"HIV's acquisition of its ability to counteract human tetherin appears to be a stepwise evolutionary gain where mutations gradually improved the ability, since "chimeras within each region yielded intermediate phenotypes. In other words, each mutation made HIV increasingly better at counteracting tetherin. How can it be IC if it's a gradual path?
In other words, each step was advantageous to improve the mechanism.....
The principle of evolutionary continuity, succinctly formulated by Albert Lehninger in his Biochemistry textbook. An adaptation that does not increase the fitness is no longer selected for and eventually gets lost in the evolution (in the current view, only those adaptations that effectively decrease the fitness end up getting lost). Hence, any evolutionary scenario has to invoke – at each and every step – only such intermediate states that are functionally useful (or at least not harmful).
In the end, this is NOT an example of an irreducibly complex system at all as said before. The system lost, and then (re)gained its function.
From pages 55-56 in chapter 3 of Edge of Evolution:
Suppose that P. falciparum needed several separate mutations just to deal with one antimalarial drug. Suppose that changing one amino acid wasn’t enough. Suppose that two different amino acids had to be changed before a beneficial effect for the parasite showed up. In that case, we would have a situation very much like a combination-drug cocktail, but with just one drug. That is, the likelihood of a particular P. falciparum cell having the several necessary changes would be much, much less than the case where it needed to change only one amino acid. That factor seems to be the secret of why chloroquine was an effective drug for decades. How much more difficult is it for malaria to develop resistance to chloroquine than to some other drugs? We can get a good handle on the answer by reversing the logic and counting up the number of malarial cells needed in order to find one that is immune to the drug. For instance, in the case of atovaquone, a clinical study showed that about one in a trillion cells had spontaneous resistance. In another experiment, it was shown that a single amino acid mutation, causing a change at position number 268 in a single protein, was enough to make P. falciparum resistant to the drug. So we can deduce that the odds of getting that single mutation are roughly one in a trillion. On the other hand, resistance to chloroquine has appeared fewer than ten times in the whole world in the past half-century. Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance to chloroquine is roughly one in a hundred billion billion. In shorthand scientific notation, that’s one in 10^20.
page 60: "Recall that the odds against getting two necessary, independent mutations are the multiplied odds for getting each mutation individually. What if a problem arose during the course of life on earth that required a cluster of mutations that was twice as complex as a CCC? (Let’s call it a double CCC.) For example, what if instead of the several amino acid changes needed for chloroquine resistance in malaria, twice that number were needed? In that case the odds would be that for a CCC times itself. Instead of 10^20 cells to solve the evolutionary problem, we would need 10^40 cells."
A "CCC" is Behe's own term. "chloroquine-complexity cluster"
it's what he calls the two simultaneous mutations needed for p. falciparum (the parasite that causes malaria) to evolve resistence to the drug chloroquine.
Can Random Mutations Create New Complex Features?
the data suggest many structures might in fact not be evolvable by Darwinian evolution--especially when multiple mutations are needed to convey any advantage on an organism.
In 2004, Michael Behe co-published a study in Protein Science with physicist David Snoke showing that if multiple mutations were required to produce a functional bond between two proteins, then "the mechanism of gene duplication and point mutation alone would be ineffective because few multicellular species reach the required population sizes."
In 2008, Behe and Snoke's critics tried to refute them in the journal Genetics, but failed. The critics found that, in a human population, to obtain only two simultaneous mutations via Darwinian evolution "would take > 100 million years," which they admitted was "very unlikely to occur on a reasonable timescale.
Douglas Axe demonstrated the inability of Darwinian evolution to produce multi-mutation features in a 2010 peer-reviewed study. Axe calculated that when a "multi-mutation feature" requires more than six mutations before giving any benefit, it is unlikely to arise even in the whole history of the Earth.
protein folds in general are multi-mutation features, requiring many amino acids to be fixed before the assembly provides any functional advantage.
Another study by Axe and Ann Gauger found that merely converting one enzyme into a closely related enzyme -- the kind of conversion that evolutionists claim can easily happen -- would require a minimum of seven simultaneous changes,6exceeding the probabilistic resources available for evolution over the Earth's history. This data implies that many biochemical features are so complex that they would require many mutations before providing any advantage to an organism, and would thus be beyond the "edge" of what Darwinian evolution can do.
An empirical study by Gauger and biologist Ralph Seelke similarly found that when merely two mutations along a stepwise pathway were required to restore function to a bacterial gene, even then the Darwinian mechanism failed.7 The reason the gene could not be fixed was because it got stuck on a local fitness maxima, where it was more advantageous to delete a weakly functional gene than to continue to express it in the hope that it would "find" the mutations that fixed the gene.
The paper says "the results revealed that four TMD amino acid substitutions (E15A, V19A, I25L and V26L) were sufficient to render the SIVcpz Vpu active against human tetherin". So they are changing amino acids at positions 15, 19, 25, and 26 in that diagram.
Blue is chimp SIV and yellow is human HIV. they mix and match the pieces.
- is no anti-tetherin activity
(+) is a little bit
+ is some
++ is a lot.
In the first column under "release". Note how they never test amino acids 25 and 26 separately. Also note how they never test position 15 separately from either position 19 or position 25-26. Since they didn't test every path, they can't say it is or isn't gradual. Also note that some of the paths they tested were gradual. We go from - to (+) to + to ++. This is on the evolution of HIV-1 group N's anti tetherin activity.
That paper is inconclusive about whether all four amino acids had to change at the same time.