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

Jonathan Edwards said:
Properly controlled trials should be set up but I suspect that bureaucracy will get in the way. The real problem is that the service is so flat on its back that nobody will have time to even think of setting up trials. If the policy had been to lock down and slow things down realistically then these things might have got set up.
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Yes, lockdown ASAP would have been hard to fault.

What do you think about the Moderna mRNA vaccine? Isn't that a realistic hope for a vaccine in a shorter time than conventional methods?

https://pipelinereview.com/index.ph...-Coronavirus-mRNA-1273-for-Phase-1-Study.html
 
boolybooly said:
Yes, lockdown ASAP would have been hard to fault.

What do you think about the Moderna mRNA vaccine? Isn't that a realistic hope for a vaccine in a shorter time than conventional methods?

https://pipelinereview.com/index.ph...-Coronavirus-mRNA-1273-for-Phase-1-Study.html
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To answer my own question, with a crash course in immunology for today's homework, TWiV have a report on the fast track vaccine candidates.
http://www.virology.ws/2020/03/11/sars-cov-2-the-vaccine-landscape/

TWiVs Helen Stillwell is reporting the phase 1 preliminary vaccine test results might be in by August.

One caveat, Dr Jose Esparza (who was once at IVIC, where I briefly studied nociception before ruling myself out of post grad due to still being too ill and undiagnosed,) comments on a need to pretest the vaccine before human trials due to a potential for Antibody Dependent Enhancement of Infectivity (ADE), whereby viruses benefit from immune reactions, in this case coronavirus protein spikes are thought to bind (EDIT CORRECTION) to ACE2 receptors in the lungs, arteries, heart, kidney, and intestines but an antibody to the vaccine might bind to the virus without neutralising it and allow it to gain access to different cells due to the antibody acting as a link.
https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndrome_coronavirus_2
https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2
https://en.wikipedia.org/wiki/Antibody-dependent_enhancement

If I remember correctly Moderna have chosen the SARS-CoV-2 spike sequence as their antigen.

Wikipedia comfortingly reports ADE complications in vivo are rare, which is good, as I would hate to die a common death!

(re EDIT I am sorry but I had a bad day the first time I tried to study this and misunderstood.)
 
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Substantial undocumented infection facilitates the rapid dissemination of novel coronavirus (SARS-CoV2)
16th march 2020

Abstract
Estimation of the prevalence and contagiousness of undocumented novel coronavirus (SARS-CoV2) infections is critical for understanding the overall prevalence and pandemic potential of this disease. Here we use observations of reported infection within China, in conjunction with mobility data, a networked dynamic metapopulation model and Bayesian inference, to infer critical epidemiological characteristics associated with SARS-CoV2, including the fraction of undocumented infections and their contagiousness. We estimate 86% of all infections were undocumented (95% CI: [82%–90%]) prior to 23 January 2020 travel restrictions. Per person, the transmission rate of undocumented infections was 55% of documented infections ([46%–62%]), yet, due to their greater numbers, undocumented infections were the infection source for 79% of documented cases. These findings explain the rapid geographic spread of SARS-CoV2 and indicate containment of this virus will be particularly challenging.
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https://science.sciencemag.org/content/early/2020/03/13/science.abb3221
 
I hope this is the right thread to put this. It has been reported in The Age today as an important breakthrough which could help speed up finding a vaccine:

"Doctors took four blood samples before and after her recovery and identified the antibodies recruited by the body to fight the illness.

Laboratory head Katherine Kedzierska said the scientists found the woman's immune system responded to coronavirus in the similar way humans fight off influenza.

This suggests an otherwise healthy person could be expected to fight off a mild to moderate case of coronavirus in about three days.

"We found that although COVID-19 is caused by a new virus, in a previously healthy patient robust immune responses can be elicited and associated with clinical recovery," she said.

"What we found was that three days after the patient was admitted, we saw large populations of several immune cells, which are often a tell-tale sign of recovery during seasonal influenza infection, so we predicted that the patient would recover in three days, which is exactly what happened."

The findings, which were published in the Nature Medicine Journal on Tuesday, are the first time a broad immune responses to COVID-19 has been reported globally."

https://www.theage.com.au/national/...ghts-in-vax-breakthrough-20200316-p54ap7.html

ETA - I found the article from Nature Medicine:
https://www.nature.com/articles/s41591-020-0819-2
 
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There are some interesting bits in that paper @Sarah94.
COVID-19, PNEUMONIA & INFLAMMASOMES – THE MELATONIN CONNECTION

Coronaviruses like SARS-CoV-2 use viroporins to STIMULATE immune responses as part of their pathogenicity.

