The Achilles Heel of the Coronavirus

Post by simion314 » Mon, May 17, 2021, 11:21 AM UTC

roenxi wrote: post #37

IAmGraydon wrote: post #20

Earlier quoted context omitted.

The article doesn’t say it’s “rarely used”. It says it “rarely happens”. It is not supposed to happen: > Frameshifting almost never happens in our cells. It would lead to dysfunctional cellular proteins. So the drug would disable an aberrant behavior that coronaviruses depend upon to replicate. This doesn’t sound like a bad thing. It’s also why trials exist.

There is a level of confidence in your post which is wholly unwarranted given how complicated the human body is. There is no design committee at work here, nobody is telling any body what the bits are supposed to do. It is all evolutionary equilibriums. The point of this drug is to shut the coronavirus down to the point where it cannot restart; it is not at all out of the question that something obscure but important…

Post by webwielder2 » Mon, May 17, 2021, 11:24 AM UTC

tryonenow wrote: post #17

>Frameshifting almost never happens in our cells. It would lead to dysfunctional cellular proteins; however, certain viruses, such as coronaviruses and HIV, depend on a frameshifting event to regulate levels of viral proteins. For example, SARS- CoV-2 - the virus that causes COVID- 19 - is critically dependent on frameshifting promoted by an unusual and intricate fold in the viral RNA. God is a hacker.

Post by pessimizer » Mon, May 17, 2021, 11:43 AM UTC

Clostridium wrote: post #54

roenxi wrote: post #47

Earlier quoted context omitted.

If we disable oxygen to the lungs for 30 minutes then switching it back on doesn't help. The lung owner is probably dead. Some of this stuff causes permanent changes. There is reason to be optimistic, because if for it to be really bad then there'd need to be: * Permanent change * Causing negative symptoms * Which took a long time to be symptomatic (which, coincidentally, HIV/AIDS exposure is a great example of) Now…

There are always risks, and ignoring a novel approach is also a risk. The issue is to gauge risk intelligently, based on extensive prior medical, biological and physicochemical knowledge and modelling, and on sound clinical testing using randomized controlled trials (the kind of trial that proved dexametasone and disproved ivermectin, hydroxyquinoline etc. as a therapeutic for covid).

Post by pessimizer » Mon, May 17, 2021, 11:46 AM UTC

ARandomerDude wrote: post #23

gmuslera wrote: post #10

For me sounds scary to disable a mechanism in all our cells that is "rarely used". Negative knowledge covers what we don't know and what we don't know that we don't know, and that rarely could be less rare than we thought, doing maybe not do frequent but anyway essential things, for all or some cells.

Yeah I always laugh for the same reason when people describe organs as "vestigial."

Post by 542354234235 » Mon, May 17, 2021, 11:54 AM UTC

roenxi wrote: post #56

Clostridium wrote: post #51

Earlier quoted context omitted.

Au contraire, this is exactly the thing that we should look into in an emergency! RNA-slippage is a well-known mechanism that a healthy cell has safeguards against. The corona virus exploits this slippage, so disabling it using a drug is a novel and smart approach as this presents a likely very specific attack surface (meaning side-effects will likely be few). Ignoring this mechanism would be very imprudent. What mak…

> What makes you think the usual precautions (cell lines, animal models, phase I, II, III trials) will not be taken as per usual? You've skipped one of the usual phases, which is Phase IV trials. Cell lines -> Phases III trials aren't enough to catch long term side effects, because they are all done quickly. An experimental mechanism passing Phase III trials is insufficient to prove it is safe. It proves that any neg…