Neither of them are malaria. They both cause malaria. Malaria is a disease.
That makes sense. Otherwise, genetic diseases like cystic fibrosis would be considered examples of convergent evolution. Which would just be silly.
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I donât follow. Disregarding the specific case of CQ resistance, if it really is independent evolution of the same adaptation in parallel, (if there is no gene-flow between sub-populations), then why is that not convergence?
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Just a point of nomenclature. Malaria is the name of the disease, while Plasmodium is the name of a clade of parasites that contains the species that causes malaria. Like Covid-19 is the name of the disease caused by the virus named SARS-Cov-2.
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That seems to describe pathways through which convergence towards the same set of high-resistance conferring mutations can (and have been observed to) occur?
Yes, their biology are very different, as the title of the paper I referred to indicates: here it is:
« Why Plasmodium vivax and Plasmodium falciparum are so different? A tale of two clades and their species diversities »
Here is a possibility discussed in the paper below:
The evidence for pvcrt upregulation in CQ-R P. vivax, as well as previously demonstrated effects of PvCRT in heterologous systems[11],[12]raise intriguing questions about the native function of this transporter and its role in drug resistance. Why is PvCRT able to transport CQ, whereas wild-type PfCRT in P. falciparum can do so only when it harbors specific amino acid mutations[12]? How might these various observations relate to findings of different stage-specific drug responses of P. vivax and P. falciparum[31],[41],[42] or to possible effects on resistance from post transcriptional modifications of the protein[43]? How do PvCRT and PfCRT differ in their molecular functions? In view of these questions, it is interesting to consider a proposed model in which the mutations of P. falciparum CQR might convert the carrier function of PfCRT from an exchange-only activity to a net transport function for the drug[44]. In the case of PvCRT, net transport of CQ may already be an inherent directional property of the transporter. Structural explanations for the different properties of PfCRT and PvCRT will have broad implications for our understanding of the CRT family of carriers, the natural functions of which remain unknown.
Ok, I will modify my claim as follow: it is only through a few point mutations in the same pre-existing protein that P. Falciparum developed chloroquine resistance. Am I correct now?
- my focus on the terminology is warranted
- I am not ignoring the mechanism of resistance
- I avoid nothing
You understand that the cited paper is a review, yes? Itâs an assessment of the full literature at the time of publication. Did you read it? Do you disagree with its method? Is it grossly wrong?
Around 5% of those examined.
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Taken from the CDC site:
Chloroquine-resistant P. falciparum first developed independently in three to four areas in Southeast Asia, Oceania, and South America in the late 1950s and early 1960s. Since then, chloroquine resistance has spread to nearly all areas of the world where falciparum malaria is transmitted.
Whatâs wrong with the following claim? : cases have been observed where separate populations of the same species independently converged to the same solution when confronted to a given challenge.
Now, in the case of cystic fibrosis, can you tell what is the challenge to which humans are confronted to and what is the solution that has been found ?
Well, youâre doubly wrong here.
First, the paper by Summers et al that you cite doesnât refute the point that I was discussing, ie that populations of the same species can independently converge to the same solution when confronted to a given challenge, chloroquine resistance in P. Falciparum being a good example.
Second, ironically and contrary to what you think, the same very paper, far from refuting Beheâs main inference in the Edge of Evolution, in fact vindicated it, said inference being the need for multiple, specific changes in a particular malarial protein for the development of resistance to chloroquine.
Because thatâs not the definition. Because tweaking a transporter is relatively trivial, and because in the context of evolutionary biology, it refers to far more distant relationships and more complex traits, the classic example being flight.
organisms that are not closely related
I do.
No, it did not address the full literature at the time of publication. Know how I know for certain?
Yes x3. Itâs obviously lame, but thatâs what happens when you give in to confirmation bias, as you and Larry appear to have done.
So 1000 (of the 20000 mammalian genes) meets some definition of âhandfulâ? Never heard that before. 
Whatâs your point? There are only 3 ways I can think of to evolve resistance: break down the compound, keep it from coming in, or sequester/pump it out after it gets in.
Do you disagree?
Great! Do you agree that Behe grossly misrepresents the literature available at the time he wrote his book, and that the literature published since his book weakens his case even further?
That wasnât the inference, though. Behe asserted (his inference was fatally flawed) that two specific substitutions were required, neither of which conferred any chloroquine resistance on its own.
The paper definitely refutes all of Beheâs claims regarding chloroquine resistance.
