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

I just saw a twitter thread about a study comparing the transmission of coronavirus by vaccinated vs. un-vaccinated people.

First tweet - "A study out of the University of Illinois shows vaccinated individuals with a 'breakthrough' infection are LESS likely to shed infectious virus at a given viral load, shed for a SHORTER period of time compared to unvaccinated individuals, AND report fewer days of symptoms."

Code:
https://twitter.com/sailorrooscout/status/1433788553465679906

I don't have the scientific background to analyze this study, so please don't ask me what it means! Just passing along the information! :)

Link to study (from last tweet in the twitter thread) - https://www.medrxiv.org/content/10.1101/2021.08.30.21262701v1
 
https://www.bbc.co.uk/news/health-53467022

Stephen Holgate is a co-founder of Synairgen. They originally developed this for asthma and COPD etc

"The treatment from Southampton-based biotech Synairgen uses a protein called interferon beta which the body produces when it gets a viral infection."

"The initial findings suggest the treatment cut the odds of a Covid-19 patient in hospital developing severe disease - such as requiring ventilation - by 79%"

 
Can't think of a better place to post this:

(UK) Charges to be introduced for Covid lateral flow tests within ‘months’ in ‘reckless’ move

https://www.msn.com/en-gb/news/ukne...ckless-move/ar-AAOzR5W?ocid=ASUDHP&li=BBoPWjQ

Absolute genius. Discourage people from getting tested by making them pay for their LFTs. A great way of keeping track of the disease. Not. Because it will cost the NHS so much less if we have additional outbreaks requiring hospitalisation than it will to pay for the kits. :banghead:
 
[Not sure if this has been posted elsewhere...]

Merck has announced that they have developed an antiviral pill, "molnupiravir," that has cut Covid-19 hospitalizations and deaths in half. "The pills could be available by late this year."

The Merck drug — named for Mjölnir, the hammer wielded by the thunder god Thor in Norse mythology — is designed to stop the coronavirus from replicating by inserting errors into its genetic code. Doctors will prescribe the treatment to patients, who will receive the pills from pharmacies. The drug is meant to be taken as four capsules twice a day for five days — a total of 40 pills over the course of treatment.
https://www.nytimes.com/2021/10/01/business/covid-antiviral-pill-merck.html

A limitation of the drug is that, like some other Covid-19 drugs, it is more effective when taken earlier in the disease. This requires rapid diagnosis as well as quick access to the drug.
 
[Not sure if this has been posted elsewhere...]

Merck has announced that they have developed an antiviral pill, "molnupiravir," that has cut Covid-19 hospitalizations and deaths in half. "The pills could be available by late this year."



A limitation of the drug is that, like some other Covid-19 drugs, it is more effective when taken earlier in the disease. This requires rapid diagnosis as well as quick access to the drug.

This is great news, though I can't seem to find published results yet. If the results aren't nearly as good as monoclonal antibodies then I'll be slightly less excited.

Prior data was reported here, but an effect on clinical outcomes wasn't measured. https://www.medrxiv.org/content/10.1101/2021.06.17.21258639v1
 
Study reveals why some people get Covid toe condition

(looks rather like gout, and often hurts like hell!)

Study reveals why some people get Covid toe condition - BBC News

Scientists believe they can explain why some people who catch Covid develop chilblain-like lesions on their toes and even fingers.

Covid toe appears to be a side effect of the body switching into attack mode to fight off the virus.
The researchers say they have pinpointed the parts of the immune system that appear to be involved.
The findings, in the British Journal of Dermatology, may help with treatments to ease the symptoms.

Continues at link, dated 6.10.21
 
Fingers, too. But I guess that's lost because it's not as visible. Lots of things get lost because they aren't obvious at first. So many things, almost all the things.

I had this for years, fingers and toes (almost like it's about extremities...), so it's not a temporary switch to fight off infection, it can clearly be chronic, but medicine won't see that for years, if ever, because once you remove the obvious discoloration, it just becomes another symptom that can't be verified.
 
The Swedish guidelines for covid-19 testing will be changed on November 1st. Those who are fully vaccinated or have recently had covid-19, and children younger than 6 years old, will no longer be recommended to get tested when they have symptoms.

This will obviously affect everything, including research. :(:grumpy:

Currently about 79% of the Swedish population 16 years or older have been vaccinated with two doses. Approx 64% if you include the whole population.

An opinion piece published in SvD last week explains some of the problems with this approach:

”Fel att sluta testa vaccinerade personer”
https://www.svd.se/fel-att-sluta-testa-vaccinerade-personer
Auto-translate said:
"Wrong to stop testing vaccinated people"

Testing, genetic surveillance and tracing of all cases of covid-19 are crucial tools to keep society open in the coming winter.

