The biology of coronavirus COVID-19 - including research and treatments

Snow Leopard said:
But this doesn't demonstrate whether people are able to be infected through such contact.
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Yea what we really need is insight like: 90% get coronavirus through close contact (via droplets in the air) i.e. in enclosed spaces and not wearing a mask ---- 1% get it through contact with a surface on which the virus has survived 24 hours +

All fictitious of course, but I'm not sure whether there are realistic ways to assess the % of people acquiring the virus through specific routes --- grateful to be corrected though.
 
I've seen suggestions to this effect before, but:

People with blood type O may have lower risk of Covid-19 infection and severe illness, studies suggest

http://www.msn.com/en-gb/news/newsl...es-suggest/ar-BB1a2JGS?li=AAnZ9Ug&ocid=ASUDHP

People with blood type O may be less vulnerable to Covid-19 and have a reduced likelihood of getting severely ill from the virus, according to two new studies.

The two independent studies, carried out by researchers in Denmark and Canada and published in the journal Blood Advances, found that individuals with blood types A and AB are most vulnerable to the disease.

The research provides further evidence that a person's blood type may play a role in their susceptibility to coronavirus and could shed further light on why the illness proves deadly for some but others only experience mild symptoms, or none at all.
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I'm not sure how statistically significant the numbers are, but am I right in thinking that non-O blood groups tend to be more prevalent in people of BAME origin?
 
Wits_End said:
I've seen suggestions to this effect before, but:

People with blood type O may have lower risk of Covid-19 infection and severe illness, studies suggest

http://www.msn.com/en-gb/news/newsl...es-suggest/ar-BB1a2JGS?li=AAnZ9Ug&ocid=ASUDHP
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Interesting! Here’s a useful explanation of blood groups: https://www.nhs.uk/conditions/blood-groups/

Edit to add - I’m not sure the differences are great enough to draw this conclusion though!

In the Danish study, researchers found that among 7,422 people who tested positive for Covid-19, only 38.4 per cent were blood type O.

This is despite people with that blood type making up 41.7 per cent of a control group of 2.2 million people from the general population who were not tested.

By comparison, 44.4 per cent of those who were blood type A tested positive, while in the wider control group that blood type made up 42.4 per cent.
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SARS-CoV-2 infects the brain choroid plexus and disrupts the blood-CSF-barrier in human brain organoids

https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(20)30495-1

Highlights
  • SARS-CoV-2 entry factors are expressed in choroid plexus (ChP) cells
  • More mature lipid-producing ChP cells could be more susceptible to SARS-CoV-2 infection
  • SARS-CoV-2 productively infects ChP, but not neurons in organoids
  • SARS-CoV-2 infection damages the ChP epithelium causing leakage of this brain barrier
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Here, we use human pluripotent stem cell-derived brain organoids to examine SARS-CoV-2 neurotropism. We find expression of viral receptor ACE2 in mature choroid plexus cells expressing abundant lipoproteins, but not in neurons or other cell types. We challenge organoids with SARS-CoV-2 spike pseudovirus and live virus to demonstrate viral tropism for choroid plexus epithelial cells, but little to no infection of neurons or glia. We find that infected cells are apolipoprotein and ACE2 expressing cells of the choroid plexus epithelial barrier. Finally, we show that infection with SARS-CoV-2 damages the choroid plexus epithelium, leading to leakage across this important barrier that normally prevents entry of pathogens, immune cells and cytokines into cerebrospinal fluid and the brain.
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Professor Holgate spoke briefly tonight in the Southampton University Distinguished Lecture about the similarities between long COVID and ME/CFS.

In answer to the question that you put, Trish, Stephen Holgate said that the ME community is a neglected one, with the existence of the illness often being denied. He thinks that COVID will put a spotlight on post viral illness, leading to an understanding of the seriousness of the illness, and that it is an exciting time for the ME community. There is a lot to learn from us.

A link to a recording of the lecture is to come.
 
Prof Holgate also said something along the lines re ME "there is almost a denial in medical circles of its existence, let alone how serious it is".
He was very pleased to be asked this question "as he has spent the last 7? years working on ME, that it is a very exciting time for the ME community...there are lessons to be learnt"

As a Southampton alumnus I heard about this early. Were you at Southampton @Frankie, or is it just your nearest Uni?
 
Here is an article from the university of British Columbia (UBC) about a clinical trial for COVID

Drawing closer to COVID-19 treatment breakthrough

A new clinical trial may uncover a treatment method for COVID-19 that could save countless lives worldwide. The study’s lead investigator Dr. Josef Penninger, professor of medical genetics at UBC, answers some key questions about the potential breakthrough research.

It’s vital to improve treatment therapies now for people with COVID-19 so we can save lives until a safe vaccine is developed. Even when we have a vaccine, we’ll still need therapy and treatment for people who are already sick. Improving treatment is also a key step in quelling some of the fear, and helping the world adapt to the new normal.

Tell us about the clinical trial you’re leading.

