SARS-CoV-2; CoVID-19; Coronavirus; Updates and Information

[Takkyu_ga_suki]

Not too bad. A bit preliminary. Would like more details on how they did odds ratios to account for various comorbidities.

A large percentage of people these days are deficient in D.

The video claimed 70%. That figured shocked me.

Sure some of it is bad diet and other bad practices, but maybe too much time spent in the office as well. ;-)

 

[Der_Echte]

There could be a lot of links to post with a lot of the research and study with Vitamin C and its positive effects vs virus, but this recent study in China cites a lot of the background and is convenient to see, if you can get through many pages of the background.

This is a study of IV Vit C to treat Corona Virus.

There is the NIH article and the link to the full article on a link from inside the NIH article (NIH somehow doesn't show but the beginning of the text) The link on NIH re-direcs to the bottom science article link.

Intravenous Vitamin C for reduction of cytokines storm in Acute Respiratory Distress Syndrome

https://www.ncbi.nlm.nih.gov/pubmed/32322486

https://www.sciencedirect.com/science/article/pii/S2213434420300153?via=ihub

 

[Baal]

Some years ago they checked vitamin D levels in various hunter and gatherer societies (not many left on the planet), and they found everyone had a vitamin D levels above 40 ng/ml. Very few people in any developed nation are at that level! Normally people are considered "deficient" if they are under 20 ng/ml, which is actually the level that prevents really bad bone disease in kids, not a level that produces optimal health. A lot of people would say that you ought to have a level of at least 30 ng/ml (bearing in mind that different labs use different methods and can come up with slightly different numbers).

Probably the biggest reason for widespread deficiencies is spending all of life indoors. You can't actually get very much from diet except for certain fatty fishes or vitamin D they add to milk and some juice drinks. This is especially true for vegans or vegetarians. I take a supplement, especially these days.

The paper below breaks it down by age, race, and country with helpful maps. The darker your skin is, the more likely you are to be deficient in vitamin D.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4018438/

 

[Baal]

There could be a lot of links to post with a lot of the research and study with Vitamin C and its positive effects vs virus, but this recent study in China cites a lot of the background and is convenient to see, if you can get through many pages of the background.

This is a study of IV Vit C to treat Corona Virus.

There is the NIH article and the link to the full article on a link from inside the NIH article (NIH somehow doesn't show but the beginning of the text) The link on NIH re-direcs to the bottom science article link.

Intravenous Vitamin C for reduction of cytokines storm in Acute Respiratory Distress Syndrome

https://www.ncbi.nlm.nih.gov/pubmed/32322486

https://www.sciencedirect.com/science/article/pii/S2213434420300153?via=ihub

Sadly DE, that paper from some dudes in Saudi Arabia is a hot mess and it appears to have received minimal peer review because it is filled with problems. Normally Elsevier journals do better than that. For example in the section where they claim that ascorbic acid is anti-viral (based on a study that Linus Pauling, by then crazy, did in 1971 using industrial strength concentrations on isolated virus particles) in practically the next sentence they mention that "It was found that a very high-dose of one sodium salt of ascorbic acid (90 mM) kills Candida albicans in-vitro". First, 90 fricking millimolar!!!!!!!!!!! That is almost as high as extracellular sodium, the most abundant entity in extracellular fluid after water. Second, Candida albicans is definitely not a virus.

Too many of the case reports they cite are not adequately documented and are published in journals devoted to "orthomolecular science" which is fancy quackery. Clicking on some of the papers they cite as evidence leads to "results not found", a VERY key one in the context of Covid-19 being number 115. A few times the authors cite themselves, to another review article almost identical to this one and with no clinical data of their own. If one doesn't check and look, one could get the impression that there was something relevant there.

This doesn't mean they are wrong. But I think the paper is a piece of shyte and they should be embarrassed.

If you want to read something far more credible, check this one out. It is more balanced, more thorough, and comes from people with a strong track record (Harvard guys) and it appears in a journal that is actually peer-reviewed rigorously. It includes both positive and negative results and some mention even of the potential risks. They raise some of the same points but they are far more thorough.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6201324/

Here is one actual case report for a virus-induced ARDS (the lowest standard of evidence, and in this case not for Covid-19) from people in Virginia. It is from 2017, and the authors claim to be the first to try high dose IV vitamin C for ARDS. It worked in this case.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295174/

Bear in mind though that we already know that Covid-19 doesn't always produce the effects one expects based on other viruses. So will it work for Covid-19, especially in later stages? Maybe. Anecdotes are out there. I hope so. But far from proven. Probably worth a try.

