No, not at all. Quite the contrary in fact!
I wonder if you understood what this thread is about. Let me explain again.
Bases on theoretical analyses and experimental data, Sanford claims that strains of RNA viruses such as influenza circulating in the human population degenerate rapidly through genetic entropy. Critics of this thesis argue that if this were true, then flu viruses should have been extinct for a long time, but since this is not the case, the thesis is therefore false. However, this objection only works if the genetic entropy of influenza viruses occurs at the same rate in all hosts and in the various environments in which the viruses exist. However, as we have seen in this thread, there is evidence that influenza viruses are subject to less genetic entropy in their natural biotic or abiotic reservoirs than in humans. So this particular objection to GE in RNA viruses doesnât work.
The data he seems to be ignoring is the continuing existence of influenza viruses, contrary to the predictions made by his model.
You would need to explain why this is. Influenza is continually replicating and infecting new hosts in all of the species it is found in. If it isnât continually replicating and infecting new hosts it would immediately go extinct.
Those articles directly contradict Sanford because Sanford predicts that influenza should be accumulating slightly deleterious mutations that reduce fitness over time. Instead, influenza is in evolutionary stasis which means it isnât accumulating slightly deleterious mutations over time.
Those viral strains ARE CONTINUALLY REPLICATING THE ENTIRE TIME. Please let this sink in.
Gil, you have presented no relevant facts, just a series of equivocations.
I do; my graduate training is in virology. I even know Luis Villareal from that time at UCSD.
Your explanation is Tufnelesque.
He is misrepresenting the data, Gil. He is misrepresenting reassortments as mutations.
False. He claims this universally, so youâre just moving the goalposts.
We donât merely argue, Gil, we point to the evidence that you and Sanford ignoreâlike reassortment. It is sadly predictable that you eschew evidence to portray science as mere rhetoric.
Letâs see your math.
You have shown zero evidence for or against genetic entropy, just a bunch of equivocations.
No, not at all. What Sanford says is that influenza is prone to rapid degeneration during outbreaks but relatively protected from GE in its natural reservoirs, being biotic or abiotic. And it happens that his view is supported by many level of evidences, as this thread demonstrated.
Are you serious? Have you been following this thread. Obviously not, otherwise you wouldnât have made this remark, for the whole point of the thread was to show that there are very good reasons to think that influenza is less prone to GE in its natural reservoirs than during outbreaks.
Yes, because in evolutionary stasis, it is still replicating and mutations are still occurring. Why wouldnât it be? Please answer without any equivocations or cut/pasting.
I did not; it made no sense. Iâm confident that @T_aquaticus did not miss it either.
The more an RNA virus replicates, the more it mutates. The more it mutates, the more it departs from evolutionary stasis and the more it is prone to genetic entropy. So obviously, you were plain wrong when you said that a virus that is in evolutionary stasis should be MORE susceptible to GE, not less.
You say that, but youâll note that the word âstasisâ doesnât appear anywhere in the paper.
They document that the substitution rate of AIV in wild birds is about 40% lower than in poultry (~2.5 vs ~4.0 x10-3 substitutions per site per year), and they explain that this can likely be explained by several factors, including a latent phase involved in transmission between wild birds reducing the number of viral replications or the heightened contact between poultry driving up the number of replications. There are also different selection pressures from the immune systems of the different groups.
The question the study was addressing was whether or not AIV substitutions rates differ between wild birds and poultry, not whether or not AIV experienced âevolutionary stasisâ. Youâll note that in the 2006 study I referenced before, they were able to dismiss the idea of âevolutionary stasisâ based on the fact that AIV had a substitution rate â>10-3 substitutions per site per yearâ. This 2015 only further supports this by finding that even in wild birds, the substitution rate is ~2.5x10-3.
Look at Figure 1 of the 2006 paper, and compare it to Figure 1 of the 2015 paper.
When placed on the same scale (below), itâs clear that the results are consistent. The 2015 study was just performing a more detailed comparison of two specific groups - wild birds and poultry. Coarsely, AIV substitution rates are pretty constant between groups, and certainly high enough to not be considered in âstasisâ, but there are differences between groups at the finer scale. These differences are significant enough to be interesting to virologists, but not enough to explain away the persistence of AIV if genetic entropy is true.
Thanks for these precisions. I agree with you that if the flu rate of molecular evolution is only 40% lower in its natural reservoirs (wild birds) than during outbreaks in other hosts, this difference is probably not enough to explain away the persistence of AIV if genetic entropy is true. But isnât the key to this enigma the frozen evolution phenomenon, I.e., the fact that influenza viruses can persist for prolonged period of time in an abiotic form in the environment?
