This Week in Evolution

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)