Discussion thread IV - COVID-19 (new coronavirus)

[mscox]

Does SARS-CoV-2 utilize antibody-dependent enhancement? - LessWrong 2.0

 

[mscox]

Evaluation of Antibody-Dependent Enhancement of SARS-CoV Infection in Rhesus Macaques Immunized with an Inactivated SARS-CoV Vaccine | SpringerLink

 

[mscox]

Reinfection could not occur in SARS-CoV-2 infected rhesus macaques | bioRxiv

 

[mscox]

Medical Countermeasures Analysis of 2019-nCoV and Vaccine Risks for Antibody-Dependent Enhancement (ADE)[v1] | Preprints

 

[mscox]

Is COVID-19 Receiving ADE From Other Coronaviruses? - PubMed

 

[mscox]

Molecular mechanism for antibody-dependent enhancement of coronavirus entry | Request PDF

 

[mscox]

Virus Eradication- Abstract Detail (Coronovirus SARS 1) ADE

 

[mscox]

My apologies for all those posts, however if it turns out that sars-cov2 exhibits ADE then we are in for a very, very rough time. If immunity to Covid-19 makes second infections more deadly and vaccines more complicated..... Well, it does have me personally worried :/

 

[bertrand789]

Merci, mais, en pr?alable, ce ne serait pas bien de repr?ciser la fiche de danger. Je veut dire que vu les su et les r?gles souvent limitatives en place, si l'objectif soci?tal est:
en absence de vaccin, d'obtenir un taux de contamination soci?tale acceptable, quelles sont les strat?gies soci?tales possibles ?

- les Chinois ont ? plus de 80% opt? pour la m?decine traditionnelle. C'est, ce que j'ai lu, mais dans les faits, disposer de ce stock c'est possible, et cela a ?t? fait pendant les confinements, d'une part, d'autre part, comme dans les ?tudes, dites scientifiques, on ne sait pas s'ils en ont us? ou pas, on fait comment ?
- d'autres ont laiss? l'usage libre de certains traitement anti paludisme, sans rien enregistrer , soit disant ...

etc
Les possibles potentiels quand il n'y a aucun stock disponible, pour une soci?t?, cela sert ? quoi en phase de pand?mie ? ah oui pour le prochain tour ...

Donc les objectifs soci?taux sont formalis?s et accessible ou ?

Maintenant, si l'on admet l'usage de m?dicament pr?liminaire . Perso, je trouve mieux la version sans antibiotique, d'une part et d'autre part , entre un produit avec 40 ans de retour et des produits autres, donc encore dans les tuyaux, on a un avis pes? comment ?

 

[Emily]

Thanks for sharing those. Could be we are seeing ADE in those cases that are very severe in the context of the individual's age group. If Sars2 interacts with other coronaviruses, that is a plausible explanation for why some regions are so badly affected.

 

[sharon sanders]

MARCH 26TH, 2020
Epidemiologist Behind Highly-Cited Coronavirus Model Admits He Was Wrong, Drastically Revises Model

By Amanda Prestigiacomo

Epidemiologist Neil Ferguson, who created the highly-cited Imperial College London coronavirus model, which has been cited by organizations like The New York Times and has been instrumental in governmental policy decision-making, offered a massive revision to his model on Wednesday.


Ferguson’s model projected 2.2 million dead people in the United States and 500,000 in the U.K. from COVID-19 if no action were taken to slow the virus and blunt its curve.
However, after just one day of ordered lockdowns in the U.K., Ferguson has changed his tune, revealing that far more people likely have the virus than his team figured. Now, the epidemiologist predicts, hospitals will be just fine taking on COVID-19 patients and estimates 20,000 or far fewer people will die from the virus itself from from its agitation of other ailments.
Ferguson thus dropped his prediction from 500,000 dead to 20,000.....
:tiphat:https://www.dailywire.com/news/epide...revises-model/

He cleared this controversy up:



neil_ferguson
@neil_ferguson
1/4 - I think it would be helpful if I cleared up some confusion that has emerged in recent days. Some have interpreted my evidence to a UK parliamentary committee as indicating we have substantially revised our assessments of the potential mortality impact of COVID-19.
5:52 PM ? Mar 26, 2020?Twitter for iPhone
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2/4 -This is not the case. Indeed, if anything, our latest estimates suggest that the virus is slightly more transmissible than we previously thought. Our lethality estimates remain unchanged.
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3/4 - My evidence to Parliament referred to the deaths we assess might occur in the UK in the presence of the very intensive social distancing and other public health interventions now in place.
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4/4 - Without those controls, our assessment remains that the UK would see the scale of deaths reported in our study (namely, up to approximately 500 thousand).
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[JimO]

Thanks mscox for all the information. The worst part of this pandemic is all the uncertainties.

