And are you basing this on evidence? You should be able to recognize a theme by now. Speculation is not how scientists advanced ideas, this is the realm of evidence. I think a large amount of the friction generated by your posts is the lack of understanding of this fundamental concept. When conjectures and pronouncements based on rhetoric and guessing are strewn about haphazardly, the scientists here object to that - sometimes rather strongly! This type of approach to science might work in a Facebook group, but it will not go over well in a group comprised mostly of professional scientists and scholars.
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Your own thinking appears to be tightly locked up inside the YEC box. And thatās a very small box.
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You were asking me about my opinion about why there could be bias. I donāt know how scientists think. I donāt know how clinical trials are determined. There may be no bias at all. I was merely asking for your analysis.
But why are scientists above the public asking general questions about methods and decision-making? Scientists are people too. Everyone has a worldview and bias on something whether they admit it or not. For example, I really, really like my family doctor but I will push back if I think I need care Iām not getting - or getting too much care that was a waste of time and money (thatās happened when I had gestational diabetes too). Itās my life and other peopleās lives too.
This again demonstrates my point. You have already determined that scientists are above the public asking general questions when you have not demonstrated anything of the sort.
You are correct, I did ask your opinion. I should have known to phrase it in such a way that indicated I was interested in your educated and informed opinion, rather than your knee-jerk response. So let me check - what are your reasons for suspecting that scientists have overlooked this particular drug, which just coincidentally seems to match up with what you believe from your understanding of Sanfordās explanation of GE?
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No, that was my response based on your response to me. It seemed like you were pushing back on me for asking the question at all.
I already answered that question.
Not at all, questions are valuable. However, they are most valuable if they are based on something, rather than just random guesses.
No, you really didnāt. You didnāt supply any reasons (evidence) at all. All you said was āthey just arenāt thinking outside of the box as much as they could.ā without any explanation of why you think that is the case. You have offered only your unsupported opinion, and have not offered any reasons for it.
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Would you go to an auto mechanic for medical treatment? Expertise, training, and knowledge mean something.
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Yes, because I was asking IF there was bias. You asked me for possible reasons. I gave possible reasons. Again, there may be no bias. I was asking for a critical review. You and Steve initially responded both in a nice way.
Also, I couldnāt be insinuating theyāre not considering the drug because they donāt know about GE. That makes no sense since I cited papers from mainstream scientists who are promoting it as a possible option and they also describe countries that have used it!
No. Of course. I also question my auto mechanic. Probably most of do occasionally.
You are misunderstanding me. Your OP indicates that you believe there IS bias. What Iām asking for are reasons why you think that. If you donāt know if there was a bias, why would it even come up in your OP?
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Since the papers indicated it was a more novel approach, I wondered if āstoppingā the virus from replicating is seen as the goal, and many scientists not really thinking about lethal metagenesis leading to the same end. Sometimes slow and steady wins the race? But again, I donāt know how scientists think about anti-virals and how to make them effective.
The proof of the pudding is in the eating. Ultimately, they judge a treatmentās worth by how effective it is and how safe it is. They would also be looking at how quickly a treatment works, especially in the case of an acute infection.
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Ok, so I think we can agree that your reason for suspicion of bias is rhetoric, and not data. I know Iām rehashing this a lot, but Iām still not convinced that you see this as a distinction, much less an important one.
At the risk of leaving the first point unresolved, letās go ahead and move on to the drugs themselves. As I mentioned in another thread, Remdesivir can work both by blocking replication of the viral genome and by mutagenesis. The Favipiravir article mentions that it is an RDRP inhibitor. What I did not mention earlier is that Remdesivir is also an RDRP inhibitor. These two drugs essentially work in the same way. They are both nucleoside analogs (I think I did use that term) that can essentially interfere with the ability of the viral polymerase to produce accurate copies of the viral RNA - inhibiting the replication of the genome AND introducing mutations.
This article (https://asunow.asu.edu/20200518-mutational-meltdown-can-we-push-sars-cov-2-evolutionary-cliff) discusses mutational meltdown, focusing on Favipiravir, but also mentioning Remdesivir in the same context.
Again, the worry that scientists are biased (for whatever reason) against drugs that actually work against SARS-CoV-2 is not a reasonable worry.
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I donāt make that distinction when weāre discussing how people think. You see that in rhetoric.
The data is the fact that we havenāt had more clinical trials on this particular drug while remdesivir was approved a long time ago.
Yes, didnāt I say that in my explanation of the mechanism of action? They still have subtle differences. It seems favipiravir may be more effective at lethal mutagenesis from what I read.
When communicating science, the data is more important than what the author says about the data. In this specific example, you are concerned that there may be bias among scientists that have prevented them from fully exploring Favipiravir as a treatment for SARS-CoV-2 infection. Your suspicions are not based on evidence. Your suspicion is based on someone writing that mutational meltdown was a novel treatment strategy.
Alright, you are getting closer. This is indeed a fact. The next logical step would be to examine if remdesivir and favipiravir work through different mechanisms. Butā¦ they donāt. Another follow-up question could be - does one of the two possibly work better against this particular virus? Perhaps. Studies have been done and continue to be done.
If you mentioned that remdesivir is also an RDRP inhibitor, I must have missed it.
And weāre back to the cliffhanger again. You have made an unsupported statement. What are the differences between the two regarding their efficacy against SARS-CoV-2? What did you read about the more effective lethal mutagenesis of favipiravir compared to remdesivir? Statements like these require support in order to be taken seriously.
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Not that remdesivir looks likes itās any great shakes when it comes to COVID-19.
By the way, our Boston-area first-wave SARS-CoV-2 paper is finally out: Phylogenetic analysis of SARS-CoV-2 in Boston highlights the impact of superspreading events | Science
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Correct. One can easily describe early termination as a mutationāas a deletion of the 3ā end of the viral genome.
I didnāt correct you, I pointed you directly to the evidence from primer extension experiments.
Itās predictable that you didnāt even bother to look at evidence, though.
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Preach it, brother!
Thanks. This was very interesting, and very readable. Im sure it will be very important.
With the possibility of vaccines that protect against disease but not infection, this consideration may be increasingly important.
Even if you are vaccinated, you could spread COVID-19? I hadnāt thought about thatā¦ 
Congratulations !
We donāt know yet. Current trials looked at safety and efficacy. Next theyāll study whether it prevents spread. It may. We just donāt know yet.
I saw an article about a potential trial that would use college kids, but I donāt know if thatās actually happening or not. I think they were going to vaccinate them in January and then do Covid tests frequently to see if they have an asymptomatic case. The existing trial did check for Covid infection at the time of each shot, and symptomatic Covid was tested for as needed (we were given a test to self-administer at home and mail in if we have symptoms), and they check blood work for antibodies at beginning of trial, a couple months in, and 6 months in. But that doesnāt tell you if a vaccinated person had an asymptomatic case. Youād need to do frequent Covid tests for that, as the potential study I mentioned was wanting to do.
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