No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2?

I have trouble seeing how you could not see those qualifications. However, that failure is consistent with your false portrayal of science as debate over preexisting data.

Why not answer them, then? If you don’t answer the questions, you are demonstrating your insincerity.

That is very hard, given that you implicitly or explicitly claim expertise greater than mine in virtually every post.

Only if you don’t act like it fits.

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I assume that very few Christians who affirm a YEC have any idea that any of the science of evolution has to do with health. I did not until very recently. I have answered this question before and said perhaps there will be. I will consider this question asked and answered.

I’m not him so I couldn’t tell you why he chooses not to participate in this particular forum, but he’s answered questions when I’ve asked him. I will also consider this question asked and answered.

How would you characterize the continuous research over data and science adding to a body of knowledge over all aspects of science? It appears to me, based on just the research that started this conversation that there isn’t consensus on how mutations affect fitness. I had scientists giving me different answers.

I do not have expertise greater than yours. However, it is obvious by now to everyone that I do believe current evolutionary theory is bad science. I do not like bad science. Creationists’ hypotheses about evolutionary theory seem to be simple and profound. When I read about evolutionary theory in mainstream texts, they also seem to confirm their ideas.

And where creationists would posit created diversity, scientists currently appeal to natural selection or an unknown process. Why aren’t scientists able to show the science definitively rules out creationist hypotheses? Why do Christians and others continue to question current evolutionary theory? How do you know the science of evolution will never change? What would convince you it’s wrong?

First, while you don’t do it above, it’s clear that below you are conflating “Christian” with YEC. That’s really offensive.

Evolution permeates all of biology. If it is false, it is leading us astray in all of those fields. If YEC “science” is correct, scientists using it should be outcompeting us in every field. Not only are they not outcompeting us, they aren’t even trying. Actions speak louder than words.

None of the explanations for their inaction make YEC “scientists” look good from either a secular or a Christian perspective.

We don’t “research over data,” Valerie. In the vast majority of cases, we produce new data. Jeanson has quit doing that in favor of cherrypicking the data of others. It’s really, really lazy. He doesn’t really work in the sense that we scientists use the term. That’s another reason why his refusal to appear here is so telling.

You’re looking at text, not research. It’s not that complex. Fitness is a measure of differential reproduction. The complexity comes in when we consider how many things might/do contribute to differential reproduction.

Did you watch the video of the Birds of Paradise?

Or more likely you’re not understanding them because you’re trying to support a position without much background knowledge. You’re also doing textual analysis instead of examining the evidence for yourself.

And we have expertise greater than Jeanson’s, Steve orders of magnitude more. Jeanson is a dilettante in this field.

It’s also obvious that you do not have any evidence to support that belief, just hearsay.

You lack sufficient knowledge to judge.

The words are not the evidence. Your claim that Jeanson’s paper is “detailed” is absurd.

Why should they bother when creationists are so lazy? It’s my responsibility to rigorously test my own hypotheses. Why should evolution be an exception?

It’s only a minority of Christians. Why are you misrepresenting Christianity as a single bloc?

Why do so many of those same people claim that SARS-CoV-2 is a hoax, some right up until they die from it?

I don’t. What I do know is that lazily cherrypicking the data produced by others is not ever going to do it. It’s going to be from those who currently accept evolution and are actively working.

Evidence, the same thing you should be examining now but won’t. The same thing that Jeanson should be producing, but won’t. Textual analysis doesn’t cut it either way.

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I used a qualifier there. We both agreed those were important. That you’re misrepresenting my views is disappointing.

You are correct. You used a qualifier at the top, but not below. I was wrong and apologize.

Here’s where you do conflate them:

I have no intention of doing that. Are you going to use your accusation as a way to avoid addressing the points I made?

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As others have pointed out, fitness is reproductive success. Now what goes into reproductive success? In the macroscopic world we see, no lethal mutation, viability and vigor to compete in the wild of tooth and claw, beating off the competition for mates, and a providential environment. Reproductive success integrates all of these factors, and all that is captured by fitness.