We are running a placebo-controlled, double-blinded phase 2b clinical trial involving 200 patients with severe cases of COVID-19 in Austria, Germany, Denmark, the United Kingdom, the United States and Russia. One hundred patients are receiving standard COVID-19 care, while the other 100 are also receiving twice-per-day intravenous doses of soluble recombinant angiotensin-converting enzyme 2 (or ACE2)—an enzyme on the surface of cells in our organs, including the lungs, heart, gut, kidney, and blood vessels

ACE2 is the critical entry receptor for SARS-CoV-2, which causes COVID-19. Basically, when any virus, including a coronavirus, enters our body, it must enter cells through a specific receptor—SARS-CoV-2 needs the entry gate ACE2. But when we intravenously introduce more ACE2 into the body, the ACE2 enzymes look like receptor cells and essentially act as decoys for the virus. Therefore the virus cannot find the “real” gate anymore. We have already shown that this approach works by significantly reducing this novel coronavirus’ infection rate.
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Link to article

 
MEMarge said:
Prof Holgate also said something along the lines re ME "there is almost a denial in medical circles of its existence, let alone how serious it is".
He was very pleased to be asked this question "as he has spent the last 7? years working on ME, that it is a very exciting time for the ME community...there are lessons to be learnt"

As a Southampton alumnus I heard about this early. Were you at Southampton @Frankie, or is it just your nearest Uni?
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Hello MEMarge. Yes, I was at Southampton Uni as a mature student from 1985 to 1988. I wonder if we overlapped?
 
This sounds very exciting: https://www.ox.ac.uk/news/2020-10-1...elop-extremely-rapid-diagnostic-test-covid-19

Article said:
DPhil student Nicolas Shiaelis, at the University of Oxford, says: ‘Our test is much faster than other existing diagnostic technologies; viral diagnosis in less than 5 minutes can make mass testing a reality, providing a proactive means to control viral outbreaks.’
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But:

Article said:
They hope to incorporate the company by the end of the year, start product development in early 2021, and have an approved device available within 6 months of that time.
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Remdesivir has 'no meaningful impact' on COVID-19 survival, huge study finds

http://www.msn.com/en-gb/health/med...tudy-finds/ar-BB1a6un2?li=AAnZ9Ug&ocid=ASUDHP

Admittedly, not yet peer-reviewed, but still:

"The big story is the finding that remdesivir produces no meaningful impact on survival," Martin Landray, a professor of medicine and epidemiology at Oxford University, said in a statement, according to The Associated Press. However, Dr. Peter Chin-Hong, an infectious diseases expert at the University of California, San Francisco, told The New York Times that the trial results might be somewhat skewed.

The trial participants were treated at 405 different hospitals around the world, each with their own treatment protocols, so factors beyond remdesivir may have impacted patient survival, he noted. In addition, remdesivir may still offer benefit to patients if given early in the course of their illness, but that wasn't specifically addressed by the new study, Dr. Maricar Malinis, an infectious diseases physician at Yale University, told the Times.
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Title : Covid-19 Vaccine Protocols Reveal That Trials Are Designed To Succeed

Link : https://www.forbes.com/sites/willia...s-reveal-that-trials-are-designed-to-succeed/

Moderna, Pfizer, AstraZeneca, and Johnson & Johnson are leading candidates for the completion of a Covid-19 vaccine likely to be released in the coming months. These companies have published their vaccine trial protocols. This unusually transparent action during a major drug trial deserves praise, close inspection of the protocols raises surprising concerns. These trials seem designed to prove their vaccines work, even if the measured effects are minimal.
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If this article is true then having a covid vaccine is unlikely to prevent people getting the disease, it will allegedly, at best, just reduce the severity of symptoms. So, Covid-19 has brought in an entirely new definition of what a vaccine is intended to achieve. So, start expecting more of these useless vaccines that we will all be expected to have in future, whether we like it or not.
 
Arnie Pye said:
If this article is true then having a covid vaccine is unlikely to prevent people getting the disease, it will allegedly, at best, just reduce the severity of symptoms. So, Covid-19 has brought in an entirely new definition of what a vaccine is intended to achieve. So, start expecting more of these useless vaccines that we will all be expected to have in future, whether we like it or not.
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I think this point is overblown. Most vaccines are not "sterile" immunisations - they do not completely prevent infection, yet we are able to prevent spread all the same, since the infection is significantly limited.
Lots of people are talking shit about "mucosal immunity" without understanding what that is. IgG is found in the respiratory mucosa, and several vaccines have shown IgA antibodies, so the claims that there will not be any "mucosal immunity" from intramuscular injection method of administration are not evidence-based.

Fact is, that if the vaccine can significantly reduce symptoms, it will reduce spread due to lowering the number of days which an individual has high enough viral load to infect others.
 
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Snow Leopard said:
Lots of people are talking shit about "mucosal immunity"
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But not me.

Snow Leopard said:
Most vaccines are not "sterile" immunisations - they do not completely prevent infection, yet we are able to prevent spread all the same
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I use as my yardstick the vaccinations I got as a child or young adult. I don't hear of outbreaks of (for example) diphtheria and whooping cough in the UK, and I was vaccinated against those.

Before Covid-19 the fastest development of a vaccine from beginning to end was the one created to prevent mumps, and that took four years.

I am not an anti-vaxxer. But my hackles have been raised by several things about any possible Covid-19 vaccination.

1) It's apparently going to be tested on the elderly - the frailest possible group.

2) I have never been happy about the fact that pharmaceutical companies are no longer held liable for their mistakes in connection with vaccines. I want the general population to have some kind of leverage to keep pharma companies honest.

3) Any Covid-19 vaccine will be delivered without any knowledge of possible long term effects.

4) Covid-19 is a coronavirus. There are, as yet, no vaccines or antiviral drugs to prevent or treat human coronavirus infections. So, my trust in any Covid-19 vaccine is limited by that.
 
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