Folding Forum

wuffy68 wrote:Los Alamos National Laboratory/University of Sheffield paper (pre-print - still under review)

...and here in lies the danger ... "still under review".

Whilst the paper and the science behind it may well be valid/correct it has not yet been checked as such ... Yes it is important to get information/knowledge out there - but at the same time it is important to check/validate/confirm/recheck/etc.

Scientific history is littered with examples of where un-validated or hurriedly-validated science has done some pretty bad things ... pre-peer reviewed and un-validated science is a bit like a tweet, it can be totally miss leading/incorrect but can be retweeted quickly because the essence of where it has come from, its veracity, its provenance, any caveats it should have had are lost or overlooked.

What may be totally normal language and science in the scientific domain can appear very alarming in the non scientific media (hey, that is what media does best isn't it?).

I'm not saying it may not be really, really important ... but jumping to conclusions not warranted by the actual paper before it is even peer reviewed may not be the best thing for the media to be doing?

I think the real question is: So what?

It is more transmissible than the original, but it seems to be the one we have been dealing with since February.
So all of our statistics in the West are presumably based on it. The paper is interesting science no doubt, and may say something about the mutation rate.
But the next mutation may be less transmittable.

JimF wrote:It is more transmissible than the original, but it seems to be the one we have been dealing with since February

I think that's the question ... back in February, looking at the charts in the paper, we still had the Wuhan version as the predominant strain. Today, the Italian version seems to be prevalent, which could mean we would need to start working on modeling a second spike protein for a vaccine. Again, we cant give it too much weight since it's still waiting for peer review, but the institutions involved seem highly credible.

Unfortunately it is very logical and quite possibly true. The most transmissible mutations will survive while the less tarnsmissible will disappear. That is natural selection, isn't it? Just this way, not an opposite.

Does the RNA mutate or do the protein spikes change? Is it possible to get these protein spikes to release their RNA payload prematurely? Hit each virus once with an activation signal seems easier than de-activating all the protein spikes on every virus.

InDebtBigTime wrote:01:55:04:WU01:FS01:Requesting new work unit for slot 01: READY gpu:0:[Radeon RX Vega M XT] from 192.0.2.1
01:55:04:WU01:FS01:Connecting to 192.0.2.1:8080
01:59:24:ERROR:WU01:FS01:Exception: Failed to connect to 192.0.2.1:80: Connection timed out

Your Vega MXT is supported by FAH but it looks like it's not set up correctly. we need to see the first few pages of FAH's log (assuming you're running either Windows or Linux.) Is OpenCL installed on your system?

TPL wrote:Unfortunately it is very logical and quite possibly true. The most transmissible mutations will survive while the less tarnsmissible will disappear. That is natural selection, isn't it? Just this way, not an opposite.

I'm not a doctor but I think I can answer in laymans terms - real PhDs can probably give a deeper answer ...

... my understanding is, a vaccine would block the spikes from binding - it doesn't necessarily cause them to release their RNA prematurely. This would require creating a protein that perfectly matches the ACE-2 entry receptors of the human body, so you would continue to see infections - since the virus would either bind with a pseudo-ACE-2 receptor, OR an actual cell wall. If it were even possible (and that's not necessarily how coronavirus works), something like that would merely slow the infection rate - but perhaps let asymptomatic people spread the disease for a longer period before succumbing to it themselves. Having pseudo-ACE-2 receptor proteins floating in the body would probably cause some other issues - for one, these would bind to whatever other healthy molecules our cells use -either denying the body of nutrients, or preventing our cells from expelling waste products efficiently, and in chemical signaling, they could adversely effect patients' cardiovascular systems as ACE-2 binding sites in heart regulate blood pressure, and all sort of other bodily functions.

Once blocked by a vaccine, free-floating "blocked" viruses are dealt with by the bodies immune systems while it "learns" to seek out future infections - the creation of anti-bodies. Vaccines give the body extra time to react to the virus before it's allowed to infect and damage large numbers of cells - causing inflammation, and leading to co-morbid conditions like bacterial pneumonia.

Anti-virals on the other hand, actually "treat" already infected cells. These are called Protease Inhibitors which prevent the virus from maturing properly once they egress (released from the infected cell). The infected cell still dies, BUT the viruses it manufactures are essentially made non-viable (inert).

It's very complicated, because any foreign agent in the body that may block coronavirus, has a chance of interfering with healthy cells - that's why new drugs can take years, and cost billions of dollars to develop.

From what I've read, novel coronavirus is somewhat unique, in that it's very good at avoiding detection by the human body's immune system after initially being contracted.

Please note I was not talking about any cure or vaccine. I was talking only about natural selection and how it normally works. It includes viruses too. Some mutations can be more infective, some less. And the most infective will spread while less infective slowly disappear.

That is completely different thing than fatality. This recent virus incubation period is long and I think fatality may be somewhat irrelevant in this case. It have time to spread before symptoms. Either the same, more or less, no one knows. Also, no one knows about possible immunity yet. So, we don't actually know yet if any vaccine will ever be effective. One thing that WHO has warned about.

What comes to mutation rate, it was told to be slow. Well, the more infections the quicker it will be.
SARS-CoV-2 family tree.

Many reasons to fold on.

Do the recent National Institutes of Health cuts to EcoHealth Alliance have any adverse effects on the collaboration between the Folding@home Consortium and Hong Kong University of Science and Technology (HKUST)?

Apparently not. HKUST grad students are still initiating a number of new projects.

bruce wrote:Apparently not. HKUST grad students are still initiating a number of new projects.

Thanks good to know - IMO, the decision to cut funding to the EcoHealth Alliance during a pandemic wasn't wise (politics aside).

The guys from Rosetta@Home claim to have found antivral proteins for the virus.

https://twitter.com/RosettaAtHome/statu ... 9390555136

I hope it's not only effective in a test tube, that it's also safe in the human body.

Development of new drug is complicated, as even if it's effective, there is a chance it may induce severe side effects, and thus, a complicated multiphased clinical trial is necessary. However, we need everything we have to find useful cure. A new invention is always a good news, as from 100 new invention, there might be 1 that actually works. No such thing as wasted effort.

They start with animal testing first before injecting the antiviral protein in humans.