Genetic Entropy

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.

Your articles create a false impression upon laypeople (including you) because they omit critical information.

Its purpose is to convince religious laypeople of something not supported by the data.

But that’s not how it works!

The new strains originate primarily by reshuffling of the genome segments in one of the reservoirs and secondarily by mutation. The viruses are always “jumping” between species. We just don’t notice them unless a new reassortment causes overt disease.

This happens every year! That’s why there are different vaccines every year, and some of them miss the mark. There may be 2 or more new reassortments and one is missed, or an antigen is changed by the fixation of a new (or old) mutation.

That documented reality makes your articles moot and extremely misleading.

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You’re being pedantic. You said “that’s not how it works”, but then you go on to confirm that what I said is happening all the time. So it does work that way, after all. Again, nothing C&S or I have written is inconsistent with these facts, but I understand and respect you have a different interpretation of them.

Thanks again, as usual, for your time, and I’ll attempt a second time to extract myself here because I’ve shared all I need to on it.

What if someone reads your articles, concludes that H1N1 is extinct, so that s/he doesn’t need this year’s H1N1 vaccine, then dies from H1N1?

No, you claimed that the jumping itself is the deciding factor.

Your “now beginning” is simply false. The reality is that the reassortment is the cause. You strategically omit that.

Your conclusions are completely inconsistent with them, as was your misleading labeling of the data itself.

Then include the facts about segmentation and reassortment and see if you can make your article make any sense at all.

It doesn’t even have to be a new virus strain (i.e. without reassortment).

HA is hemagglutinin, the H of HxNx. Mutations in that gene can switch host species specificity. You can also shuffle the genes from an avian virus with a human virus that already has an HA specific to humans. Either way, you get genes that have been evolving in a different species which the human population hasn’t seen and hasn’t developed a herd immunity against.

This is where zoonotic diseases are so interesting. There is no telling how the human immune system is going to react to a new bug. There can be cases like Ebola where it is passed around among bats without any problems, but it causes a massive overreaction by the human immune system, resulting in life threatening disease. There can also be cases where the human immune system doesn’t overreact, and is able to keep viral load down. @Mercer can correct me if I am wrong, but it seems to me that it is largely a crap shoot when it comes to virulence.

The real question is if virulence and mortality is a beneficial pathway for viruses in the long term. Transmission and avoidance of the host immune system seem much more viable, at least in my eyes.

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Don’t worry, that won’t happen. Nothing we wrote implies in any way that H1N1 as a whole is extinct and/or that flu vaccines are unnecessary. CMI is very much pro-vaccines:

No, you claimed that the jumping itself is the deciding factor. The reality is that the reassortment is.

Not intentionally, if so. The point is that the jumping does happen.

Your conclusions are completely inconsistent with them

That’s your opinion, and I respect it.

as was your misleading labeling of the data itself.

That has been corrected with your help, and I thank you.

You are not wrong, which is why misrepresenting how this works puts laypeople in literal danger for their lives, if they believe you.

There’s no way that you can assume that someone reading your misleading article has also read your nonmisleading one.

No, your point was:

That’s not true, because as you just conceded, jumping is happening all the time.

I know that this discussion has about run its course, but I think it should be emphasized that holding up flu viruses as an example of GE totally and completely ignores the roles genomic organization, importance of rearrangements/reassortments, and differing contributions that the various genome segments make to disease, infectivity, and the like. Properly factor these in, and flu viruses pretty clearly refute the notion of GE.

(The same could be said of almost any virus.)

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Because virus can persist for very long periods of time in a dormant state and can re-emerge from « natural reservoirs ». This is probably what happens for the 1918 strain of flu.

RNA viruses don’t do that.

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That’s why I’m suggesting that @PDPrice privately and independently insert all of the info about segmentation and reassortment, just to see if the article still makes any sense.

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You keep saying things like this, about how your really don’t understand important details about this topic. Nothing wrong with that, of course. Learning is why many of us are here.

But what I don’t get is what makes you feel entitled to write articles, that will be read by thousands, about things you admit you do not understand. Don’t you worry about misleading people?

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I didn’t say I didn’t understand the content of the article itself. You’re the one misleading people with this. I said that my understanding of that specific question (which goes beyond the scope of the article I actually wrote) was a bit fuzzy.

There is a reason that I had Dr. Carter as the co-author on that article to make sure that scientific statements were accurate. There is by all means a stringent review process before anything gets published to the site, and lots of people see it before it goes live.

You’re alleging things that are simply not the case here.

This is an interesting thread that ran its course. I’m looking forward to seeing how @PDPrice takes this forward: A Trust Building Excercise on Genetic Entropy.