I already got mine 
Why? If you’re right, it’s a waste of time.
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Look at the arrow pointing DOWN (swine) in 1918. It’s not as simple as you pretend it to be.
I believe that is in reference to the fact that the strain apparently jumped not only from the duck to the humans, but also from the duck to the swine.
I think that your belief is founded entirely on wishful thinking. That cartoon, as complex as it is, is still a huge simplification. It’s disturbing that you cite the cartoon as though it represents all of the relevant data. Do you see my point, Paul?
The paper states that the rate at which mutations became fixed during the spread of the 2009 pandemic strain was the same as the rate during time periods where it wasn’t spreading like crazy. The paper says just the opposite of what C&S are claiming.
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The paper IS what they are claiming. If I understand it correctly (and I may not) they are saying that the swine flu outbreak was still attenuated and still harbored the mutational load of previous H1N1 strains. Note that the 2009 swine flu scare was a far cry from being anything like the 1918 outbreak.
I think it’s a naive distinction, illustrated by the discussion here.
Recombination is a huge source of heritable variation that is generally ignored by evolution denialists. Influenza is a turbocharged version of that, given that coinfection of the same cell by two different viruses produces massive variation.
Note that segmentation is described in the journal article, while in the two creation.com articles, readers are told absolutely nothing about the segmentation and the massive variation it creates. You’d think that influenza A had a single, linear genome and that all of the variation comes from mutations.
The data in the paper don’t support the claims that they make in words in the paper.
The 1918 strain would have also harbored the mutational load from the 1,000’s of years of mutations that preceded it. So how could the 1918 strain be so virulent?
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This is where my understanding gets fuzzy, but I think he’s saying the virus is something that is beneficial in the waterfowl and the waterfowl have natural regulatory mechanisms in place to keep the virus in check and mutations low:
However, when it jumps to pigs and people, it burns like wildfire because we do not have the natural regulatory mechanisms that aquatic waterfowl apparently do.
(From creation.com/fitness)
That makes a crystal-clear, falsifiable, empirical prediction: that we will never find any evidence for a pre-1918 outbreak.
Pass the popcorn…
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Yeah, if you mean specifically H1N1. I think that would be a prediction, if I understand everything correctly. Dr. Carter & Sanford would have to say for sure if that would be something they’d predict.
Your understanding is extremely fuzzy. You’re also back to equivocating between mutations occurring and mutations being fixed. The former is biochemistry and the latter is population genetics, a branch of evolutionary biology.
I think they are making it up.
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I do.
Your understanding is not fuzzy there.
That’s not how science works, Paul. Hypotheses must be mechanistic and stated clearly so that we all agree that the hypothesis itself, not any particular person, is making the predictions.
The scientific method is about baking in all interpretations and assumptions before we see the data.
We get excited about that.You seem to be different.
“Spetnerian metrics”.
Of course. I only mean that I am not placing my own understanding of the work on such a high pedastal as to presume to speak for them.
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That is not what is happening. This is why omitting the genome segmentation in the creation.com articles is so deeply misleading.
The genome has 8 segments–different RNAs. It does not have a simple, linear genome as you are assuming with your “jumping” bit here or as any layperson would infer from your article.
These big, epidemic-producing reassortments are caused by two or more viruses infecting the same cell in the same host, shuffling those genome segments, not just a couple of mutations or one strain of virus “jumping,” whatever that means.
But you are clearly clinging to the idea that you understand it better than I do, while shrinking from testing hypotheses independently–the quickest way to really learn.
Nothing we wrote would be inconsistent with that, and I can assure you that C&S do understand this, as their paper bears out. The purpose of the creation.com article is clearly not to act as a textbook on how these RNA viruses work at a genomic level.
Jumping obviously means that this new virus strain which originated from one type of host is now beginning to affect a completely different host.