Look at panel A:
https://www.pnas.org/doi/10.1073/pnas.1322965111#fig01
And all of these isolates:
https://www.pnas.org/doi/10.1073/pnas.1322965111#fig02
Arenât there more than 2 substitutions presented, and donât many of them confer resistance by themselves?
Wikipedia is your friend.
Evolution
The ÎF508 mutation is estimated to be up to 52,000 years old.[185] Numerous hypotheses have been advanced as to why such a lethal mutation has persisted and spread in the human population. Other common autosomal recessive diseases such as sickle-cell anemia have been found to protect carriers from other diseases, an evolutionary trade-off known as heterozygote advantage. Resistance to the following have all been proposed as possible sources of heterozygote advantage:
- Cholera: With the discovery that cholera toxin requires normal host CFTR proteins to function properly, it was hypothesized that carriers of mutant CFTR genes benefited from resistance to cholera and other causes of diarrhea.[186][187] Further studies have not confirmed this hypothesis.[188][189]
- Typhoid: Normal CFTR proteins are also essential for the entry of Salmonella Typhi into cells,[190] suggesting that carriers of mutant CFTR genes might be resistant to typhoid fever. No in vivo study has yet confirmed this. In both cases, the low level of cystic fibrosis outside of Europe, in places where both cholera and typhoid fever are endemic, is not immediately explicable.
- Diarrhea: The prevalence of CF in Europe might be connected with the development of cattle domestication. In this hypothesis, carriers of a single mutant CFTR had some protection from diarrhea caused by lactose intolerance, before the mutations that created lactose tolerance appeared.[191]
- Tuberculosis: Another possible explanation is that carriers of the gene could have some resistance to tuberculosis.[192][193] This hypothesis is based on the thesis that CFTR gene mutation carriers have insufficient action in one of their enzymes â arylsulphatase - which is necessary for Mycobacterium tuberculosis virulence. As M. tuberculosis would use its hostâs sources to affect the individual, and due to the lack of enzyme it could not presents its virulence, being a carrier of CFTR mutation could provide resistance against tuberculosis.[194]
That criterion with being âclosely relatedâ is rather arbitrary. Itâs easy to understand what convergence is by just contrasting it with divergence. Things can either diverge, run in parallel, or converge. So divergence and convergence are just opposites.
It doesnât make sense to have this requirement that convergence requires some particular distance of relationship. How closely is âcloselyâ related anyway?
A much better way to understand the concept is just this:
If two lineages independently evolve the same or highly similar traits/adaptations, regardless of the degree of relatedness of those lineages, they have converged on the same/similar solution. If they have converged instead of diverged, then it is convergence. Instead of divergence.
If two separate populations of Plasmodium falciparum independently evolve the same small set of resistance conferring mutations, that is an example of evolutionary convergence.
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I do not, but it would be nice of you to tell me.
Could you tell me just whatâs wrong with the methodology? And could you suggest a review on the subject that you think has proper methodology?
Thatâs an estimate, not a count of known cases. Arguing about whether 1000 is a handful is not of great interest to me. But your claim is that 10,000 is a better estimate, right? What is the basis for that estimate?
And again, does this have anything whatsoever to do with the title subject?
IMO itâs an important mechanistic distinction, but then I very clearly stated that itâs not my definition.
âââââââââââ
It certainly would, but given your arrogance, should I? You canât guess? It would probably be more likely to be correct than your other guesses on this subject.
Hint:
After all, your condescending questions and claim:
âŠobviously represented blind guesses. Should one really expect niceness in response to that?
The pathetically limited search terms, for starters.
Are you denying that immuglobulin genes arenât functionally alternatively spliced? Are they mentioned in what you touted as âan assessment of the full literature at the time of publicationâ?
I know, because I read the lousy paper you cited as someone elseâs source, remember? Weâre discussing your confident claim:
That claim was not made in the context of the paper you then sorta, kinda cited as a reachthrough. Now you seem to be saying that 5% supports your claim. 5% of known genes is 1000. Would anyone in his/her right mind call 1000 âonly a handfulâ?
Of course not! One usually loses interest in supporting oneâs guess when one realizes that one cannot support it empirically.
My claim? Nice try. I havenât made that claim. It would be nice if you used a quote instead of a fabrication. Here it is:
Now I do admit that youâve since shown me a lower estimate, but itâs ludicrous.
I pointed this out as one of many potential problems with the hidden alignments on which the paper depends. You chose to challenge me and make a claim without knowing what you were talking about. At this point, itâs only about whether and when youâll quit digging.