Everyone else is doing my writing for me

I'm still working on finishing up 3 manuscripts (one book, 2 journal articles) so I've not blogged quite as much this week as I generally do. Next week I should be back up to speed, and have a few topics in the queue that I want to get to. Luckily for you, though, John Hawks has a pair of excellent posts discussing infectious disease issues, Sciencblogs neighbor RPM at Evolgen has a post on microbial diversity, and fellow PT contributor Mike Dunford has a post discussing the CCR5 deta 32 mutation, HIV resistance, and West Nile over at The Questionable Authority. Discussion of these and a few of my own comments below the fold...

The first discusses an article in Discover magazine (if anyone wants to send that article my way, I'd muchly appreciate it, btw) suggesting that "some of the most major epidemics that killed the Aztecs and other ancient American populations may have been caused by an indigenous hemorrhagic fever." It's an interesting hypothesis (and John includes the links to 2 other peer-reviewed papers on the topic as well). It's long been assumed that these epidemics were due to the introduction by the Spanish of smallpox and similar diseases, against which the native populations had no immunity. The viruses burned through the indigenous populations, leaving the Europeans essentially unscathed--a miraculous feat in the eyes of the natives, leading some to attribute god-like powers to the Spainards. But were these epidemics really due to smallpox, or were they caused by native diseases, such as a hemorrhagic hantavirus?

It's not just an academic question, either. We're always on the lookout for emergingand re-emerging diseases, and a better understanding of what really occurred when these two populations met up would supplement our knowledge of what we've been seeing in the modern day.

The second post deals with prion disease; specifically, what type of selection have the alleles that encode the prion protein (PRNP) been subjected to? (Much more of the background can be found over at Hawks' site). A 2006 paper suggests "a complex history of selection including mainly positive selection..." --essentially, that there has been selection pressures leading to the divergence of these alleles, apparently followed by drift and/or purifying selection. The question John ends with is, why? What was it that led to this divergence?

So for a gene that had no coding changes in humans or chimpanzees, why would there recently have been two successive selected changes in humans?

For a highly conserved brain-expressed gene, why would there recently have been two successive selected changes in humans?

Hmm...

The authors don't even speculate in their manuscript--interesting in itself, since that's one of the fun things about conclusions like this.

Over at Evolgen, RPM says:

Apparently, not much known about the genetic diversity of bacterial populations -- or so I've heard. As a eukaryotic geneticist, I can say that we know a whole bunch about multicellular organisms -- mostly because they're a lot easier to see and catch, and they're more like us than are prokaryotic relatives.

I've written about microbial diversity previously here and touched on it in this post, but those are both discussing microbes associated with humans, while the paper RPM cites deals with soil bacteria, finding that pH is the major factor contributing to diversity in this environment. I wonder what a meta-analysis of the diversity of human-associated bacteria would find? For example, we already know that diversity can vary even by location within the colon; we also know that the pH of different areas in the body can vary (due not only to bodily secretions but also other bacterial flora that may be present). How much is this a factor in the diversity in our own normal flora?

Finally, Mike discusses the CCR5 delta 32 allele, which has been found to confer resistance to HIV. (I've also written briefly on this topic, here). Mike cites a press release for a new study showing that people with this mutation, while resistant to HIV infection, appear to be at a greater risk for severe West Nile disease. Mike uses this as a springboard to discuss the role of environment iin determining what is a "beneficial" mutation--a concept creationists often throw around without really understanding what that means.

So, who's up to write my posts tomorrow? :)

Smallpox, Infectious disease, Prions, Hemorrhagic fever, HIV, Microbial diversity