I'd say the achilles heel is most likely in the genomic structure, which unlike influenza, is less likely to recombine.
The Achilles Heel of the Coronavirus
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Re: The Achilles Heel of the Coronavirus
#12A bit redundant. We know how to “kill” the SARS-CoV-2 virus in vitro (in a test tube). Ammonia, bleach, UV light. Heck, even diluted mouthwash will do the trick. The problem is that none of these approaches are safe in vivo (in the body). All of the approaches the article talks will require years of human testing. The drug EIDD-2801 does similar things but has yet to pass testing even after 12 months of studies.
This trial says UV light can be safe. Take it for what you will.
https://www.medrxiv.org/content/10.1101/2021.03.05.21252997v...
Re: The Achilles Heel of the Coronavirus
#13For 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.
I wouldn't want to do it permanently but doing it temporarily, to treat a severe acute infection, seems like a pretty good tradeoff. Especially after you've done your clinical safety trials to be sure.
Re: The Achilles Heel of the Coronavirus
#14Earlier quoted context omitted.
I did a thought experiment about how the immune system must work and came up with a simple system using only mechanisms that I know are available molecularly. If you could have a bunch of random protein sensors that undergo a training phase where they learn what "Host" is. Anything that makes a "detection" during training is discarded. Anything that doesn't is either never going to detect stuff, or might detect somet…
Perhaps an improved auto-recognition "self" system that uses something like public key crypto and a challenge-response.
The biggest advantage we have is that we might identify the responsible bad signaler, and then target it for removal somehow. I wouldn't want to mess with it more than that...for now.
Re: The Achilles Heel of the Coronavirus
#15For 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.
Doing it just long enough in people with a severe infection so they don't die of the infection seems like a reasonable trade off.
Nobody's suggesting we use this as a daily supplement in healthy people.
Re: The Achilles Heel of the Coronavirus
#16A bit redundant. We know how to “kill” the SARS-CoV-2 virus in vitro (in a test tube). Ammonia, bleach, UV light. Heck, even diluted mouthwash will do the trick. The problem is that none of these approaches are safe in vivo (in the body). All of the approaches the article talks will require years of human testing. The drug EIDD-2801 does similar things but has yet to pass testing even after 12 months of studies.
The article's about a method they hope will be safe in the body.
Maybe they're right maybe they are wrong, but hardly seems redundant.
Re: The Achilles Heel of the Coronavirus
#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.
Re: The Achilles Heel of the Coronavirus
#18>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.
https://en.wikipedia.org/wiki/Viral_evolution#:~:text=Bubble...
you might find this interesting. bubble theory imagines that interacting molecules, let's call them 'scripts', formed simple self replicating metabolisms inside the cavities of hydrothermal vents. At a script level there are two successful strategies: participate in a co-operative network or exploit a co-operative network to self replicate you. At a community level, excluding non-contributors is beneficial and this pre dates and perhaps leads to the development of cell membrane. In this view cells and viruses co-evolve from the same origin by pursuing different strategies.
It's game theory and tragedy of the commons from day one.
Piast, Radosław W. ‘Shannon’s Information, Bernal’s Biopoiesis and Bernoulli Distribution as Pillars for Building a Definition of Life’. Journal of Theoretical Biology 470 (7 June 2019): 101–7. https://doi.org/10.1016/j.jtbi.2019.03.009.
https://www.sciencedirect.com/science/article/pii/S002251931...
Re: The Achilles Heel of the Coronavirus
#19Earlier quoted context omitted.
This isn't about "killing" the virus, it's about inhibiting its ability to reproduce. Pointedly, it's about doing so without introducing mutagens like EIDD-2801, but instead by inhibiting a specific ribosomal behavior induced by a component of the virus. Finding a safe mechanism to do so is the next step in their research. I suspect your interpretation of the article might be off. This work is a great example of the…
Suppose protein folding simulation and manufacturing can rapidly advance well beyond current levels. It seems like a hypothetical synthetic immune system that whitelists every configuration of every protein an individual can possibly generate and excludes everything else (if possible) would be a way to blanket eliminate unknown unknowns proactively like SELinux for the body.
Such a system would effectively halt evolution, though.
Re: The Achilles Heel of the Coronavirus
#20For 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.
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.