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Sourced Coronavirus Information & Links

Started by Sheffield Wednesday, March 14, 2020, 09:42:19 AM

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Zetetic


jobotic

Oh yeah, sorry.

Was looking for mine so didn't really pay attention.

Head Gardener


steveh

Male pattern baldness? You will probably get Covid-19 worse.

QuoteIn January, one of the first publications on those sickened by the novel coronavirus in Wuhan, China, reported that three out of every four hospitalized patients were male. Data from around the world have since confirmed that men face a greater risk of severe illness and death from COVID-19 than women and that children are largely spared. Now, scientists investigating how the virus does its deadly work have zeroed in on a possible reason: Androgens—male hormones such as testosterone—appear to boost the virus' ability to get inside cells.

A constellation of emerging data supports this idea, including COVID-19 outcomes in men with prostate cancer and lab studies of how androgens regulate key genes. And preliminary observations from Spain suggest that a disproportionate number of men with male pattern baldness—which is linked to a powerful androgen—end up in hospitals with COVID-19. Researchers are rushing to test already approved drugs that block androgens' effects, deploying them early in infection in hopes of slowing the virus and buying time for the immune system to beat it back.

https://www.sciencemag.org/news/2020/06/why-coronavirus-hits-men-harder-sex-hormones-offer-clues

fat_abbott

All it needs now is a link to Phimosis and CAB is as good as dead

steveh

Blood type A? You will probably get Covid-19 worse.

QuoteResearch published last week prior to peer review suggested blood type may play a role in the severity of patients' reactions to SARS-CoV-2. That study looked at the genes of more than 1,600 patients in Italy and Spain who experienced respiratory failure and found that having type A blood was linked to a 50% increase in the likelihood a patient would require a ventilator. An earlier Chinese study turned up similar results regarding a person's susceptibility to Covid-19.

The research found that individuals with type O blood are between 9% and 18% less likely than individuals with other blood types to have tested positive for the virus. However, there was little difference in susceptibility among other blood types, the study found. When the researchers adjusted the data to account for factors like age and pre-existing illnesses, as well as when it restricted the data to only those with high-probability of exposure like health-care workers, the findings were the same.

https://www.bloomberg.com/news/articles/2020-06-08/23andme-provides-more-evidence-that-blood-type-plays-role-in-virus

KennyMonster

Quote from: Dewt on April 14, 2020, 11:05:43 AM
I am very interested in not getting this virus and I will live like a hermit until there's a vaccine.


Ooooh "vaccine, vaccine, vaccine", that's all I bloody hear about!

Are my anti-Covid Immunoglobulins not good enough for ya?

Sheffield Wednesday


steveh

Some interesting things I read this week.

They're getting more of an understanding of how the virus affects the immune system, which has some parallels with HIV in the treatment needed and helps explain why the after-effects go on so long.

QuoteOne of the most striking aberrations in Covid-19 patients, the investigators found, was a marked increase in levels of a molecule called IP10, which sends T cells to areas of the body where they are needed.

Ordinarily, IP10 levels are only briefly elevated while T cells are dispatched. But in Covid-19 patients — as was the case in patients with SARS and MERS, also caused by coronaviruses — IP10 levels go up and stay up.

That may create chaotic signaling in the body: "It's like Usain Bolt hearing the starting gun and starting to run," Dr. Hayday said, referring to the Olympic sprinter. "Then someone keeps firing the starting gun over and over. What would he do? He'd stop, confused and disoriented."

The result is that the body may be signaling T cells almost at random, confusing the immune response. Some T cells are prepared to destroy the viruses but seem undermined, behaving aberrantly. Many T cells apparently die, and so the body's reserves are depleted — particularly in those over age 40, in whom the thymus gland, the organ that generates new T cells, has become less efficient.

https://www.nytimes.com/2020/06/26/health/coronavirus-immune-system.html

It's also affecting the production of insulin, which in some patients is causing them to have diabetes.

QuoteVarious viruses, including the one that causes severe acute respiratory syndrome (SARS), have been linked with autoimmune conditions such as type 1 diabetes. And many organs involved in controlling blood sugar are rich in a protein called ACE2, which SARS-CoV-2 uses to infect cells.

The latest clue comes from an experimental study in miniature lab-grown pancreases published last week suggests that the virus might trigger diabetes by damaging the cells that control blood sugar.

https://www.nature.com/articles/d41586-020-01891-8

The virus has been found to use tentacles (filopodia) to better infect nearby cells, something HIV also does.



QuoteThe discovery that the coronavirus initiates the sprouting of filopodia in infected cells suggests that it has, at some point in its evolution, developed more than one way to ensure it gets passed quickly from cell to cell.

Typically, a rapid rise in infected cells will raise a victim's viral load, make her feel sick and promote the transmission of the virus to other people. UC San Francisco's Nevan Krogan, one of the paper's senior authors, said there is much about the coronavirus that doesn't match scientists' expectations.

