Then GE is neither inevitable or even a problem for evolution, but merely something that happens under special circumstances that virtually never occur in nature.
So actually no, you have no such reference. The entire viral population doesn’t cross through repeated nor persistent bottlenecks, rather typical host-to-host transmission events only feature relatively small numbers of viral particles. But of course typically many thousands to tens of thousands of individuals carry the disease (millions on a global scale), and so at any given moment hundreds of thousands to millions of particles are transmitted.
A transmission bottleneck between two hosts does not a persistent population bottleneck make. At all.
Thanks. Unlike you, they define their use of the term and use it consistently. It’s a great paper.
Please show, using math, why you think that 1000 generations would give a different answer.
Then, scientifically, why don’t you go and do the experiment in Sanford’s lab? Today, it would be cheap and Creation Ministries has plenty of money to fund it.
I see you’re playing your game with “bottleneck” now. As Rum pointed out, the bottleneck produced by transmission of a virus from one host to another is not a population bottleneck.
In other words, as I’ve been saying for years, it’s essentially equivalent to “error catastrophe”, which doesn’t occur in nature but may be inducible experimentally. Or it may not be.
Given that 1) T7 genome is ~40 000 bp long and 2) the intrinsic mutation rate of the virus (in absence of mutagens) is ~10^-6, I see no difficulty for children of T7 baramin to make it to Springman’s lab, sunny day or not! What you have to consider here is that the authors of the T7 paper assessed the fitness of the virus in presence of a mutagen that enhances the mutation rate by two to three orders of magnitude above the baseline rate.
Do you understand why none of what you’re saying makes any sense in the context of Sanford’s hypothesis? The whole point is that the vast majority of mutations are both slightly harmful and also unselectable. There is no combination of mutations, nor a combination of mutations, mutation rates, and population/ecological conditions that arrest the supposed decline. That’s the whole point. T7 should be GE’ing itself to extinction, and bumping the mutation rate by a few orders of magnitude should just make it go faster. If, as Sanford claims, virtually all mutations are harmful, independent of context, then these results are impossible. If GE is context specific then…it isn’t GE!
In the absence of mutagens, the probability that a single mutation arise within the T7 genome during a replication event is ~ 1/25. This means that at the end of an infectious cycle, a lot of unmutated T7 infectious particules are available for jumping to another host, making T7 largely immune to GE.
Again, missing the point: If you can’t select out the mutations, and they just accumulate and accumulate, then they eventually go extinct anyway. It just happens faster under mutagenesis.
Have you read Sanford’s book? Because you’re not making the argument he is making. You are making the argument population geneticists make to refute his argument.
His point is that the mutations are selected out, right @Giltil ?
Here are my layman’s points again - the main argument Sanford makes with GE is random mutations plus selection could have never given rise to humanity. Selection acts entirely differently depending on the context. The reason no one engages only that argument and instead on the forum all discussions lead to simple organisms is because evolution is an entirely different ballgame in those contexts. Actually it is the evolution that to me is the most fascinating and the most obvious.
Thanks. I will take a deeper look, skimmed a bit, but need to read when my brain is better rested in order to respond - which I hope to do.
Not sure to understand your point. Can you elaborate a bit?
This is utterly false. As the authors state: Fully 28 mutations in the population had frequencies of ≥0.75 (54 sites with mutation frequencies >0.5), those possibly representing adaptive changes or boosted to high frequency by virtue of being closely linked to adaptive changes (Figure 3).
What’s utterly false is your conflating mutation with fixation of mutant alleles. In your defense, the authors of the paper contributed to that with sloppy terminology.
I am afraid that you have not carefully thought through what you are saying for the trick of horizontally multiplying the transmission events does not erase the bottleneck problem.
No, that’s because the evolution of “simple” organisms is much more easily studied on the timescales of human lives due to their very short generation times. Thus it is in these organisms we’re most likely to be able to detect the claimed effects of Genetic Entropy in real time. And yet we’re not seeing it happen.
You’re welcome to hang around for a million years to see if we go extinct to GE of course. Oh wait you can’t. You’d be forced to do historical inference instead, but then “you weren’t there” and we can’t have historical inference as then … well all of creationism would collapse. So this is where we are, you all reject historical inference and insist on seeing things appear before your eyes on the timescales of a few months to years.
Now notice something curious. In response to observations of continous fitness increases in bacterial experiments, GE proponents have started to say that perhaps, maybe, sorta kinda, things like bacteria don’t suffer from Genetic Entropy. It’s all rather vague and it appears like they can’t decide on whether they think it happens or not(or they change the subject away from fitness and start blathering about loss of function mutations and “degeneration” instead of reproductive fitness).
And when we point out it doesn’t appear to be happening to viruses either we’re told (for example) we just have to wait longer to see Genetic Entropy of the Corona virus, or that it’s because viruses are able to hide away in natural reservoir species for long periods of time and re-emerge as vital as ever in the human population over and over again.
So if we can’t test in viruses because we haven’t waited long enough, or because viruses can keep reemerging from dormant states, how do we test it? Where will you be in a million years?
For transmission events to represent a population bottleneck, each infected host would have to represent a completely separate population from all of the other infected hosts.
Do you think that is a reasonable way to describe a viral population during an epidemic?
Think about it like this:
For the host-to-host transmission bottleneck to take effect on a population-wide scale there must be no competition between different host’s viruses to infect new hosts. That is to say there must be no factors able to have the effect of discriminating among the transmission-success of the virus-variants carried and transmitted by different hosts.
But clearly there are such factors at play. A virus emerging from one host with a significant increase in probability of successful infection, tha is incrased transmissibility, is more likely to transmit to new hosts before another, which will eventually make them unlikely to be ligible/effective future carriers for competing transmission.
And isn’t that exactly what we are seeing in this current pandemic right now, with highly infectious variants having taken over and become the dominant carriers in many areas?
Look. Imagine that the patient zero of an epidemic transmits the virus to two other persons, that these two persons each transmit the virus to two other persons, etc. After n generations, 2^n people are going to be infected. Now, due to strong bottleneck, we know that after each transmission event, the « best » viral genotypes within the first viral swarm have a small probability of being transmitted to the next host. Imagine for the sake of the argument that this very probability is 10%. And imagine the epidemic after 20 generations. In this case, the number of infected individuals (after 20 generations) will be 1 048 576. Now if you take any of these infected persons, the chance that they will be infected with the best viral genotype of the initial viral swarm is 10^-20! Now, if we assume a mean reduction in fitness equal to 0,001 after each transmission event and initial fitness of 1, the mean fitness after 20 generations will be equal to 0,999^20, that is 0,98, corresponding to a 2% reduction in fitness.
So yes, individual inter host bottlenecks translate into global loss of fitness at the population level.