Let’s pretend your claim is here is not your usual patent nonsense, and accept for the sake of argument that loss of virulence is loss of function.
It would follow from this that gain of virulence is gain of function.
It is all but certain that SARS-CoV-2 evolved from an earlier virus that was far less virulent.
So once the zoonotic origin of SARS-CoV-2 has been confirmed, you will have to come up with another argument in support of design, because it would have been demonstrated that random mutations can meet your personal criteria for gain of function.
Just giving you a heads up here. You should probably start working on your excuse now.
You still can’t understand parallelism. To use an analogy, if it takes 5 years to build a skyscraper then you must think that only 1 skyscraper in the whole world is built every 5 years.
You also seem to forget that multiple neutral mutations are fixed in each generation, about equal to the mutation rate. On top of that, a mutation doesn’t need to be fixed in order to be beneficial.
You have been shown all of these things multiple times, and yet here you are repeating the same mistakes. What gives?
Except that Lynch provided literature support of the assumption. So… not false.
Which isn’t even relevant to the Lynch/Behe debate.
Which isn’t the same as reduced function.
No, it isn’t. Virulence is the damage caused by infection. Extreme virulence may be advantageous if it results in large inoculums from higher viral loads, or disadvantageous if it results in reduction in exposure to new hosts either because of shorter infectious periods or potential hosts avoiding infected persons. Delaying the death of the host and extending the infectious period would then be a beneficial function in cases where contact between potential hosts and infected persons is low. Say, when people are being careful because of the active pandemic. You know, reality.
But we can use calculations to evaluate probable causes, in the instance of evolution, particularly. And in the case of evolution, it is not guaranteed that some such structure will appear, but in the case of my appearance, it is very likely that some egg will be fertilized and someone will be born.
Which comes down to a particular candidate for God, can we know him, and what he might and might not do? I believe we can.
Again, the validity of reason is a postulate, so I am assuming reason is valid. I then note that this entails a conclusion that my thoughts are not the complete products of mindless atoms. That makes reasoning supernatural. And if I am a created being, then my reason is a gift from the Creator, who must have greater reasoning ability than I do, to be able to create me with reason.
It is likely that SARS-CoV-2 modification that allowed it to bind to the human ACE 2 receptor was an experimental modification in the lab.
How do you think random change caused a virus with 29000 nucleotides to modify its sequence and produce a protein that binds to a human receptor. Unlucky accident
Viewing this event before the fact, it is improbable, but after the fact, the probability is 1. If you predict you will win the lottery, and you win it, then we suspect shenanigans.
Well, I don’t know how my car was assembled, and I need not know this to know it was designed. Think of SETI, they are looking for a signal which would imply intelligence, without knowing how it was produced.
Fitness is reproductive success. Relative to the virus the ability to replicate is fitness.
The real weakness in your argument is that a virus is a poor example of evolution as it requires a host to replicate thus fitness is dependent on the virus and the host which is not true for other organisms.
Fitness is a term that is a measure of micro evolution. The main issue in macro evolution is new function. A new function could either lose or gain fitness. The loss of a function could either lose or gain fitness.
well, at least we can agree about the minimal chance to get a new anatomical trait ?(such as the beginning of a new organ). i mean, do you think this is likely to get such a new trait in one in say 1000 births? (which means that one in about 1000 people has the beginning of feathers or wings for instance). or do you think its a very generous number?
Also, the existence of a god does nothing to resolve the question of whether our minds are reliable. An omnipotent god could easily create our minds such that they are completely unreliable, but we are convinced of the contrary. That seems at least as likely as that evolution could have left us with minds that give us a completely inaccurate view of the world which somehow does not result in our immediate death as we stumble in front of moving cars or off steep cliffs because our senses do not tell us they are there.
That has never been more than an unfounded conspiracy theory.
Random mutations change the tertiary structure and the distribution of charge and hydrophobicity of the S protein, and those changes increase binding to human ACE2. It’s not that hard to understand. Additional random changes have also modified protein-protein interactions between the S protein and existing antibodies within the human population.
I’ll start by pointing out that the claim that “very weak” is “strong” is not one that would convince an objective person.
Most mutations are neutral in the usual sense which is all Lynch’s argument needs. It is certainly not the case that the majority are strongly deleterious. So Lynch’s model makes a reasonable simplifying assumption - and if it is wrong it could simply be fixed by reducing the mutation rate to account for it. Behe’s model ignores variation in the population by assuming that all mutations would be strongly deleterious - which is quite simply wrong, and Behe’s defence implicitly admits it.
So objectively Lynch is ahead.
Thousands of years are not a long time in evolutionary terms. Even then I think you are overestimating.
Since that statement is gobbledygook I would have a problem with it. But I don’t think any model makes such a claim at all.
Because other coronaviruses have similar proteins that can also bind to ACE2. Just not as well, meaning that a mutation can increase affinity. Not complicated. And it had happened before, because it isn’t that unlikely.
Maybe if you assume that the coronavirus was engineered to be especially virulent, but that’s not the sort of function that evolution is concerned with. The essential functions of the virus - when it comes to being a successful virus - don’t require a high virulence.
Displacing other strains is moving towards fixation, so I really don’t see that this objection makes any more sense that the first.
What are you basing your thoughts on? A new gene with new functional information. How many changes on average to you think it takes to land on a new function? How many new unique functional sequences did the Lenski experiment produce?
