SoylentNews is people
SoylentNews
Supercomputer crunches data on COVID-19:
A genetic study of COVID-19 patients, powered by the Summit supercomputer, may have taken us a step towards understanding how the new coronavirus causes disease.
Summit, located at the Oak Ridge National Lab in the US, analysed 40,000 genes from 17,000 samples earlier this summer in an attempt to understand the virus, AI expert Thomas Smith explained in an article on the Medium platform.
While the machine is the second-fastest computer in the world, the process required it to analyse 2.5 billion genetic combinations — a feat that took over two weeks.
Its results pointed to the fact that bradykinin, a natural chemical compound that regulates blood pressure, could explain many facets of COVID-19 and some of its symptoms.
The findings may shed light on why the virus causes vascular problems in certain patients, from strokes to inflammation of the skin or toes, as well as indicating new potential therapies to treat its worst symptoms.
[...] The researchers suggested that efforts to find a treatment for symptoms should be focussed on curbing bradykinin storms.
"Further experiments identified several existing medicinal drugs that have the potential to be re-purposed to treat the Bradykinin Storm," they wrote.
"A possible next step would be to carry out clinical trials to assess how effective these drugs are in treating patients with COVID-19.
"In addition, understanding how SARS-Cov-2 affects the body will help researchers and clinicians identify individuals who are most at risk of developing life-threatening symptoms."
Also at: Medium.com
Journal Reference:
Michael R Garvin, Christiane Alvarez, J Izaak Miller, et al. A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm, (DOI: 10.7554/eLife.59177)
[Ed Note: Added link to related story.]
(Score: -1, Offtopic) by Anonymous Coward on Saturday September 05 2020, @09:58PM
It turns out that, thanks to the miracle of the NIH grant funding model, every research project has a connection to COVID-19.
(Score: -1, Troll) by Anonymous Coward on Saturday September 05 2020, @10:31PM
Soon a teen launches DDoS attack [soylentnews.org] on Oak Ridge so he can stay home longer and masturbate.
(Score: 1, Interesting) by Anonymous Coward on Sunday September 06 2020, @03:09AM (6 children)
This one, for example, attaches to the very same ACE2 receptor:
https://en.wikipedia.org/wiki/Human_coronavirus_NL63 [wikipedia.org]
However, while causing "approximately 4.7% of common respiratory illnesses", it caused no media storm whatsoever since its discovery 16 years ago.
(Score: -1, Troll) by Anonymous Coward on Sunday September 06 2020, @03:49AM
Because we collectively have no spare capacity for pandemic bullshit on top of the Trump bullshit. There. I let you in on the global conspiracy.
(Score: 0) by Anonymous Coward on Sunday September 06 2020, @04:16AM
Maybe because in its thousand years of existence it still hasn't killed as many people as the current coronavirus has in six months.
(Score: 3, Interesting) by choose another one on Sunday September 06 2020, @09:10AM (3 children)
Short answer would appear to be "it does do it", in severe cases, with many of the same symptoms as covid (even down to the kawasaki-like disease link).
Real question is why it doesn't have the same _impact_ as covid with >1% IFR, possibilities:
* SARS-COV-2 is _better_ at doing the same thing (IMO, very possible)
* SARS-COV-2 is _better_ at spreading (maybe, it is quite good with long incubation and asymptomatic spread, but good as the common cold?)
* SARS-COV-2 is new, and we have no innate resistance to it or tolerance of it
I reckon the last point is the best bet, for historical example of the same thing look at european colonization of south america, where indigenous death rates are now estimated at ~90% from things like flu and measles which kill well under 1% in historically exposed european populations.
That would be good news in a way because it suggests that we will build a long term population immunity to it, but it's very bad news for those who are known-vulnerable like me because we'll all have to catch it (survival odds similar to Russian Roulette) to achieve that immunity, and tolerance/adaptation will be over several generations (we don't have herd-immunity to common cold, we have adapted to tolerate it). Those 90% of south americans didn't all die in the first wave.
(Score: 0) by Anonymous Coward on Sunday September 06 2020, @05:24PM (2 children)
The real question is, what IS the real impact? To know the real IFR, you need to divide actual (not inflated) fatalities by actual (not only detected) infections. A few days ago, Icelanders have published their attempt at the latter, and their result was 0.3% (three times less than the 1% figure you used).
https://www.nejm.org/doi/full/10.1056/NEJMoa2026116 [nejm.org]
A number of similar studies in other countries came to about the same figure or less. Rather unlikely that all those locales have some very different breed of humans than the rest.
Yes, for the elderly the virus is several times more dangerous than that population-average rate, but then, all infections are.
(Score: 2) by choose another one on Sunday September 06 2020, @10:16PM
I am using UK figures
- 52k dead (ONS death certificate figures)
- 67M population
- 6-7% infected so far (large scale antibody testing studies)
That gives ~1.2% UK IFR, in line with various published estimates of same. Also in line with published analysis of epidemic in worst affected areas of Italy, where they got close to 1% PFR, not IFR.
(Score: 2) by choose another one on Sunday September 06 2020, @10:24PM
Just to add a couple of references on UK IFR:
BMJ: https://www.bmj.com/content/369/bmj.m2484/rr [bmj.com] " Finally, they estimate an Infection Fatality Rate of 1.1% (0.9%--1.4%)."
Lancet: https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(20)30135-3/fulltext [thelancet.com] "with 44 000 deaths (using death certificate data4), this suggests an IFR of 1·0%."