Covid-19 fatality rate
% is probability of dying if infected by the virus (based on two sets of Chinese data of 50,000 + and 70,000+ people, one from the WHO joint mission, dated at the end of Feb)
There's a link to the source of the data.
Image_COVD-19-Fatality-Rate-by-Age.jpg


This is the theory - children produce lots of melatonin and production of it drops off with age. and you need melatonin to inhibit the inflammasome.
The fact that the pro-inflammatory cytokine storm effects are induced by the activation of NLRP3 inflammasomes, the ability of melatonin to INHIBIT NLRP3 inflammasome elevates this powerful molecule to a truly unique position in the fight against COVID-19. This also means that if a patient, regardless of age, has adequate melatonin, the infectiousness of COVID-19 will be greatly reduced, and the chances of developing ARDS/ALI significantly diminished.
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It is no wonder that none of the pregnant mothers infected by COVID-19 admitted to Zhongnan Hospital of Wuhan University, Wuhan, China, developed severe pneumonia or died; nor were their babies infected by COVID-19 [89]. Why?
Melatonin secretion in the third trimester of pregnancy is more than doubled compared to the first trimester.
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But there are quite a few exclamation marks and I kept waiting for the ad for a special melatonin +ascorbic acid supplement.

And here's the details about the author:
Doris Loh is an independent researcher and writer specializing in the investigation of familiar and innovative health topics using unique perspectives in traditional and quantum biology. Her training as a classical pianist allows her the freedom to explore concepts and theories with a curiosity that often results in distinctive conclusions. Recent works by Doris are focused on how health and disease are greatly affected by electromagnetic radiation that surround us everywhere we go. Her works on EMF offer insight and solutions to the challenges humans and other living organisms face during this era of change. Major works by Doris include an in-depth series on deuterium, as well as a startling series on the birefringent quantum properties of the major REDOX balancer, Vitamin C (ascorbic acid).
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So, yeah.
 
Merged thread
Fecal-oral transmission may be part of the COVID-19 clinical picture, according to two reports published in Gastroenterology. The researchers find that RNA and proteins from SARS-CoV-2, the viral cause of COVID-19, are shed in feces early in infection and persist after respiratory symptoms abate.

But the discovery is preliminary. "There is evidence of the virus in stool, but not evidence of infectious virus," David A. Johnson, MD, professor of medicine and chief of gastroenterology at the Eastern Virginia School of Medicine in Norfolk, told Medscape Medical News.

The findings are not entirely unexpected. Both of the coronaviruses behind SARS and MERS are shed in stool, Jinyang Gu, MD, from Shanghai Jiao Tong University School of Medicine in Shanghai, China, and colleagues, note in one of the newly published articles.
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Article continues here : https://www.medscape.com/viewarticle/926682
 
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Hutan said:
There are some interesting bits in that paper @Sarah94.
COVID-19, PNEUMONIA & INFLAMMASOMES – THE MELATONIN CONNECTION

Coronaviruses like SARS-CoV-2 use viroporins to STIMULATE immune responses as part of their pathogenicity.

Covid-19 fatality rate
% is probability of dying if infected by the virus (based on two sets of Chinese data of 50,000 + and 70,000+ people, one from the WHO joint mission, dated at the end of Feb)
There's a link to the source of the data.
Image_COVD-19-Fatality-Rate-by-Age.jpg


This is the theory - children produce lots of melatonin and production of it drops off with age. and you need melatonin to inhibit the inflammasome.





But there are quite a few exclamation marks and I kept waiting for the ad for a special melatonin +ascorbic acid supplement.

And here's the details about the author:

So, yeah.
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Oh dear. But I guess even a stopped clock can be right sometimes? I don't care about the author's credentials, only about the quality of the science in this particular article. Which might be dubious, I don't know.
 
Not sure if this has been posted yet, there is new data showing that being infected once leads to immunity according to this study in rhesus macaques.

"Taken together, our results indicated that the primary SARS-CoV-2 infection could protect from subsequent exposures, which have the reference of prognosis of the disease and vital implications for vaccine design."

This was mentioned in today's press conference by our CDC as well as by one of our leading experts (Christian Drosten), so I think there is reason to be hopeful.
 
Coronavirus survives on surfaces up to 72 hours. Here’s how to protect yourself

Then there’s the new coronavirus. Its survival on surfaces is similar to that of the SARS virus, to which it’s related. On plastic, after eight hours only 10% of what researchers deposited was still there, according to a study published on Tuesday in the New England Journal of Medicine. But the virus didn’t become undetectable until after 72 hours. On stainless steel, the numbers began plummeting after just four hours, becoming undetectable by about 48 hours. On copper and cardboard, virus was undetectable by eight hours and 48 hours, respectively.
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https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/
 
hinterland said:
Interesting. How do we know that the other common coronaviruses have been circulating in humans for thousands of years? Is that a fact?

If we managed to get through millennia while only acquiring 4 human coronaviruses yet 3 have jumped species in the last 20 years, that's a worrying trend! It's not the bat's fault...
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Yes that seems a bizarre statement surely that would make it a virus that wouldn't cause symptoms in us?

So why did this suddenly change if that is true?
 
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