back ancestral viruses are doing so with controlled methods that allow the viruses to divide only once. This significantly reduces the risk of the virus spreading and evolving to reinfect humans and other organisms. Other than that, I see no other risk of this line of scientific inquiry.
And contrary to Luis P. Villarreal’s perspective that Africans will be nearly eradicated by the HIV virus, I think research on endogenous retroviruses will be hugely influential for developing nations and the world. Repopulation will not have to occur before HIV immunity develops.