The same basic principle of reproductive success extends the notion of fitness to the microbial world, but the way it operates is a bit more funky. Viral fitness in a particular individual host is not the same as fitness in regards to a population, but both are valid concepts which should be defined when presenting a measure of fitness. A given viral attachment generally varies in its affinity to potential host species, so fitness varies there. As infection spreads and the host population develops immunity, that impacts fitness. So there is not some objective fitness which can be assigned to any given pathogen without regard to the context of the host population, and as such fitness is always, always, a moving target. As a virus, you are always up against a resource requirement that is either dying on you, or developing impenetrable defenses.

Which is why mutation, far from being an inexorable harbinger of pathogenic decline, is vital to the success of pathogens. Only by mutation can the progressive development of host population defenses be countered or new host populations be penetrated. Mutability is in and of itself a survival tactic; it is a feature, not a … wait for it…a bug.

Here is a paper which discusses aspects of fitness in regards to infection bacteria. Ellipsis mine:

The virulence‐transmission trade‐off hypothesis has provided a dominant theoretical basis for predicting pathogen virulence evolution… The central prediction of this hypothesis is that pathogen fitness is maximized at intermediate virulence due to a trade‐off between infection duration and transmission rate. … Further, in support of the key prediction, there was no evidence for directional selection on a quantitative proxy of pathogen virulence and, instead, isolates of intermediate virulence were fittest. Surprisingly, however, the positive relationship between virulence and transmission rate was not underpinned by variation in pathogen load or replication rate as is commonly assumed. Our results indicate that selection favors pathogens of intermediate virulence at disease emergence in a novel host species, even when virulence and transmission are not linked to pathogen load.

Experimental evidence for stabilizing selection on virulence in a bacterial pathogen

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Thank you. I accept your apology.

My point was that there ARE Christians who question evolutionary theory along with others (at least a few in the ID camp who are not Christians) but in no way did I mean that only those who question evolution are Christians. I think that is the plain meaning of what I wrote and saying it’s otherwise doesn’t follow logically.

I’m becoming weary of answering your questions because it doesn’t seem to lead to fruitful conversation. Thus, my choices are either to ignore you completely or only answer the ones I think may lead to fruitful conversation or where I think it’s important to clarify something.

No, could you link this again?

Evolution is obvious, but yes if it is misunderstood it is leading you astray so I care whether it’s being understood correctly. It is an interesting topic in general and fascinating to understand the progression of the science of it in my lifetime.

They are trying. And yes, eventually they should be able to outcompete you if correct.

Who is trying? Who is working on empirically testing their own biological hypothesis? There are plenty of book and blog authors that are mining data that has already been published, but there seems to be a dearth of individuals doing any sort of work in the lab. Millions of dollars are spent on elaborate efforts to keep their base entertained, but I don’t know if any YEC “wet” research. I’d be very happy to be corrected here.

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That all depends on what we consider to be fruitful. For me, it is getting you to see the elisions Jeanson executes that are blatant to those of us with expertise. It appears that you define “fruitful” as helping to support Jeanson and your “worldview.”

That’s disappointing, but predictable. It’s what made sexual selection obvious to Wallace.

They are not trying. They are only trying to convince people like you that they are trying. And there’s no need to qualify with “eventually.” It would become obvious right away if they were trying.

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And the adaptive immune system itself would be impossible if mutations were only ever destroying functions or reducing fitness.

You have to wonder why the adaptive immune system employs a mechanism of somatic hypermutation to literally increase the mutation rate by a factor of over a million during affinity maturation, as that would seem to only speed up the decline of antibody fitness if creationists are right about mutations can only ever reduce or destroy fitness and function.

The immune system literally employs classical random mutation and positive-selection-driven Darwinian evolution as a mechanism and strategy to fight off novel infections.