 

[JimO]

Thanks Sharon. That does clear up a lot of my confusion.

 

[cartski]

Which paper? NEJM was 72 hours. MMWR was 17 days on the cruise ship conditions. Not heard of 7 days on poly. Not heard anything about ineffectiveness of washing fresh produce. Not heard anything about ineffectiveness of disinfecting packaging of frozen produce.

J.

 

[cartski]

This changed tube media report has been debunked by Ferguson. See post #101 in this thread.

 

[mscox]

Experiments with toy SIR models. Whilst these may be overly simplistic models, they clearly illustrate the sensitivities and impacts of different behaviours, controls and inherent infectivity.

 

[gsgs]

weekly deaths from 122 US-cities in MMWR was discontinued some years ago. Do we still have some weekly deaths ? e.g. New York City ?

 

[gsgs]

Ferguson now thinks it's more transmissional than he had first thought.
[ many mild cases, some % of London already infected --> lower mortality ?]
but insists on the 510000 deaths estimate without measures+working healthcare.
However the current measures should be effective --> <20000 deaths.
I don't see much effect of any measures in Europe including Italy with its nationwide lockdown on Mar09.
Why should the English measures be so much better ?
And why still 510000 deaths with so many infected already

and what about the ~5fold increase of deaths from all causes in Lombardy ? (--> >2Million deaths in USA projected ! )

 

[JJackson]

Thanks for that, an excellent simple model with clear explanations making a great introduction to the interface between epidemiology and public health interventions.

 

[JJackson]

I noticed in one of today's news links that Spain was stopping use of a rapid test kit as it was not sufficiently accurate. Unfortunately it did not say how this test worked but I have concerns about the tests in development. Most of the ones I have seen in development test for antibodies. Early in the disease the body produces IgM before shifting to IgG which makes these test very useful as, if they test both, you can see the point in disease progression and post infection antibody decay rates. The problem with SARS-2 is IgM levels climb from about 4 to 8 days post infection with IgG becoming dominant after that. These are both produced as a reaction to a disease having been circulating in the host for a while. As no one has any partial immunity, that can be boosted, the adaptive immune response has to start from scratch. COVID seems to be highly infectious around symptom onset which falls before even the IgM levels reach test sensitivity. Where these test should be useful is in hospitalised patients for whom the test is just a confirmation of the clinical diagnosis. Using the test for this will free up RT PCR capacity which can be directed to early case identification where virus levels are still low and the patient can be usefully isolated.
[Edit]
This is an extract from an old post taken from this thread - https://flutrackers.com/forum/forum...son-s-workshop/8326-tales-from-the-front-line
It gives a very basic look at the immune response to a novel infection - may be useful of you are new to such things.

If we assume an H5N1 viron has entered the body but not infected a cell but has made first contact with the immune system. Step one is the immune system needs to see it as ‘not self’. Only the external surfaces of the virus are ‘visible’ and in our case that principally means parts of the H & N proteins. Ignoring all the detail of what happens next the salient points are that certain surface features of these proteins’ tertiary structure (antigenic sites) are ‘learnt’ and communicated (antibodies are produced by the B-cells) to the rest of the immune system which then gears up to fight the infection. This is an important step change; the immune system has changed from looking for any thing that is ‘not self’ (generalised xenophobia) to identifying a specific threat and targeting it. A second viron – with identical surface feature – will now have a much lower chance of successfully reaching its target cell type as it is being actively targeted. If the surface features are similar – but not identical - then protection will fall somewhere between the two states. This learnt protection is not based on the whole overall viral surface shape but on lots of small features with an antibody produced for each.