So, it's great that they're investigating, but this reads a bit too breathless to be taken entirely seriously:
"stop virus in its tracks"
"a potential game changer"
"ground-breaking study"
...but further down:
"The question now is how to turn this new knowledge against the virus itself and defeat the pandemic."
Yes, that would be the question, which is much closer to the beginning of the process of developing and producing and rolling out a new treatment, than it is to the end.
In other words, while it's great that this kind of thing is being investigated, it is extraordinarily unlikely to impact _this_ pandemic. No doubt Covid-19 will come back again, several years after this pandemic has run its course, and it's great to investigate how to be better prepared for that. But this is not going to result in a treatment fast enough that this pandemic will not already have spread to its (historically normal, typical, well-nigh-inevitable) conclusion.
COVID-19 (SARS-CoV-2) won't "come back again" because it will never go away in the first place. It has already spread so widely that it is now endemic in the worldwide human population (plus some other mammal species). Just like at least 4 other coronaviruses.
> In rhinovirus, a virus causing the common cold, a similar pocket was exploited to develop potent small molecules that bound tightly to the pocket distorting the structure of the rhinovirus, stopping its infectivity. These small molecules were successfully used as anti-viral drugs in human trials, defeating rhinovirus in the clinic.
So why isn't there a cure for the common cold? If there still isn't a cure for the common cold, why should we expect this drug target to be different?
Surely whoever wrote this article should have anticipated these questions?
The "common cold" refers to a benign, self-limited upper respiratory viral infection by over 200 viral subtypes, including many strains of coronavirus (causing collectively 10-15% of colds), adenovirus, enteroviruses (echovirus, coxsackievirus) rhinovirus (over 100 serotypes, collectively causing 30-50% of colds), metapneumovirus, bocavirus, influenza and parainfluenza viruses (~5% of colds each), and respiratory syncytial virus (another 5%).
I think this is general lay knowledge. Certainly, any article that uses the words "glycoprotein" is aiming at the sort of audience that knows "common cold is a syndrome caused by a buncha different viruses."
The common cold isn't any specific virus, it's a huge range of viruses that cause "cold" symptoms. Some coronaviruses cause "colds" as well. Common cold viruses are research targets to discover knowledge that can be weaponized to prevent pandemics.
>These small molecules were successfully used as anti-viral drugs in human trials, defeating rhinovirus in the clinic.
Because it's still in trials, and not widely available, due to the long process of approving such medicines.
It still seems possible that there will be a drug that can be used to combat rhinovirus, as well as coronavirus someday, possibly sooner rather than later.
I almost never comment, but the answer here is simple: markets.
The common cold doesn't kill. There's almost no economic impetus for a cure. Note, I said "almost." There may be some, but there's still not enough to drive R&D in a corporate lab, and certainly not enough to drive policy in a government lab.
There are 100 other questions that would follow from science to logistic once you answer: Can we create a drug that kills infection in clinical tests?
"Enabled by Oracle high-performance cloud computing, ..."
Anyone know why that phrase is in there? It sounds very much like product marketing, but I can't see why the researchers or this story's author would be motivated to promote Oracle.
> Funding: ... This work received generous support from the Oracle Higher Education and Research program to enable cryo-EM data processing using Oracle’s high-performance public cloud infrastructure (https://cloud.oracle.com/en_US/cloud-infrastructure) ...
Why this summary of the work includes it prominantly, rather than in the footnotes like in the original paper, I'm not sure. Perhaps it was a condition the authors had for contributing to the article. Or perhaps it was Oracle's PR that got them the article in the first place. There is a comment from Oracle later in the article.
"Should I acknowledge Oracle support for my research project work, for example, in publications or on websites?
Please acknowledge the “Oracle for Research” program in any publications or on websites."
> Unexpectedly, the research team's analysis revealed the presence of a small molecule, linoleic acid (LA), buried in a tailor-made pocket within the Spike protein.
> LA is a free fatty acid, which is indispensable for many cellular functions. The human body cannot produce LA. Instead, the body absorbs this essential molecule through diet.
> Intriguingly, LA plays a vital role in inflammation and immune modulation, which are both key elements of COVID-19 disease progression. LA is also needed to maintain cell membranes in the lungs so that we can breathe properly.
> From other diseases we know that tinkering with LA metabolic pathways can trigger systemic inflammation, acute respiratory distress syndrome and pneumonia. These pathologies are all observed in patients suffering from severe COVID-19.
> A recent study of COVID-19 patients showed markedly reduced LA levels in their sera.
I’m wondering if a long strip of tape, the ability to move left or right, and the ability to write a symbol to the tape could generate 3-D structures of SARS CoV-2 Spike proteins.
There are plenty of covid-19 vaccine trackers, but I can't find trackers for antivirals, especially novel, non-repurposed ones. E.g. what happened to compound 11a from this paper? https://science.sciencemag.org/content/368/6497/1331
The best I have a Lancet review for repurposed drugs found via computational methods (published last week). Ignore the "AI;" most of these are just graph algorithms or vanilla neural networks. I haven't seen anything this comprehensive for novel therapeutics.