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What makes it survive can also be what makes it decline…

Don’t you remember that I was the one sharing this paper in the forum? :wink:

I read the link, but not understanding it yet. Can you provide me with the high school biology version?

Also this one:

https://science.sciencemag.org/content/early/2020/11/11/science.abe8499

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I’m sure you can just google the terms and find various resources.

Very succinct, and simplified explanation:
The underlying principle is mutation+recombination, and selection facilitated by a sort of feed-back loop where more successful immune cells that are better able to bind to pathogens, are rewarded more resources, and so basically outcompete unsuccessful mutants (IIRC very unsuccessful mutants are eventually killed off).

The are the well-known antibody proteins (so-called immunoglobulins) that the immune system employs to target and kill invading pathogens (usally just drawn like like the letter “Y”).

These antibody proteins have to be able to bind somewhere on the surface of the pathogen. If one of the antibodies can bind the pathogen, even if only very weakly, this will trigger an adaptive reaction such that the cells that produce the antibody will be rewarded with resources and start dividing so the daughter cells that inherit replicated DNA suffer mutations.

As the immune cell replicates it’s DNA, the gene encoding the antibody has an elevated mutation rate (a million-fold higher than the “normal” chromosomal mutation rate), and the gene encoding the antibody protein also has a section that undergoes a lot of recombination in a process known as VDJ-recombination.
New daughter cells with mutations and rearrangements that have higher affinity than before are rewarded with more resources so they can go on replicating themselves, with new daughter cells suffering more mutations, and thus among these new mutant daughter cells there will eventually be some that have evolved even better affinity.

In this way the affinity between antibody and pathogen is gradually increasing generation by generation of immune cells, and this process of improving the binding ability of the antibody by positive-selection driven evolution is called “affinity maturation”.

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And constant negative selection to eliminate self-reactive antibodies and T-cells. When that fails, people get autoimmune diseases.

It’s a turbo version of Darwinian evolution. If God designed us from scratch, He has a great sense of humor.

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I had seen this variant was in the news, but there were few details until this came up in my feed. Interested in any thoughts.

“Preliminary genomic characterisation of an emergent SARS-CoV-2 lineage in the UK defined by a novel set of spike mutations - SARS-CoV-2 coronavirus / nCoV-2019 Genomic Epidemiology - Virological” Preliminary genomic characterisation of an emergent SARS-CoV-2 lineage in the UK defined by a novel set of spike mutations - nCoV-2019 Genomic Epidemiology - Virological

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It’s a sound and sobering report. The strain it’s describing may not be more transmissible but there’s a good chance it is, which is not going to improve an already dire situation. The whole group of researchers is good and the lead author is one of the best and most cautious in the field, so I take it very seriously.

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Looks like the scientists are being cautious, but if this is the same variant, public health officials are already saying it’s up to 70% more transmissible! (They’re basing that on other scientists doing modeling) COVID-19: New mutation in every part of UK except Northern Ireland, says expert | UK News | Sky News

I was seeing some pushback on Twitter just checking quickly - it looks like some of the public isn’t buying it while the UK puts in place more lockdowns and the European countries are looking at banning travel from the UK. Major social ripple effects.

It’s a sad situation all around. I appreciate understanding the science of this better than I did months ago and seeing how it’s transmitted to the government and then to the public.

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The massive increases in cases here in the last week suggests it is a lot more transmissible. We’re seeing a sharper rise in new infections that we did in September, despite the increased precautions including a second six-week lockdown.

Sure, some of the rise may be due to lock-down fatigue, or Xmas shopping, but we’re seeing a steeper growth now than we did when schools opened in September.

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2020: the year that keeps on giving. At least we haven’t had a nuclear war yet.
[Looks around nervously.]

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I saw one group yesterday was suggesting that it may be more transmissible in children. Coronavirus: Impact of new variant on children investigated I am interested to find out if they will determine that to be the case.

Hopefully you can have a nice Christmas in spite of the confusion and lockdowns!