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

Amw66 said:
Just when you thought things could not get more confusing....
Anti vaxxers will have a field day
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From the article - “If a second dose of the vaccine a patient originally received isn’t available, or if the manufacturer of the first shot isn’t known, another vaccine may be substituted, health officials said.”

Wait... what?
Is this even.. a thing?

The U.K. is not only making up it’s own protocol and changing times which Pfizer who actually made the vaccine said there is no data on its safety and efficacy for, it is now saying you can mix up different types of vaccines? When one of them is a totally new type of vaccine and none of them have been tested together yet? I cannot believe they’re using as a reason (in the article), that’s it’s “due to be tested next year”. Lots of things are due to be tested next year. Does that make them all safe and effective?!

The thing that worries me a lot is that it now looks like they are going to end up messing up the one thing (vaccination) that actually might have helped a little bit if they’d done it right. Since they’re clearly not going to be doing any of the elimination things that other countries do.
 
Sly Saint said:
New Covid-19 Strains: What Scientists Know About Coronavirus Variants
the Wall Street Journal
https://www.wsj.com/articles/new-co...s-know-about-coronavirus-variants-11609466017
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(Cant read all of that sorry not subbed to WSJ.)

Interestingly though, Prof Vincent Racaniello is saying on TWIV the high rate of spreading is not supported by any reliable evidence and could be due to the founder effect.

https://www.virology.ws/2020/12/24/sars-cov-2-uk-variant-does-it-matter/

This video was recorded on Monday, 21 December 2020. Since then additional data on the UK variant have been released but they do not change my view: there are no biological data in humans showing that the virus has increased transmissibility. The variant is certainly spreading in the population, but that could be due to other situations that have not been ruled out.
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I think he has a point, the pattern we are seeing is consistent with founder effect in a youthful demographic who are breaking quarantine in a way which causes superspreader events.

e.g. "France: More than 2,500 break virus restrictions at illegal rave."
https://www.bbc.co.uk/news/world-europe-55513167
 
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"However, the advice said that while every effort should be made to complete the dosing regimen with the same vaccine, if the patient is at “immediate high risk” or is considered “unlikely to attend again” they can be given different vaccines."

:confused:
 
Mij said:
"However, the advice said that while every effort should be made to complete the dosing regimen with the same vaccine, if the patient is at “immediate high risk” or is considered “unlikely to attend again” they can be given different vaccines."

:confused:
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What the govt says is even worse than that.. from the FT https://www.ft.com/content/afa31d12-c393-402b-9677-1fb312cfa1cf

“The government’s Green Book for vaccinations says “every effort” should be made to complete the immunisation course with the same vaccine. But it also says: “For individuals who started the schedule and who attend for vaccination at a site where the same vaccine is not available, or if the first product received is unknown, it is reasonable to offer one dose of the locally available product to complete the schedule.

Health officials said this would only happen under very limited circumstances.

The guidelines stress this would involve individuals who are likely to be at high risk or unlikely to attend the appointment again. The two UK-approved vaccines share the same mode of action, targeting the spike protein of the virus, which makes it “likely the second dose will help to boost the response to the first dose”, the rubric says.”


“Where the product received is unknown.” Unknown?!

Also haven’t Pfizer and AZ confirmed they have enough vaccines and are sending enough to the U.K. at the right time for them to complete the vaccination schedule. So why would the same vaccine be unavailable?

And why would someone be unable to attend for a second dose, when they’ve already attended for a first dose? Why are home visits and visiting them in the community suddenly being ruled out? None of it makes sense to me.
 
NIH News Releases NIH study uncovers blood vessel damage and inflammation in COVID-19 patient's brains but not infection

“We found that the brains of patients who contract infection from SARS-CoV-2 may be susceptible to microvascular blood vessel damage. Our results suggest that this may be caused by the body’s inflammatory response to the virus” said Avindra Nath, M.D., clinical director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope these results will help doctors understand the full spectrum of problems patients may suffer so that we can come up with better treatments.”

...
“We were completely surprised. Originally, we expected to see damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases,” said Dr. Nath.

Finally, the researchers saw no signs of infection in the brain tissue samples even though they used several methods for detecting genetic material or proteins from SARS-CoV-2.

“So far, our results suggest that the damage we saw may not have been not caused by the SARS-CoV-2 virus directly infecting the brain,” said Dr. Nath. “In the future, we plan to study how COVID-19 harms the brain’s blood vessels and whether that produces some of the short- and long-term symptoms we see in patients.”
 
boolybooly said:
(Cant read all of that sorry not subbed to WSJ.)