And none of this means that taking a vitamin C supplement will help you. I do anyway because why not?

 

[NextLevel]

The video claimed 70%. That figured shocked me.

Sure some of it is bad diet and other bad practices, but maybe too much time spent in the office as well. ;-)

Some of it is that it is a fat soluble vitamin, and it is harder for the body to produce and use it optimally if you aren't getting the right fats in your diet.

 

[zeio]

4/26
https://www.theguardian.com/world/2...-drosten-germany-coronavirus-expert-interview

Q: Germany will start to lift its lockdown gradually from Monday. What happens next?
A: At the moment, we are seeing half-empty ICUs in Germany. This is because we started diagnostics early and on a broad scale, and we stopped the epidemic – that is, we brought the reproduction number [a key measure of the spread of the virus] below 1. Now, what I call the “prevention paradox” has set in. People are claiming we over-reacted, there is political and economic pressure to return to normal. The federal plan is to lift lockdown slightly, but because the German states, or Länder, set their own rules, I fear we’re going to see a lot of creativity in the interpretation of that plan. I worry that the reproduction number will start to climb again, and we will have a second wave.

Q: If the lockdown were kept in place longer, could the disease be eradicated?
A: There is a group of modellers in Germany who suggest that by prolonging lockdown here for another few weeks, we could really suppress virus circulation to a considerable degree – bringing the reproduction number below 0.2. I tend to support them but I haven’t completely made up my mind. The reproduction number is just an average, an indication. It doesn’t tell you about pockets of high prevalence such as senior citizens’ homes, where it will take longer to eradicate the disease, and from where we could see a rapid resurgence even if lockdown were extended.

Q: If there were such a resurgence, could it be contained?
A: Yes, but it can’t happen based on human contact-tracing alone. We now have evidence that almost half of infection events happen before the person passing on the infection develops symptoms – and people are infectious starting two days prior to that. That means that human contact-tracers working with patients to identify those they’ve been exposed to are in a race against time. They need help to catch all those potentially exposed as quickly as possible – and that will require electronic contact-tracing.

Q: How close we are to achieving herd immunity?
A: To achieve herd immunity we need 60-70% of the population to carry antibodies to the virus. The results of antibody tests suggest that in Europe and the US, in general, we are in the low single digits, but the tests are not reliable – all of them have problems with false positives – and herd immunity is also not the whole story. It assumes complete mixing of the population, but there are reasons – in part to do with the social networks people form – why the whole population may not be available for infection at any given time. Networks shift, and new people are exposed to the virus. Such effects can drive waves of infection. Another factor that could impact herd immunity is whether other coronaviruses – those that cause the common cold, for example – offer protection to this one. We don’t know, but it’s possible.

4/28
https://www.theguardian.com/world/2...-stay-home-amid-covid-19-infection-rate-fears

Germans have been advised to stay at home as much as possible and continue to apply physical distancing as official data appeared to indicate the spread of the Covid-19 pandemic was once again accelerating.

The basic reproduction number (R), indicating how many new cases one infected person generates on average, has come to be seen as the key indicator over whether restrictions on public life can be loosened after Angela Merkel stressed the importance of keeping the number below one.

On Tuesday, the German government’s disease control agency, the Robert Koch Institute (RKI), announced the reproduction number for Monday 27 April had risen to 1, after having put it as low as 0.7 in mid-April.

Lothar Wieler, the RKI’s president, later specified that the reproduction rate for Monday was 0.96, and there technically still below one.

A really good Rt 101 on what needs to be in place before lifting lockdowns and what to do to keep it suppressed afterwards.

http://www.chelseanewsny.com/news/the-r-factor-NF1117870

The 'R' Factor
An important metric shows that the lockdowns are working in New York

...

In other countries R has become a part of the public conversation. In Hong Kong, the School of Public Health issues a regular update (R was .2516 last Friday). Chancellor Angela Merkel gave the German public a tutorial on R that reminded everyone of her doctoral training in quantum chemistry.

