Which state is less degraded?
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I don’t think so.
I was studying biology during the swine flu outbreak in 1977; no one called it the Spanish flu then.
I am confident that the little pig on the chart represents a new reassortment that was confidently attributed to swine, typically defined by new antigen(s). Each of the isolates represented by arrows is different. Note that the whole bottom part of the figure represents swine.
Perhaps this might help you reach a deeper understanding of the complexity that your article is dangerously oversimplifying:
https://jcm.asm.org/content/45/11/3807
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According to C & S, it would be the avian benign one. The pathogenic version “burns hot and fast” and eventually reaches an attenuated state and suffers from mutational meltdown.
Why did the chart you posted have an arrow pointing down into the pig area for 1918?
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Ok, but if it’s a copy of the Spanish Flu (C & S say it is), then it’s Spanish Flu, not swine flu.
But there remain H1N1 outbreaks every year. How can that be?
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1918 shows a duck, not a pig. It was an avian host.
New strains keep jumping from swine and/or avian hosts, apparently.
Not so, the attenuated state is selected because it is more fit for long term survival.
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C&S seemed to have been so focused on one viral strain that they missed the overall picture. If we take a holistic approach, we see that viral DNA/RNA has a long history and a continuous ancestry going back to the first influenza virus. For those ready with their nit picking combs, this is an oversimplification, but the basic facts hold true.
Let’s use a car as an analogy. The GE supporters are saying that the parts in the car wear down over time to the point that the car can no longer function. There are also other cars puttering about in this same world. If I take car parts out of a 50 year old car and put them in my car, does that 50 year old part suddenly act as if it is new? No. This is analogous to the types of swaps that happen between influenza strains. Parts are swapped back and forth, but those parts are old themselves.
What GE calls “new” virus simply isn’t. It is a reshuffling of old virus. If GE predicts that the 2009 pandemic H1N1 should die out because of GE in just 10 years, then how is it that these other parts from other viruses are still kicking around after at least 1,000’s of years (limiting this to a YEC time window for now)? How are they still functional and able to combine into viable and virulent viruses?
GE just doesn’t make sense.
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I think we would all like to see some references that back up this claim.
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It’s clear that C&S don’t know what they are talking about. Please look at the evidence in Table 1 and Figure 1 in the paper I cited and explain how your simplistic bifurcation can possibly be accurate, or useful for anything but deception.
Note that we can only make trees from individual genome segments, as shown in Fig. 1. Each segment (M in the figure) gives a different tree. That’s the incredible complexity that you’re oversimplifying into a bifurcation. There are no bright white lines, Paul.
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A good place to start would be for you to read their paper, which is one such reference as what you’ve requested.
This adhom is not supported by the evidence. It’s clearly significant that the CDC colored the 1977 outbreak red, exactly the same as the 1918 strain. What, didn’t they have the imagination to think of any other colors? This doesn’t stack up. The whole point of said chart is to delineate the different strains in existence. You’re saying they were just lumping different strains together under one color, but that would defeat the whole point, and you can see they’ve got different strains shown in different colors.
I did. I can see how bad it is, even though I last did virology in 1990. Why are you arguing with me from a position of ignorance?
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It’s not an ad hominem. The data, particularly the data they omit, do not support their conclusion. They present ZERO evidence to support the claim of a meltdown.
The significance of red in the CDC cartoon is that both are H1N1.
I appreciate your opinion on this, I really do. Thanks for your time. I think I’ll bow out of this for the time being because I’ve contributed all I really can to the discussion.
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Just so there isn’t any confusion, could you please specify which of their papers you are referring to, and which of their references should contain this info?
You’re welcome. I hope that you continue an independent study of the complexity of H1N1 and don’t forget your flu vaccine this fall.
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