Interestingly though, Prof Vincent Racaniello is saying on TWIV the high rate of spreading is not supported by any reliable evidence and could be due to the founder effect.

https://www.virology.ws/2020/12/24/sars-cov-2-uk-variant-does-it-matter/



I think he has a point, the pattern we are seeing is consistent with founder effect in a youthful demographic who are breaking quarantine in a way which causes superspreader events.

e.g. "France: More than 2,500 break virus restrictions at illegal rave."
https://www.bbc.co.uk/news/world-europe-55513167
Click to expand...

I’m not sure. This new strain had several mutations (spike protein?) that could lead to it making things worse and spreading more quickly. I’m not saying there’s not superspreading going on but why could the new mutation not be playing a role too? London and some areas in the south are in a really bad state, and this strain is very dominant here and has increased really quickly (see the picture on the right). I find it doubtful this is all due to young people breaking quarantine. Is there any way to know definitively from research, whether the new mutation (or not) is what’s making things worse? Data from the ONS:

 
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lunarainbows said:
And why would someone be unable to attend for a second dose, when they’ve already attended for a first dose? Why are home visits and visiting them in the community suddenly being ruled out? None of it makes sense to me.
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It makes no sense to me either. If the first dose didn't cause any allergic reaction, then home visits for the second jab would be safe.

In my province they've decided to vaccinate fewer people and save the second jab for them at the later date. Mixing of vaccines is not recommended here in Canada.
 
Sounds consistent with Byron Hyde’s theory of M.E being a diffuse microvascular injury to the brain.
Kalliope said:
NIH News Releases NIH study uncovers blood vessel damage and inflammation in COVID-19 patient's brains but not infection

“We found that the brains of patients who contract infection from SARS-CoV-2 may be susceptible to microvascular blood vessel damage. Our results suggest that this may be caused by the body’s inflammatory response to the virus” said Avindra Nath, M.D., clinical director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope these results will help doctors understand the full spectrum of problems patients may suffer so that we can come up with better treatments.”

...
“We were completely surprised. Originally, we expected to see damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases,” said Dr. Nath.

Finally, the researchers saw no signs of infection in the brain tissue samples even though they used several methods for detecting genetic material or proteins from SARS-CoV-2.

“So far, our results suggest that the damage we saw may not have been not caused by the SARS-CoV-2 virus directly infecting the brain,” said Dr. Nath. “In the future, we plan to study how COVID-19 harms the brain’s blood vessels and whether that produces some of the short- and long-term symptoms we see in patients.”
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Note point 6. This point is something that Hilda Bastian was asking about (on Twitter) as well.



(which suggests that immunity acquired from prior infection or vaccination will protect against the "new" UK variant.)



(Claims of increased B117 viral load may simply be sampling biases.)
 
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(continued)



(So the presence of S:N501Y.V1 in other countries where there is community transmission and genomic surveillance will be the true test to confirm whether this variant is in fact more transmissible.)



The "gap" between other UK variants and this variant reported by others suggests to me that it developed elsewhere, in a place with a high rate of spread, but a lack of genomic surveillance.

https://www.newindianexpress.com/na...f-new-coronavirus-strain-experts-2239499.html
 
Kalliope said:
we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases,” said Dr. Nath.

Finally, the researchers saw no signs of infection in the brain tissue samples even though they used several methods for detecting genetic material or proteins from SARS-CoV-2.
Click to expand...

If these patients did not have a history of a positive infection in the recent past would it now be trumpeted that there was no evidence longcovid was caused by a virus so it must be mass hysteria?

Because everyone knows there is no viral cause to ME because they did not manage to detect any using 1950's technology.
 
Mithriel said:
If these patients did not have a history of a positive infection in the recent past would it now be trumpeted that there was no evidence longcovid was caused by a virus so it must be mass hysteria?
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Not only that, it would be used as proof positive that hysteria, anxiety and depression DO cause physical symptoms. Just look at all those people with anxiety and depression who have physical symptoms!

This is beyond circular reasoning, it's circular failure. Millions of people present with symptoms for which a cause cannot be identified, the symptoms are dismissed as not real and reduced, compressed with massive loss of information, into anxiety and/or depression. Now look back at the same patients again, they have a "diagnosis" or anxiety and/or depression and wow do they have many physical symptoms now, all attributed to some combination of hysteria/anxiety/somatization/depression.

Literally pointing at failure to commit failure. Amazing. Straight up amazing, you could not parody this, it is already beyond satire.
 
[ETA: The following was a response to a post which has now been deleted. The post was removed because I had got confused (often happens) and misunderstood it, so there were concerns it might have caused confusion for others too. This post remains the same just with the original references to the deleted post removed]

Efficacy is simply the percentage reduction of disease in the vaccinated group of people compared to the unvaccinated group. It doesn't tell you what percentage of the trial population fell sick or were hospitalisised (for that you need to look at the trial data).

