Darwin’s Surprise

Charles Darwin’s work was restricted to fossil records, comparative anatomy, and biogeography, so he would be surprised to find that, with the advent of molecular biology, research suggests that our elusive common ancestor may be even more revolutionary than previously thought. The idea that humans may have descended from endogenous viruses that significantly affected our evolutionary development may come as a surprise because we do not even consider viruses living. They are simply DNA or RNA wrapped in a protein coat—yet somehow potent enough to possibly give rise to the distinctions between mammals and reptiles. Thierry Heidmann suggests that endogenous retroviruses led to the development of a placenta in mammals, which offers protection for the fetus while allowing it time to mature. This evolutionary development allowed mammals access to maternal nutrients that help develop large brains.

Endogenous viruses, which infect a species’ DNA to the point of actually becoming a part of the species, may have significantly impacted the direction of evolution. According to Paul Bieniasz, 10% of our DNA contains old retroviruses; “[we] evolved remarkably sophisticated defenses against them, and we would have done that only if their impact on human populations had been quite severe.” He states that retroviruses must have threatened humans multiple times in our history, and that HIV may only be one of very many.

Interestingly, although chimps are infected by the AIDS virus, it does not make them sick, despite their being our closest relatives. Scientists attribute that difference to the various copies of an endogenous retrovirus present in chimps but not in humans: Pan troglodytes (PtERV). A gene in humans codes for a protein that destroys PtERV, TRIM5α, and even after researchers modified it to function like it does in chimps, the protein blocks either PtERV or HIV, not both. It is possible that by developing defense against PtERV, we were left susceptible to HIV. After much more research and testing, drugs may be produced in the future that act much in the same way as the protein that protects chimps against HIV does.

This article has changed my understanding of viruses by broadening my perspective of them; I have always thought of viruses as parasitic, which they are, but I never considered their impact on evolution. Viruses not only infect their hosts, but they may also become a permanent part of them. Interestingly, although the rapid rate of mutations in viruses renders drugs ineffective after a while, “… endogenous viruses can enter our genome without killing us [because] they make many errors when they reproduce.”

What came as a surprise was not so much the implications of the research, but the extent to which some of it was rejected by the scientific community. In 1968, when Robin Weiss suggested not only that endogenous retroviruses in the embryos of healthy chickens may be benign, but also that they may be an essential component in placental development, he was laughed at, his interpretation denounced as “impossible.” However, after further research, Weiss discovered versions of the same virus in the red jungle fowl, an ancestor species of chickens. The implication of Weiss’ research brought up ideas about how much of human viral fragments are seen in relatives such as chimps and monkeys—a lot. Since it is unlikely that humans and chimps were infected with numerous identical viral infections over the past millions of years, those viruses must have been present in a common ancestor.

Another surprise came when Howard Temin’s theory that questioned the central dogma of molecular biology—DNA to RNA, RNA to protein—was rejected. In the early 1900s, no one understood why, despite not being viral, cancer epidemics spread across American poultry farms. Temin suggested a deviation from the central dogma—RNA to DNA, later explained by the discovery of reverse transcriptase. Despite what history has shown with the initial dismissal then acceptance of Darwin’s theory of evolution, scientists still do not seem to hesitate much when rejecting a deviation from established molecular biology. Questioning an idea is one thing; dismissing it altogether is another.

Reviving “dead” viruses is definitely not a concept to be taken lightly; the author of the article finds it analogous to Frankenstein’s monster and Jurassic Park. However, like many things, this falls across a continuum and therefore extremes should be avoided. Assembling a virus such as polio, injecting it into mice who become paralyzed and die simply to “prove that it can be done” is not an appropriate approach to take. Although at this point, the revival of dead viruses is not done at a large scale and is presumably quite contained, the article concedes that “a talented undergraduate with a decent laptop and access to any university biology lab can assemble a virus with ease.” At this point, with limited and shaky knowledge on dead viruses, resurrection could genuinely aid us in understanding and fighting the medical complications we see today. However, in the future, it is possible that our own creations could become threats, and it is essential to consider ethics at all times.

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2 Responses to Darwin’s Surprise

  1. ManzoorR says:

    I also thought it was surprising so see research being completely rejected because it did not fit the parameters of molecular biology at the time. As I first read about Robin Weiss’ discovery of endogenous retroviruses being harmless in chicken embryos and that the viruses played a critical role in placenta development, I was amazed by his theory, and even though I had never heard of endogenous retroviruses before reading this article, I did not immediately think that he was wrong that his idea was “impossible”. Even my response might have biased because I was reading an article where I know the information reported is correct, it shocked me how others soundly rejected his theory.
    I was also surprised by the fact that 8-10% of genome consists of the remains of endogenous retroviruses. Reading this made me wonder that if only 2% of our genome codes for proteins that are essential for life and about 10% is shards of endogenous retroviruses, what the rest of our DNA was. I thought it was ironic how the article talked about this 10% being “junk DNA” because it did not code for functional proteins, yet how important this 10% was in our evolution. Even though these endogenous retroviruses have been defeated by evolution, they might have protected us from viruses that were even more deadly. For example, I found it very interesting that endogenous retroviruses could have helped create one of the “hallmarks of our evolution”: the development of the placenta and live births. The placenta protected the fetus and created a barrier where maternal nutrients could reach the embryo and waste would be eliminated, increasing the survival rate of the offspring and allowing for larger brain development.

  2. safiaabdalla says:

    I, too, was very shocked to discover how many of these scientific discoveries were rejected by the scientific community. What was more surprising was to me was the fact that most of these discoveries were recent! It would appear that sometimes peer-review can be ineffective when science is verging on a new field. The fact that we evolved to have an immunity to PtERV and not HIV fascinated me as well. TRIM5alpha acts a retrovirus restriction factor, it prevents the replication of viral DNA by binding the virus’s capsid proteins and preventing the capsid from breaking apart and releasing the viral DNA. The fact that TRIM5alpha in humans affects the PtERV virus and not the HIV virus is most likely due to the fact that human TRIM5alpha proteins only have a complementary structure to the PtERV virus’s glycoproteins and not HIV’s. We simply might be seeing a snapshot of the current evolutionary TRIM5alpha process. Primates might have had HIV as a more severe threat and the emergence of an HIV restriction factor might have been more of an immediate concern for their species. Likewise, PtERV might have been a more immediate environmental pressure for our ancestors resulting in the evolution of a TRIM5alpha protein that restricted PtERV.

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