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

Well, this is interesting:

http://www.msn.com/en-gb/news/world...t-covid-19/ar-BB19ohb9?li=AAnZ9Ug&ocid=ASUDHP

A significant proportion of patients who develop life-threatening forms of Covid-19 have genetic or immunological defects that impair their ability to fight the virus, research has found.

In papers published in the journal Science, the Covid Human Genetic Effort international consortium describes two glitches in severely ill Covid-19 patients that prevent them from making a frontline immune molecule called type 1 interferon.

The patients would have carried these glitches for years before the pandemic, or in the case of the genetic errors, all their lives. The discovery may help to explain a mystery surrounding the coronavirus: why it leaves some sufferers sick or dying in intensive care, while others remain barely affected or asymptomatic.
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https://science.sciencemag.org/content/early/2020/09/23/science.abd4585

Auto-antibodies against type I IFNs in patients with life-threatening COVID-19

Science, 24 Sep 2020 (open access)

Abstract
Interindividual clinical variability in the course of SARS-CoV-2 infection is immense. We report that at least 101 of 987 patients with life-threatening COVID-19 pneumonia had neutralizing IgG auto-Abs against IFN-ω (13 patients), the 13 types of IFN-α (36), or both (52), at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1,227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 were men. A B cell auto-immune phenocopy of inborn errors of type I IFN immunity underlies life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men.
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Paging @Jonathan Edwards for comment. ;)
 
Snow Leopard said:
https://science.sciencemag.org/content/early/2020/09/23/science.abd4585

Auto-antibodies against type I IFNs in patients with life-threatening COVID-19

Science, 24 Sep 2020 (open access)



Paging @Jonathan Edwards for comment. ;)
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Potentially interesting. It would be useful to have some control antigens studied. For instance heat shock protein 60, which pops up as a non-specific result in all sorts of situations where there is B cell activation.

I am a bit puzzled by there being antibodies to all sorts of different interferons if this is a specific pathogenic pathway.

Still, it might be a factor. Antibodies that engage immune mediators could well come up at least actually with infections. Rheumatic fever may have something to do with antibodies that engage complement in an aberrant way and allow immune complexes to deposit, for instance. And of course Guillain Barre has been linked to antibody production.
 
The presence of auto-Abs was associated with a poor outcome, with death occurring in 37 of the 101 patients (36.6%)
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This seems like a fairly strong effect and the one of the most surprising COVID-19 findings (if replicated) I have seen so far.

Jonathan Edwards said:
I am a bit puzzled by there being antibodies to all sorts of different interferons if this is a specific pathogenic pathway.
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The authors also claim:

The prevalence of auto-Abs against type I IFNs in the general population was estimated at 0.33% (0.015-0.67%) in a sample of 1,227 healthy individuals
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Which seems high for what is hypothesised to be a pathological auto-antibody!?

This is a bold claim too:

Moreover, IFN-α subtypes were undetectable during acute disease in the blood of patients with auto-Abs against IFN-α, suggesting a pre-existing or concomitant biological impact in vivo. It is also unlikely that patients could break self-tolerance and mount high titers of neutralizing IgG auto-Abs against type I IFN within only one, or even two weeks of infection
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Snow Leopard said:
Which seems high for what is hypothesised to be a pathological auto-antibody!?
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I think that the problem is that a 'positive' antibody test is always defined by an arbitrary cut-off on a particular assay. There are always a few normal people who have levels a bit away from the massif the population.Nobody has a completely negative binding to an antigen.
 
Amw66 said:
I think finland have trained dogs.
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Yes. From a Swedish news article yesterday:

SVT: Finland: Hundar används i jakten på smitta
Google Translate said:
Finland: Dogs are used in the hunt for infection

The coronavirus has been shown to have an odor that is relatively easy for dogs to identify. In Finland, fifteen dogs have been trained to detect infected travelers.

A total of fifteen dogs and ten instructors have been trained for the project, which began at Helsinki Airport this week.

Standard testing takes place in parallel at the airport. The effectiveness of dogs has not been tested in scientific studies yet.

But the experiments so far show good results for finding infection, says Anna Hielm-Björkman, researcher in veterinary medicine.

- We have seen that the dogs can actually find infection before there are clear symptoms.
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We have a report here in Florida of a treatment protocol developed by AdventHealth in Ocala. (This non-profit hospital system is one of the better ones in the state in my experience.) ICAM only depends on supplements and generic drugs which can be used off-label. It has been very successful in limited use on hospitalized patients. Florida has plenty of such patients for a trial.

One of the possibilities this opens up is that weak positive results from such questionable drugs as hydroxychloroquine may have been due to other treatments not spelled out.
 
Barry said:
Although I'd be willing to contribute to all this, I'm still very content with my old iPhone 4, which is a long way short of the required spec to run the app. And I'm not prepare to spend £100s to upgrade just for that.
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What *is* the required spec? Where do I find it? I'm not sure my phone will cope with it.
 
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