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

This is a very interesting paper, albeit coauthored by a not-so popular Jos van der Meer.

They make some novel hypotheses that I think have been sorely lacking in recent discussion of COVID-19 pathology and it's relationship with ARDS.

But they also state some things I find questionable, such as:

Oh really, why does the epidemiology suggest that it is one of the strongest risk factors?

But ARDS due to COVID-19 cannot be assumed to be the same as classical pulmonary edema and requires fresh clinical observations of hydrostatic pressure and the like. There is reason to suggest that SARS-COV-2 is uniquely altering ACE2 pathways in ways that don't exist in those cited papers.

An interesting hypothesis, I think they are onto something here.

The timing is indeed coincidental...

They propose blockage of (Bradykinin) B1 and B2 receptors

But one of the comments suggests caution:

 

not everyone may develop that ace2 problems to a "threatening" extend.
it could have a genetic component.

it would be very very very interesting to see, if people with these problems respond super-well to ivermectin.

im wondering... if for quite a few of those "ace" patients other meds, like these ace2 inhibitors or other blockers may bring you to that point "between a hard place or a rock" or whatever this saying goes...

(ivermectin has shown already as something that may help, as so many other odd meds...)

today, in a german newspaper a swiss doctor stated, that ppl "of course" die of "cardiac failure"... they may play as if this is "old news", its not. its definitely not. there was no talk about cardiac failure until mid march minimum.

 

https://twitter.com/user/status/1249713002330415106


Interesting if this holds up.


Heading out now for some Marlboros....

 

Potential interventions for novel coronavirus in China: A systematic review

https://onlinelibrary.wiley.com/doi/10.1002/jmv.25707

 

https://twitter.com/user/status/1249726952602296320

 

3/6/2020Disease Briefing: Coronaviruses

https://clarivate.com/wp-content/uploads/dlm_uploads/2020/01/CORONAVIRUS-REPORT-3.6.2020_v1.pdf

 

It is very strange if smokers are more immune becasue smokers are more likely to have cardiac problems, hypertension, asthma and COPD which are all risk factors

 

nicotine may protect from covid replication (when i understood that right)
slysaint postet https://www.s4me.info/threads/the-b...vaccines-treatments.14022/page-13#post-253515

perhaps, nicotine plasters could be added to that covid-meds-lists as well?

otherwise, smokers may have a more severe disease progress... ?

 

with the ace receptor/angiotensin docking of covid virus, it would be interesting to see, if people with high ace/angiotensinII are

- more likely to die
- while having absoluty not the typical flu-symptoms (sneezing, throat...)

people with (high angiotensin II) shouldnt have any "allergy" issues, for example.
guessing, they are also unlikely to sneeze or react any much on whatsoever...

 

Is this only true of of Covid 19? Or might it also be true for other similar viruses. Just wondering if the (normally damaging) changes that occur in smokers' lungs may, rather perversely, help to thwart viral attacks on the lungs? Or even if maybe people's lungs adapt in some way to try and offset the effects of smoking, and if so could that then play a part?

For anyone who does not already know: I have no medical expertise whatsoever. Just wondering if anyone who does have such knowledge might have any thoughts.

 

No knowledge of other viruses but there's something called "cryptogenic organizing pneumonia" (COP), which is an interstitial pneumonia with no known underlying viral or bacterial or fungal cause. "Organizing" means the lung tissue becomes fibrotic and "hardens".

Here, smokers are highly underrepresented, as well, which seems very counter intuitive.

Organizing pneumonia (not kryptogenic because SarsCov2 is identified as the underlying cause) was also found in some Covid cases, accordong this study.

 

https://twitter.com/user/status/1249816957848899589

 

Could there just be another reason entirely why smokers are under-represented in hospitalised cases of Covid 19?

Hospitalised cases of Covid 19 are heavily weighted towards the higher age groups, but smokers are going to be dying of smoking related causes younger than average. Is it simply that fewer smokers are getting Covid in the upper age ranges, because less of them are reaching those ages anyway? Have controlled comparisons been made between smokers and non-smokers, where the only real difference is their smoking?

 

Has this been posted?
https://n.neurology.org/content/neurology/early/2020/04/09/WNL.0000000000009455.full.pdf

 

The UK Biobank is being used to study the coronavirus:

https://www.bbc.co.uk/news/health-52243605

 

The health programme on R4 at 8pm will be talking about clinical trials for coronavirus treatments.

 

Therefore you can perform a statistical trick - smokers without those risk factors are less likely to be hospitalised.

But these studies are inherently biased as they are sampling hospital care rates, rather than the population as a whole and should be looking at mortality rates, (or requiring intubation), rather than merely hospital admissions - there are other behavioural biases involved.

 

One of a series of youtube videos
Coronavirus Pandemic Update 37: The ACE-2 Receptor - The Doorway to COVID-19 (ACE Inhibitors & ARBs)

https://www.youtube.com/watch?v=1vZDVbqRhyM

18minutes long (I lost the drift after 10 minutes but others might understand better).