Reddit mentions of The Evolution and Emergence of RNA Viruses (Oxford Series in Ecology and Evolution)

Part 5: Summary and Question & Answer

 

There was a short summary at the end before the Q&A, in which Sanford irresponsibly attributed a bunch of things (autism, neurodegenerative disorders, a bunch of other stuff) to mutation accumulation, without evidence.

 

Oh and he didn't get to the H1N1 stuff, but he does claim that human H1N1 went extinct in 2009, which isn't true - it hybridized with a swine flu strain that continues to circulate.

 

Now to the Q&A...I'm only going to mention the relevant questions.

 

Hey, I think I know who asked that first question!

Question: Genome of 3 billion bases, 700 billion mutations for generation (because 7 billion people x 100 mutation per person) means we've sampled every mutation, a lot, right?

Answer: Yes.

Followup: So don't we then reach an equilibrium with back mutations?

Answer: Back mutations are too rare.

My notes: That's a copout answer. Do the math. For every bad mutation that happens, you remove 1 bad from the pool of possible and add 1 good (the back mutation). At some point, you hit an equilibrium. It's not hard. Sanford is denying 2+2=4.

 

Questions: Horseshoe crabs have been around for a hell of a long time, how did that happen?

Answer: ¯\_(ツ)_/¯

Me: He then went into H1N1, and oh my goodness drop it you're wrong. I don't really feel like writing it all out again, but ffs. (I'm sure I missed a post in there, but I can't find it. We've talked about this a lot.)

OMFG he also claims that there's evidence that all RNA viruses are evolutionarily young, tens of thousands of years old. THAT'S DUE TO SATURATION, DUMBASS. Their mutation rates are so high and genomes so small that after a few thousand years you can't distinguish sequence homology from convergence. So phylogenetic signals fade after 10-20k years (give or take 10 to 20k). Nobody who knows what's what actually thinks they're that age. Read a book, John. This one, to be specific.

 

Question: What's the "starting point" for the human lineage where we don't have any of these problems?

Answer: It takes time for enough mutations to accumulate to cause a problem, there isn't one "starting point" where you would say "zero mutations".

Me: See, the real answer is "6000 years ago when god created Adam," but he can't say that, so he has to hem and haw and not actually answer the question.

 

Question: RE Fischer and other early ideas - fitness isn't one-dimensional, so all of this is overly simplified, and selection preserves "evolvability" as a phenotype, right? And second, why isn't genomic entropy seen in laboratory populations of fast-mutating organisms?

Answer: Most adaptive mutations don't increase information.

Me: Can he quantify information? No.

Answer to the second part: Reductive evolution, specifically claiming that all the adaptations in Lenski experiment were loss-of-function:

>All of the beneficial mutations in the long-term Lenski experiment were loss-of-function; genes were deleted, genes were silenced, or genes were down-regulated. In one case a promoter, which is normally regulated, because an unregulated promoter.

Bull. Shit. Putting aside that this is just not true (the Cit+ line did not experience any loss of function, for example, and not all of the beneficial mutations have been figured out, which means we literally can't make the broad claim), it exposed the "heads I win, tails you lose" nature of this discourse: If a thing works in a new condition while also functioning in the old, that's a loss of specificity. If it stops working in the old and starts working in the new, that's a loss of function. See? According to creationists, no matter what happens, creationists are right! Funny how that works, isn't it?

And there's a bonus "no new information" claim. Can't quantify it, ho hum.

 

Question: This all hinges on the distribution of mutation effects, but how can we know what the distribution will look like?

Answer: Uh...Lenski! Only a few mutations were beneficial, and they were all reductive!

Me: See above.

Answer continued: H1N1! Showed a few figures from the H1N1 paper.

Me: See above. Best worst paper. So bad it's...no, it's just bad. No genetic entropy. Virulence is not a good correlate of fitness. Also, antibiotics exist now, but didn't in 1918. So bad. Just embarrassingly incompetent.

 

And that's it!

That...wasn't really anything new, was it? Was anyone else hoping for something exciting? Fireworks from the best and brightest creationists have to offer? Me too! But this is what we get. Because there isn't anything special behind the curtain. It's just the same tired arguments, misrepresentation, and basic errors over and over.

Thanks for reading.

There are quite a few points that are worth discussing in that file, Joe. I find orphan genes particularly interesting and would love the chance to work on some and try to pin down some of the mechanisms of their emergence. But to the HIV point, I see how you've arrived at your numbers but I have a problem with using these observed mutations as a proxy for HIV evolution overall and even moreso for extrapolation to other organisms' ability to evolve. My understanding of your problem is that if HIV, a rapidly evolving RNA virus, can undergo such a massive degree of sequence evolution without evolving new functions (presumably it's explored a huge amount of protein structure space but none have granted novel functions), how is it that we've done it over and over again, that is, evolved novel proteins, with our tiny population size and slow mutation rate. Is that right?

The fact is, we have no idea how much novelty was invented during the past 25 years of HIV evolution, we only know how much was invented and kept in the population as a result of its ability to improve the virus's ability to infect humans. HIV is pretty flippin awesome at infecting humans as it is, so any novel protein structures would have to be doing something really neat to outcompete the rest. If we were talking about a very dynamic environment, then these new guys may have had a leg up, but since we know that natural selection shapes allele frequencies in response to environmental conditions, and we're interested in the past 25 years of viral replication in human hosts, we really shouldn't be expecting all that much fixed novelty.
If you're interested in RNA virus evolution, I'd suggest this book by Eddie Holmes (the author of that HIV evolution review paper you linked): http://www.amazon.com/Evolution-Emergence-Viruses-Oxford-Ecology/dp/0199211132
It's fantastic.