I very much agree. Moreover, it’s intrinsically fun to learn how biology works, independent of the polemics. Don’t miss out.
36 posts were split to a new topic: YEC interest in science
If the issue is “beneficial”, that is defined as an increase of fitness. Not by an increase in “complexity” or by a “gain of function”, or by a mutation being “interesting”. You can construct an example by taking any site in the DNA where there can be a mutation that reduces the fitness. There are a great many such sites, of course. Now we know that at any site, mutations are possible from any one of the four bases to any other one. Now just consider a sequence that contains the base that reduces the fitness there, say in that case a mutation to a C from the original base, an A. Is a point mutation possible that increases fitness? Of course, just consider the mutation from C back to A. End of story. (It also shows that if you think that there is some deep information-theoretic reason why there cannot ever be a beneficial mutation, you are very wrong).
This paper discusses the earlier variant which came to dominate. In contrast with Sanford, the history of COVID accords with the usual model of viral fitness increasing with enhanced transmission and neutral or decreased virulence.
The rate of sequence variation among SARS-CoV-2 isolates is modest for an RNA virus but the enormous number of human-to-human transmission events has provided abundant opportunity for selection of sequence variants. Among these, the SARS-CoV-2 Spike protein variant, D614G, was not present in the presumptive common ancestor of this zoonotic virus, but was first detected in late January in Germany and China. The D614G variant steadily increased in frequency and now constitutes >97% of isolates world-wide, raising the question whether D614G confers a replication advantage to SARS-CoV-2. Structural models predict that D614G would disrupt contacts between the S1 and S2 domains of the Spike protein and cause significant shifts in conformation. Using single-cycle vectors we showed that D614G is three to nine-fold more infectious than the ancestral form on human lung and colon cell lines, as well as on other human cell lines rendered permissive by ectopic expression of human ACE2 and TMPRSS2, or by ACE2 orthologues from pangolin, pig, dog, or cat.
Thank you Rumraket! Yes, this is a good example of what I’m looking for. I’ll read over this one this weekend.
Well I thought you were doing well.
And yes, I see that. I’m finding myself thinking very carefully over every post, including how I ask questions.
Good question. Yes actual observed examples, not hypothetical narratives.
I guess you missed this follow-up that I posted. https://www.nature.com/articles/s41467-020-19818-2 I’m sure there will be more papers on it.
Good catch - pertinent article. I’m sure that with the unprecedented real time scrutiny devoted to this virus, that there will be much argumentation and lessons learned. It is evident, however, that this pandemic is yet another case study which discredits Sanford’s ideas in regards to origins and progression of infectious disease.
In regards to the more recent UK variant in the news, the N501Y mutation, the resulting alteration of the viral spike protein is suggested to have a greater affinity to human ACE2 receptor.
Here is the CDC summary for new variants…
Emerging SARS-CoV-2 Variants
I thought this general article in Vox was decent.
The new UK coronavirus mutations, explained
Analysis is still very preliminary, but there does appear to be an emerging consensus that the alterations of the viral spike protein in the UK and SA strains are raising transmissibility.
Yes, this is the one I was referring to. I was being lazy and didn’t feel like looking up what I was called - N501Y.
It doesn’t discredit Sanford’s ideas as far as I understand his hypothesis. There can be increased fitness in the model in the initial evolution of the strain - Fitness will just decrease eventually as mutations accumulate.
I had read the Vox article earlier. It definitely was the best popular article I’ve read on the subject. I’m definitely trying to keep up anything new written about it. If I find anything of significance I’ll post it.
But there is the usual problem with this. Was the initial baramin a benevolent virus perfectly created 4004 BC, or the pandemic inducing monster unleashed in 2019? Given the accumulation of mutations, in Sanford’s model we have past extinction, not present virulence. The unleashing of this plague does, however, fits perfectly well with evolutionary principles. And here the issue is more explicit, because recombination in corona is not as routine a mechanism as H1N1.
As for the mutations by which the virus has adapted to human transmission, do you really think that these are just “loss of function”, as in jettisoning clutter that was just getting in the way? Or from the standpoint of the virus, are real time examples of beneficial mutation and gain of function as per @jeffb OP?
The lack of recombination makes this a better virus to examine observable evolution. That’s why it interests me; hopefully we’ll learn a lot more about viruses even through all the sadness of the pandemic because of all the sequencing being done. I’m very interested now to see how the science progresses based on what I’ve learned the last few months. So I did find @Timothy_Horton comments silly.
Not enough info to know, though some indications maybe the latter.
I wonder if this is the type of thing that you had in mind, and if those qualified to assess this in the forum (not me) thought this would be an appropriate example: “A single splice site mutation in human-specific ARHGAP11B causes basal progenitor amplification” talking about a mutation leading to neocortex expansion of the brain.
I can see why the fitness of a highly letal virus may increase if its virulence decreases. But how could it be the case for a virus such as Sars-cov-2 who kills no more than 0,05% of the population and whose CFR is probably less than 0,5%?
4 posts were split to a new topic: Making A Heading in Discourse
This is one of my favorite examples that has been discussed in other threads here on the forum. This example is clearly beneficial in the context, but also serves as an example of de novo gene generation.
Here is a cool example of a mutation conferring hypoxia tolerance in a group of humans whose culture is intimately associated with water and diving:
Ah, that’s a good one! It also reminded me of this.
I don’t know how you got that idea:
Its behavior to date is consistent with what we know about virology. If it interests you, there are decades of studies that have been done and are highly relevant.
@jeffb, here’s a mind-blowing and clinically important example of the complexity of the science, which does not neatly fit your very stereotypical (sorry, can’t resist) request. The human MYH7 gene encodes the primary cardiac myosin that is also the major myosin in slow-twitch skeletal muscle. It is incredibly polymorphic:
1189 entries on 2 pages.
Unique variants in the MYH7 gene - Global Variome shared LOVD
While many of the variants are listed as “pathogenic” in this table, most dominantly causing inherited cardiomyopathy, with only a few exceptions their penetrance is very low, meaning most people with them are healthy. A simplistic understanding of evolution would predict extreme conservation, not polymorphism.
In your view, what hypothesis explains this polymorphism? I have an unpublished, empirically testable one.
The great thing about this case is that there’s really nothing one can copy/paste to address it. You know, the most devastating rebuttal conceivable would be for you to simply ignore what you perceive as sniping and dig into the science…
Agree that the baseline here is such that decreased virulence would not be as big a factor as transmission with regards to the fitness of this virus. But as a species, we are not very tolerant of even those numbers, so payback is coming for Sars-cov-2.