This Week in Evolution

This week's paper uses molecular methods to reveal new details of the evolutionary arms race between primates, including humans, and viruses. "Protein kinase R reveals an evolutionary model for defeating viral mimicry" was published in Nature by Nels Elde and colleagues in Seattle.

Protein kinase R (PKR) is an important defense against viruses in many species, from humans to yeast. When it detects a virus inside a cell, it activates eIF2-alpha, which shuts down protein production in that cell. With protein production blocked, the virus can't replicate and spread to other cells. Viruses, however, have evolved counter-measures. These include molecules that resemble eIF2-alpha. These molecular mimics interact with PKR and prevent its normal defensive activity.

Viral epidemics can be a major cause of death, so we expect populations to evolve PKR resistant to the eIF2-alpha-mimics produced by viruses. Can we find evidence of such evolution in primates?

Continue reading "Staying ahead in the evolutionary arms race with viruses" »

Posted by R. Ford Denison at 05:32 PM | Permalink | Comments (0)

My NSF grant will run out soon, so I get to spend the year in which we celebrate the 200th anniversary of Darwin's birth and the 150th anniversary of The Origin of Species as an amateur scientist, like Darwin himself. I'm not as smart or as rich as he was, but I do have imaginative and hard-working students and much better equipment.

I'm working on two grant proposals and several papers while dreaming of getting back to writing my book, so no detailed paper analysis this week. But Nature is highlighting 15 major papers on evolution they have published in the last few years.

Posted by R. Ford Denison at 05:11 PM | Permalink | Comments (0)

Not enough people voted on the Reader’s Choice, so this week’s paper is “Phylogeny and geography predict pathogen community similarity in wild primates and humans� by Jonathan Davies and Amy Pedersen, published in Proceedings of the Royal Society.

Many humans diseases, from flu to AIDS, come from other species. Similarly, diseases from dogs are an increasing threat to lions, while cat diseases kill sea otters. Are there general rules that predict how likely two species are to share diseases?

To find out, the authors analyzed several large data sets on diseases of humans and 117 other species of primate (apes, monkeys, etc.). They hypothesized that species are more likely to share diseases if they live near each other and/or if they are more closely related, that is if they share a more recent common ancestor. This is similar to how we define relatedness in humans: brothers and sisters have more recent common ancestors (parents) than cousins do (grandparents). Fortunately, the family tree for primates is relatively uncontroversial, at least among scientists.

Continue reading "Sharing diseases with relatives and neighbors" »

Posted by R. Ford Denison at 06:53 PM | Permalink | Comments (0)

I have written about evolutionary trade-offs before, starting with early posts about trade-offs between seed size and seed number in plants, and trade-offs between the ability of insects to escape predators by flying away, versus the ability to hide from them by playing dead. I have also given some examples of the increasing use of sophisticated experimental (often molecular) methods in evolutionary biology. This week's paper combines both themes.

The paper is "Restriction of an extinct retrovirus by the human TRIM5-alpha antiviral protein" by Shari Kaiser, Harmit Malik, and Michael Emerman, published in Science (vol.316 p.1756).

Retroviruses are made of RNA, but make DNA copies of themselves that can insert into the DNA of host cells they infect. HIV, the cause of AIDS, is a well-known example, but there are many others. If DNA copies of the retrovirus are inserted into cells giving rise to sperm or eggs, they can be passed to the next generation, as endogenous retroviruses. If the DNA inserts somewhere where it turns an important gene on or off, it may kill the host. Or, once in a while, this change may turn out to be beneficial. The few beneficial changes are the ones that survive and spread, just as the few mutations that are beneficial are the ones that persist.

VWXYNot has an interesting discussion of how a creationist web site misused one of her papers as evidence of "intelligent design." She shows how shared endoviruses can be used to infer shared ancestry, providing yet more evidence that we share a recent ancestor with apes, less-recent ancestors with monkeys, etc. But that's not what this week's paper is about....

Continue reading "Trade-offs in defense against retroviruses" »

Posted by R. Ford Denison at 08:28 PM | Permalink | Comments (4)

This week’s paper is “Local interactions select for lower pathogen infectivity� by Michael Boots and Michael Mealor, University of Sheffield, published in Science (vol. 315, pgs. 1284-1286) and suggested by my wife.

The evolution of greater or lesser infectiousness in pathogens has important implications for health of plants and animals, including humans. Evolution is a process that follows its own rules and humans can’t control it completely, but we can sometimes influence it, just as we may be able to constrain the course of a river or limit the spread of a forest fire.

One factor over which we have some control is the ease with which a pathogen spreads from one host individual to another. For example, a bacterium on the skin of one patient in a hospital can’t jump to another patient in a different room, but it may be able to hitch a ride with a doctor or nurse who forgets to change gloves between patients. Intestinal bacteria reach new hosts easily if untreated sewage is dumped into the same river used for drinking water, even if the bacterium is so virulent that the host is too sick to walk around and infect others.

Paul Ewald has suggested that easy transfer between hosts favors the evolution of greater virulence (Oxford Surveys in Evolutionary Biology 5:215-245). For example, cholera spreading through South America in 1991 evolved greater virulence in countries with poor water supplies, but lesser virulence in countries with better water supplies. So not only were more people infected in countries with polluted water supplies, but the infected people were sicker.

Continue reading "Less-vicious viruses evolve in viscous cannibal populations" »

Posted by R. Ford Denison at 11:42 PM | Permalink | Comments (5)