[asa] Behe's application of chloroquine resistance

Dear Friends:
 
I'm still waiting to get a copy of Michael Behe's "Edge of Evolution,"
but from reviews and blogs I gather that Behe considers Nicholas White's
estimate of the frequency of de novo chloroquine resistance in
Plasmodium falciparum (cause of the most dangerous form of malaria in
humans) to be a reliable estimate of the power of Darwinian evolution in
general.
 
White may have published the estimate in multiple articles, but I'm
working from the following review by White:
 
Antimalarial drug resistance.
J Clin Invest. 2004 Apr;113(8):1084-92.
 
From White's paper:
 
"Resistance to chloroquine in P. falciparum has arisen spontaneously
less than ten times in the past fifty years (14). This suggests that the
per-parasite probability of developing resistance de novo is on the
order of 1 in 1020 [10 raised to the 20th power] parasite
multiplications."

Reference (14) by White is a 1997 paper; more recent literature confirms
the "less than ten times" estimate, and in fact identifies four founder
events ["Genetic diversity and chloroquine selective sweeps in
Plasmodium falciparum," Wootton et al., Nature Vol 418, 2002, p.
320-323]. One founder event in Asia appears responsible for the allele
now in both Asia and Africa. Two more founder events on opposite sides
of the globe (Papua New Guinea and the Amazon) apparently independently
produced a second allele. The remaining two alleles (in Columbia, and
in Ecuador) were apparently produced by another single founder event in
South America.
 
White doesn't detail how he obtained the 1 in 10 to the 20th power
estimate. Perhaps Behe does. In any case, if we accept the estimate, I
still wonder how it can be used to estimate the limit (Behe's "edge") of
Darwinian evolution's ability to produce other biological entities.

A couple of simplistic questions come to my mind. If anyone has
possible answers, I'd appreciate knowing them.

1) As White mentions in his review, chloroquine resistance can emerge
much more frequently in the lab than in nature, for reasons having to do
with host immunity and other phenomena specific to parasitic infections.
Is the higher laboratory frequency more applicable to evolution in
general since it avoids some of the phenomena specific to parasites, or
is the in vivo frequency more relevant since it's natural?

2) Note that the lab studies grow parasites in blood only; the normal
mosquito stage is not involved. Yet it's the sexual stages in the
mosquito that can greatly accelerate, via recombination, the spread of
alleles. Clearly, strongly selected sweeps occurred to spread the four
major chloroquine resistance alleles over the past decades, apparently
requiring 20 to 80 parasite generations, which would take about 6 to 30
years in endemic areas (according to Wootton et al., Nature Vol 418,
2002, p. 320-323). My question is: once resistance alleles have spread
around the world, wouldn't any new spontaneously emerging alleles
conferring chloroquine resistance be under little if any positive
selection (because already-resistant parasites are in the same host and
vector populations), and thus unlikely to be detected? For example, I
know that in laboratory evolution studies using bacteria, mutations come
and go without being detectable as endpoints; one has to freeze samples
of the culture at various time-points to catch them before they
disappear.

I suspect that Behe is underestimating the frequencies of beneficial
random mutations.

Thanks for any help you can provide.
 
 
Charles (Chuck) F. Austerberry, Ph.D.
Assistant Professor of Biology
Hixson-Lied Room 438
Creighton University
2500 California Plaza
Omaha, NE 68178
 
Phone: 402-280-2154
Fax: 402-280-5595
 
e-mail: cfauster@creighton.edu
 
Nebraska Religious Coalition for Science Education
http://nrcse.creighton.edu <http://nrcse.creighton.edu/>
 
 

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Received on Fri, 13 Jul 2007 12:11:19 -0500