[+] [-] rossdavidh|5 years ago|reply
...but further down: "The question now is how to turn this new knowledge against the virus itself and defeat the pandemic."
Yes, that would be the question, which is much closer to the beginning of the process of developing and producing and rolling out a new treatment, than it is to the end.
In other words, while it's great that this kind of thing is being investigated, it is extraordinarily unlikely to impact _this_ pandemic. No doubt Covid-19 will come back again, several years after this pandemic has run its course, and it's great to investigate how to be better prepared for that. But this is not going to result in a treatment fast enough that this pandemic will not already have spread to its (historically normal, typical, well-nigh-inevitable) conclusion.
[+] [-] nradov|5 years ago|reply
[+] [-] jxcl|5 years ago|reply
So why isn't there a cure for the common cold? If there still isn't a cure for the common cold, why should we expect this drug target to be different?
Surely whoever wrote this article should have anticipated these questions?
(Edited to be less flippant)
[+] [-] wittyreference|5 years ago|reply
The "common cold" refers to a benign, self-limited upper respiratory viral infection by over 200 viral subtypes, including many strains of coronavirus (causing collectively 10-15% of colds), adenovirus, enteroviruses (echovirus, coxsackievirus) rhinovirus (over 100 serotypes, collectively causing 30-50% of colds), metapneumovirus, bocavirus, influenza and parainfluenza viruses (~5% of colds each), and respiratory syncytial virus (another 5%).
I think this is general lay knowledge. Certainly, any article that uses the words "glycoprotein" is aiming at the sort of audience that knows "common cold is a syndrome caused by a buncha different viruses."
[+] [-] skim_milk|5 years ago|reply
[+] [-] leptons|5 years ago|reply
Because it's still in trials, and not widely available, due to the long process of approving such medicines.
It still seems possible that there will be a drug that can be used to combat rhinovirus, as well as coronavirus someday, possibly sooner rather than later.
[+] [-] eximius|5 years ago|reply
It might be from 2019 so there may simply have not been enough time.
[+] [-] gostsamo|5 years ago|reply
[+] [-] stateofnounion|5 years ago|reply
[+] [-] mquirion|5 years ago|reply
The common cold doesn't kill. There's almost no economic impetus for a cure. Note, I said "almost." There may be some, but there's still not enough to drive R&D in a corporate lab, and certainly not enough to drive policy in a government lab.
There are 100 other questions that would follow from science to logistic once you answer: Can we create a drug that kills infection in clinical tests?
[+] [-] DoofusOfDeath|5 years ago|reply
Anyone know why that phrase is in there? It sounds very much like product marketing, but I can't see why the researchers or this story's author would be motivated to promote Oracle.
[+] [-] peeters|5 years ago|reply
https://science.sciencemag.org/content/early/2020/09/18/scie...
Why this summary of the work includes it prominantly, rather than in the footnotes like in the original paper, I'm not sure. Perhaps it was a condition the authors had for contributing to the article. Or perhaps it was Oracle's PR that got them the article in the first place. There is a comment from Oracle later in the article.
[+] [-] tyingq|5 years ago|reply
https://www.oracle.com/oracle-for-research/faq.html
Apparently pushed as a requirement for the "free" Oracle cloud resources researchers can apply for.
[+] [-] shellac|5 years ago|reply
The article itself includes Oracle in the acknowledgements, together with the various University of Bristol HPC systems used, and Archer.
[+] [-] unknown|5 years ago|reply
[deleted]
[+] [-] 0n34n7|5 years ago|reply
[+] [-] lioeters|5 years ago|reply
Following my curiosity, I found a list of dietary sources of linoleic acid:
https://en.wikipedia.org/wiki/Linoleic_acid#Dietary_sources
---
Here are the relavant passages from the article:
> Unexpectedly, the research team's analysis revealed the presence of a small molecule, linoleic acid (LA), buried in a tailor-made pocket within the Spike protein.
> LA is a free fatty acid, which is indispensable for many cellular functions. The human body cannot produce LA. Instead, the body absorbs this essential molecule through diet.
> Intriguingly, LA plays a vital role in inflammation and immune modulation, which are both key elements of COVID-19 disease progression. LA is also needed to maintain cell membranes in the lungs so that we can breathe properly.
> From other diseases we know that tinkering with LA metabolic pathways can trigger systemic inflammation, acute respiratory distress syndrome and pneumonia. These pathologies are all observed in patients suffering from severe COVID-19.
> A recent study of COVID-19 patients showed markedly reduced LA levels in their sera.
[+] [-] booleandilemma|5 years ago|reply
[+] [-] jmpman|5 years ago|reply
[+] [-] est31|5 years ago|reply
The best I could find was an overview in this survey paper: https://www.sciencedirect.com/science/article/pii/S0960894X2...
[+] [-] whymauri|5 years ago|reply
https://www.thelancet.com/action/showPdf?pii=S2589-7500%2820...
[+] [-] stevespang|5 years ago|reply
[deleted]
[+] [-] ourmandave|5 years ago|reply
Oracle's cloud API really is expanding.