We want to argue for continued broad testing to monitor the infection, deploy and evaluate targeted measures, and conduct effective tracing to keep communities open. [...]

Testing of people with symptoms of covid-19 is crucial for two main reasons: 1) at the population level, broad testing is a cornerstone of informative surveillance that can guide targeted interventions and identify new virus variants; 2) at the individual level, broad testing is a prerequisite for effective infection detection. In addition to these, there are other reasons for continued testing even of vaccinated persons, such as having test results in case of prolonged symptoms, and to have a good basis for research, but we do not go into these aspects further in this article.

Good surveillance is central to infection control as it can identify new outbreaks early, help to understand the effects of different community interventions and other external factors that influence the spread of infection, and detect abnormal patterns that may indicate new characteristics of the infectious agent. [...]

It is also of high importance to rapidly identify new virus variants with undesirable characteristics such as increased infectivity, more severe disease or where immunity from vaccines or pass-through infection no longer protects. Finding these requires three things. The first is broad testing, the second is mapping the virus' genome in patient samples and the third is good infection detection that identifies abnormal patterns such as an unusually rapid spread, a different symptom pattern or an increase in infections in vaccinated people. When this happens, it is necessary to analyse whether it is a new virus variant. Not testing vaccinees will therefore make it more difficult to detect variants where the vaccine no longer provides sufficient protection. [...]

Without testing of vaccinated people, these cases will not be detected, which increases the risk of transmission to people at risk and to health care workers who may in turn infect susceptible individuals. In order to protect the most vulnerable, it is essential to stop as many chains of infection as possible, including those that start with a vaccinated individual. [...]

This is not only a Swedish interest, but we also have a global responsibility to monitor such variants and inform the outside world of any findings.
 
Direct SARS-CoV-2 infection of the human inner ear may underlie COVID-19-associated audiovestibular dysfunction

https://www.nature.com/articles/s43856-021-00044-w.pdf

Abstract

Background
COVID-19 is a pandemic respiratory and vascular disease caused by SARS-CoV-2 virus. There is a growing number of sensory deficits associated with COVID-19 and molecular mechanisms underlying these deficits are incompletely understood.

Methods
We report a series of ten COVID-19 patients with audiovestibular symptoms such as hearing loss, vestibular dysfunction and tinnitus. To investigate the causal relationship between SARS-CoV-2 and audiovestibular dysfunction, we examine human inner ear tissue, human inner ear in vitro cellular models, and mouse inner ear tissue.

Results
We demonstrate that adult human inner ear tissue co-expresses the angiotensin-converting enzyme 2 (ACE2) receptor for SARS-CoV-2 virus, and the transmembrane pro-tease serine 2 (TMPRSS2) and FURIN cofactors required for virus entry. Furthermore, hair cells and Schwann cells in explanted human vestibular tissue can be infected by SARS-CoV-2, as demonstrated by confocal microscopy. We establish three human induced pluripotent stem cell (hiPSC)-derived in vitro models of the inner ear for infection: two-dimensional oticprosensory cells (OPCs) and Schwann cell precursors (SCPs), and three-dimensional inner ear organoids. Both OPCs and SCPs express ACE2, TMPRSS2, and FURIN, with lower ACE2 and FURIN expression in SCPs. OPCs are permissive to SARS-CoV-2 infection; lower infection rates exist in isogenic SCPs. The inner ear organoids show that hair cells express ACE2 and are targets for SARS-CoV-2.

Conclusions
Our results provide mechanistic explanations of audiovestibular dysfunction inCOVID-19 patients and introduce hiPSC-derived systems for studying infectious human otologic disease.

@Mij
 
Well that’s interesting. One of the symptoms I had whilst covid infected was earache. It was a stabbing pain occurred just over a couple of days and then just stopped. This reoccurred a few times over the next 6 months as short bouts of the same stabbing pain that would come and go in less than a couple of hours. One of my daughters who had covid at the same time reported the same thing. No visible sign of infection. I can’t say that I know what’s happened with that or what my experience means, but I’m not surprised by this:

Results
We demonstrate that adult human inner ear tissue co-expresses the angiotensin-converting enzyme 2 (ACE2) receptor for SARS-CoV-2 virus, and the transmembrane pro-tease serine 2 (TMPRSS2) and FURIN cofactors required for virus entry. Furthermore, hair cells and Schwann cells in explanted human vestibular tissue can be infected by SARS-CoV-2, as demonstrated by confocal microscopy.
 
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