This is the data from the MHRA document for the Pfizer/BioNTech vaccine:

Vaccine group (n=18,242)
Confirmed covid cases: 8 (0.04%)

Placebo group (n=18,379)
Confirmed covid cases: 172 (0.94%)

So efficacy is calculated as:
(172-8)/172 = 0.95 (95%)

The MHRA document doesn't appear to give the figures for severe disease. According to this blog by Hilda Bastian the numbers are too small for a definitive answer but 1 person who had the vaccine was classified as having severe Covid-19, versus 3 in the placebo group. The person in the vaccine group was classified as severe because their oxygen saturation level measured low at their illness visit, but they never needed medical care.

I won't bother to quote the data for the Oxford/AstraZeneca trial because according to Hilda Bastian it is not reliable, for the reasons summarized here (you need to click on the link to see all Hilda's posts relating to this):

 
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Here is a tweet expressing a counter perspective to the "rave" narrative of increased transmission.



The argument being that unsupported people living in relative poverty cannot afford to self isolate properly.

Also the age bias previously reported being debunked, which is another example of statistical phenomena due to human behaviour being misinterpreted as qualities of virus variants (as with transmissability and the founder effect).

[EDIT Fri 22 Jan '21 - re: strikethrough, higher transmissability is no longer reasonably open to interpretation as entirely due to founder effect as new data has shown there is increased mortality as well, which supports the hypothesis that the new "UK" variant has somehow developed higher rates of cell infection in patients. Previously the government's statements that there was no increased mortality cast doubt on the higher transmissability scenario.]

 
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Assessment of musculoskeletal pain, fatigue and grip strength in hospitalized patients with COVID-19, 2021, Tuzun et al
BACKGROUND: Although there are some retrospective studies to present musculoskeletal findings of the COVID-19, still the muscle strength and fatigue has not been studied in detail.
AIM: To reveal the symptoms of musculoskeletal system in COVID-19 patients, to evaluate myalgia, arthralgia and physical/mental fatigue, to assess handgrip muscle strength, and to examine the relations of these parameters with the severity and laboratory values of the disease.

DESIGN: This study was designed as a cross-sectional, single-center case series.

SETTING: This study took place from May 15,2020, to June 30, 2020 at the Istanbul University-Cerrahpaşa, Cerrahpaşa Pandemia Services.

POPULATION: Hospitalized 150 adults with laboratory and radiological confirmation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) according to WHO interim guidance were included in the study.

METHODS: The disease severity 2007 idsa/ats guidelines for community acquired pneumonia was used. Myalgia severity was assessed by numerical rating scale (NRS). Visual analog scale and Chalder Fatigue Scale (CFS) were used for fatigue severity determination. Handgrip strength (HGS) was measured by Jamar hand dynamometer.

RESULTS: 103 patients (68.7%) were non-severe and 47 patients (31.3%) were severe. The most common musculoskeletal symptom was fatigue (133 [85.3%]), followed by myalgia (102 [68.0%]), arthralgia (65 [43.3%]) and back pain (33 [22.0%]). Arthralgia, which was mostly notable at wrist (25 [16.7%]), ankle (24 [16.0%]) and knee (23 [15.3%]) joints, was significantly higher among the severe group. Severe myalgia was prevalent among myalgia sufferers regardless of COVID-19 severity. The physical fatigue severity score was significantly higher in severe cases, whereas this difference was not significant in mental fatigue score. Female patients with severe infection had “lower” grip strength, whereas grip strength among males did not differ significantly between non-severe and severe COVID-19 cases. Nevertheless the mean values in both genders and in age decades were below the specified normative values. CRP, ferritin, and LDH levels were significantly higher in women with “lower” grip strength compared to the “normal” group.

CONCLUSIONS: Aside from other multi-systemic symptoms, musculoskeletal symptoms are quite common in patients with COVID-19. Patients have severe ischemic myalgia regardless of disease activity. Although there is a muscle weakness in all patients, the loss of muscle function is more of a problem among women in connection with disease severity. Muscular involvement in coronavirus disease is a triangle of myalgia, physical fatigue, and muscle weakness.

CLINICAL REHABILITATION IMPACT: Muscle involvement in COVID-19 patients does not mean only myalgia but also a combination of physical fatigue and muscle weakness, and this should be considered in planning the rehabilitation strategies of COVID-19 patients.
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Paywall, https://www.minervamedica.it/en/journals/europa-medicophysica/article.php?cod=R33Y9999N00A21010401
 
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