Rand Paul And Fauci

After having watched and listened Rand Paul as a senator for a number of years, I’ve come to the conclusion that the only way you can tell if he’s lying is if his lips are moving. Truly, he is one of the most ignorant, disingenuous members of the Senate.

This article was published clear back in 2013.

He reminds me of a toddler who never tires of playing with his own feces.

In a contest of honesty, it’s not even a yawn to determine who is telling the truth and who is lying.

Consider yourself lucky that you only have to read about him. I live in Kentucky. I get him and McConnell both as my state politicians.

I was really hoping to avoid this sliding over into “did COVID come from the lab?” because I am actually interested in the narrower question.

I’ve read a bunch more, but some things are still not clear to me.

As far as I can tell, it’s generally agreed the Wuhan lab did research with viruses which initially could not infect humans, but in their research they modified those viruses so they could (or at least so they could infect human cells, which may not be the same thing).

From reading various definitions of Gain-of-Function, that sounds like it fits, but Fauci says not, as well as many others.

Can anybody provide a layman’s definition of Gain-of-Function viral research, and explain how this research doesn’t fit the definition?

Rand Paul is Constitutionally protected from prosecution for statements made in his official duties under the Speech or Debate Clause.

That’s why I just wished it. I also wish for a pony that poops skittles.

I guess the best we can hope for is a statement from the DOJ along the lines of “We do not conduct frivolous investigations based on false accusations from random senators trying to score political points.”

The FactCheck.org story linked by beowulff in the first reply to your original post includes a pretty straightforward definition that a layman (like me) should be able to understand:

Gain-of-function research in this context means that it would reasonably be expected to result in a virus becoming more virulent or contagious.

While there can be a debate about what constitutes a “reasonable” expectation, the EcoHealth Alliance grant was clearly not intended nor expected to create a virus that is more deadly or transmissible.

Can I have a cite where this is “generally agreed”? As far as I have read, most scientists think zoonotic transmission is, by far, the most probable explanation (as it’s happened with the majority of novel viruses throughout history). They are only keeping an open mind regarding the lab escape hypothesis.

Looking at the original paper, it seems that they were interested in the origin of SARS, and how it was able to infect humans. They found several predecessors to SARS that occurred naturally, but did not have the machinery necessary to enter human cells, so they were unable to see which of them were the likely precursor to SARS. So in order to study them they took part of the SARS virus that allowed it to enter human cells and plugged it into these viruses, and looked at what they did to human cells. They found that those that had a certain genetic sequence in common with SARS did infect the human cells, while those without it did not. This allowed them to draw the conclusion that that particular sequence was important in SARS’s ability to infect humans.

Note that there was no effort to select and propagate the versions that were particularly infectious or to create a super virus. They already had a super virus, it was called SARS. It is unlikely in the extreme that any of the new combinations would be any where near as virulent or deadly as the full SARS version.

GOF research has been used for decades in yeast and bacteria to study molecular structure or cellular pathways. They usually knock out a gene so that the yeast or bacteria doesn’t grow under certain selective circumstances. Then they reintroduce some kind of DNA library that answers their question of interest. Let’s say that some other gene complements the gene they knocked out. Well, the yeast or bacteria that received the complementary gene will grow. It will gain (or regain) the function.

Another GOF type of research would be if you put some kind of selective pressure that would kill or inhibit growth of your organism unless it mutates to survive that pressure. Or you again, introduce pieces of DNA to create different clones that will make survival proteins. You sequence the DNA of the survivors and say “hey, this mutation or gene allowed them to survive”.

Likewise, GOF research can be used with viruses. Let’s say the gain of function is binding to the ACE2 receptor. You could create a library of viruses that have mutations in the spike protein through a variety of methods. These would likely have engineering tags that would be flagged as being made in a lab. Since the SARS-CoV-2 has high spike protein similarity to the pangolin virus and other parts to the bat virus, you could take out the spike protein from the bat and splice in the pangolin. The engineering tags would be apparent unless you did shitloads of work to hide it because the SARS-CoV-2 genome shows pretty complex evolution from both the bat and pangolin viruses (this means it’s not just an accident). Or you use a random mutation method (harder to trace, I suspect) which would be forcing “evolution in the lab”.

Then you can test the viruses’ binding affinity to cells that have the ACE2 receptor in tissue culture. You isolate the viruses that bind best and propagate. That wouldn’t be easy but much easier than testing on whole animals. If you weren’t specifically going for the ACE2 receptor, you’d likely be working with whole animals and testing whether or not they get infected. Since SARS-CoV-2 virulence depends on a lot more than binding to cellular receptors (like very complex immune evasion), the GOF research would be extremely involved and, perhaps, very inefficient in animals.

Taken together, it’s clear to me that the GOF research that would have created a SARS-CoV-2 without genetic engineering tricks and prior knowledge on transmissibility and immune evasion is much less likely than what happens in nature. This is expensive, time-consuming research. Much more than the little subgrant money that they received. I’ve said this before, if you’re doing the “evolution in the lab” approach, the best evidence would be frozen sample of several stages of the “evolution” that led from a bat strain to a SARS-CoV-2. Even if you raided the lab, they could claim that these came from nature too.

Rand Paul is an evil person. Grant applications have to include exactly what kind of experiments are going to be performed and they get reviewed. So that information is available. If it doesn’t say anything about experiments that describe GOF, how is Fauci supposed to know?

It would be nice if Rand Paul could gain the function of intelligent thought. At the moment, there are several bacterium that have him beat in this department.

I didn’t say anything about SARS-CoV-2, and as hard as it may be to believe I am not trying to get to any sort of political gotcha. I’m honestly just trying to understand GoF and what we know about research that was done.

Thank you, that sounds like exactly what I said:

And then there is this:

But that’s where the rubber meets the road. Using this definition from Dahnlor, and the above description of the research from Buck_Godot, it sounds for all the world like they did exactly this. They took viruses which were known to not infect humans, and “took part of the SARS virus that allowed it to enter human cells and plugged it into these viruses” then how is that not more virulent or contagious?

Is it because:

  • The reviewers who determined it was not GoF used a different definition?
  • The fact it can infect human cells doesn’t count as “more virulent or contagious” because it’s not infecting entire humans?
  • Something else?