But the discovery of filopodia in coronavirus-infected cells suggests that this virus has developed more than one way to wheedle its way into cells and establish itself as a force to be reckoned with.

https://www.latimes.com/science/story/2020-06-26/inside-the-body-the-coronavirus-is-even-more-sinister-than-scientists-had-realized
https://eu.jsonline.com/story/news/2020/06/26/coronavirus-grows-tentacles-inside-cells-providing-clue-treatment/3235414001/

steveh

Neanderthal heritage? You will probably get Covid-19 worse.

QuoteA recent genetic association study (Ellinghaus et al. 2020) identified a gene cluster on chromosome 3 as a risk locus for respiratory failure in SARS-CoV-2. Recent data comprising 3,199 hospitalized COVID-19 patients and controls reproduce this and find that it is the major genetic risk factor for severe SARS-CoV-2 infection and hospitalization (COVID-19 Host Genetics Initiative). Here, we show that the risk is conferred by a genomic segment of ~50 kb that is inherited from Neandertals and occurs at a frequency of ~30% in south Asia and ~8% in Europe.

https://www.biorxiv.org/content/10.1101/2020.07.03.186296v1

(Not peer-reviewed, only one factor in many.)

steveh

New large survey from Korean contact tracing finds that children up to 9 transmit the virus less than adults but 10-19 are more likely to spread the virus than adults.



steveh

This is a good thread on what's now known about transmission: https://twitter.com/mugecevik/status/1308080056384843777. Full paper here: https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3692807.

The bit that's still not getting enough publicity is the importance of ventilation. OPEN THE WINDOWS PEOPLE!

Zetetic

Some very brief discussion of how dogshit vaccines might be in The Lancet:
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31976-0/fulltext

One thing that I thought was interesting:
"Challenge studies in vaccinated primates showed reductions in pathology, symptoms, and viral load in the lower respiratory tract, but failed to elicit sterilising immunity in the upper airways."

pancreas

I thought this was specifically a problem with the Oxford vaccine?

Zetetic

The Oxford[nb]AstraZeneca?[/nb] (ChAdOx1/AZD1222) and Moderna[nb]Cambridge, MA[/nb] (mRNA-1273) vaccines are referenced, on that issue. (I can't pretend to have read beyond that.)

steveh

Quote from: pancreas on September 22, 2020, 04:22:36 PM
I thought this was specifically a problem with the Oxford vaccine?

Nature published a summary of where things are with different projects today. From a quick skim I think several candidates are said to be better at producing a T-cell response than sustained antibodies. That would fit in with the Lancet piece saying:

QuoteThese observations suggest that we cannot assume COVID-19 vaccines, even if shown to be effective in reducing severity of disease, will reduce virus transmission to a comparable degree. The notion that COVID-19-vaccine-induced population immunity will allow a return to pre-COVID-19 %u201Cnormalcy%u201D might be based on illusory assumptions.

On the plus side, the Nature summary does say that safe vaccines are likely to be months rather than years away.

MojoJojo

Quote from: steveh on September 23, 2020, 12:21:40 PM
Nature published a summary of where things are with different projects today. From a quick skim I think several candidates are said to be better at producing a T-cell response than sustained antibodies. That would fit in with the Lancet piece saying:

On the plus side, the Nature summary does say that safe vaccines are likely to be months rather than years away.

I'm not sure that's true. I mean, T-cells can activate memory B-cells to produce antibodies for previously seen infections. Really I think the immune system is complicated enough that I don't think it's really possible to have a useful discussion about potential covid vaccines unless you have a relevant degree. About all you can say is they might be effective, they might not.

steveh

Yes, ignore that bit... Another summary of the paper does conclude though that "most vaccines will only protect from lower respiratory tract infection but might not induce 'sterilizing immunity'. That means they will protect people from illness, but could still allow for transmission to the unvaccinated."

This is interesting on what's being found in how the virus gets around the immune system:

QuoteThe common thread in the research is the lack of a substance called interferon that helps orchestrate the body's defense against viral pathogens and can be infused to treat conditions such as infectious hepatitis. Now, increasing evidence suggests that a significant minority of Covid-19 patients get very ill because of an impaired interferon response. Twin landmark studies published Thursday in the journal Science showed that insufficient interferon may lurk at a dangerous turning point in SARS-CoV-2 infections.

"It looks like this virus has one big trick," said Shane Crotty, a professor in the Center for Infectious Disease and Vaccine Research at the La Jolla Institute for Immunology in California. "That big trick is to avoid the initial innate immune response for a significant period of time and, in particular, avoid an early type-1 interferon response."

https://www.bloomberg.com/news/articles/2020-09-24/covid-doctors-follow-dna-trail-to-potential-immune-treatment