But in the United States we have tended to focus on other data until just the last few days.

 

[Baal]

The value of R is never discussed here, and given the situation in the US would be pretty much impossible to estimate.

But it's about to go up. Count on that.

 

[NextLevel]

The value of R is never discussed here, and given the situation in the US would be pretty much impossible to estimate.

But it's about to go up. Count on that.

Cuomo mentions it quite a bit. It is different in every state/county and it is what states use in a sense to manage their spread. I don't think "never" is fair, strictly speaking.

 

[NextLevel]

Even when people don't speak about R directly, they speak about having 14 days of declining case rates or things like that. Those are all common sense measures of R, I don't think it is wise in general to trust the general public with something that needs an appreciation of exponential functions to understand its significance.

 

[Simas]

excess deaths -no of deaths on top of historic average for the period.
% of those excess deaths reported as covid deaths.


New York attributes 93% of excess deaths to Covid, Istanbul undereports a lot, Jakarta is undereporting massively
https://www.economist.com/graphic-detail/2020/04/16/tracking-covid-19-excess-deaths-across-countries

 

[NextLevel]

View attachment 21307

excess deaths -no of deaths on top of historic average for the period.
% of those excess deaths reported as covid deaths.


New York attributes 93% of excess deaths to Covid, Istanbul undereports a lot, Jakarta is undereporting massively
https://www.economist.com/graphic-detail/2020/04/16/tracking-covid-19-excess-deaths-across-countries

Almost all the excess mortality is found in people over the age of 70 (usually with comorbidities acquired over a life of smoking or diabetic physiology). While this is not trivial and life is important, this is something that is almost never communicated when looking at these charts. They give the impression that everyone is dying when the reality is that mostly old people are getting killed by this disease. The key thing is to protect older people.

 

[Baal]

The problem with merely protecting old people is that it focuses on just one thing: deaths occurring in the immediate phase of the Covid-19 disease. I would argue it is a mistake to focus just on excess mortality right at the moment.

There are very good reasons to think that people who survive this, even people nobody would consider old, are going to have long-lasting health issues as a result. Prediction: some years down the line there will be many cases of pulmonary fibrosis as a direct result of this pandemic, with severely diminished pulmonary function. There will also be substantive increases in chronic kidney disease (which dramatically increases all-cause mortality, not to mention that life on dialysis is shyte and often short). There may well be other issues too. Heart failure, neurological issues, maybe weird autoimmune things. Some of these will disproportionately impact people who for a host of different reasons are not in a position to protect themselves now.

We are not through this thing yet, there are some biomedical likelihoods, which to me strongly indicate that it is a mistake to "just protect old people".

Edit added: Here is more on this. The second one is quite technical and strongly supports the possibility of long term effects in the kidney. It is particularly worrisome that SARS-CoV-2 virus particles are detected in cells of the renal glomerulus that cannot be regenerated. AND, this may be especially severe for a subset of people of West African descent who for certain genetic reasons (so-called ApoL1 G1 and G2 alleles) are at substantially higher risk. And that's a LOT of people in the United States. One last thing, this might happen in people who did not have a particularly severe form of the disease. It may depend on where the virus goes. I should point out that patients with HIV who have never had any symptoms of it, who have never had immune deficiencies, who have been controlled with medications without adverse affects, are now presenting with HIV-induced kidney failure, heart failure, and dementias. And this is happening because (as we now know) the virus didn't just hide in immune cells.

The fact that SARS-CoV-2 can make its way into kidney cells called podocytes (at least according to one study peer-reviewed by one of the more elite journals in the field), is ominous. Same if it can get into the brain or the heart.

https://www.sciencenews.org/article...-some-patients-may-suffer-lasting-lung-damage

http://www.nephjc.com/news/covidaki

 

[Der_Echte]

I am with Next Level in him stating the obvious, but not so often spoken, facts that corona got the weak immune system people, the large majority the very old with co-morbid stuff. I see where he is coming from in saying mainstream news highlights large numbers of total deaths instead of what risks are leading to those totals. I would not believe NL is so narrow focused only on the old (it does pay more of to focus effective actions there) but he said what he said.

I like the thinking that Baal is taking which is more inclusive and holistic in approach - must consider effects of actions and situation and time.

There are a great number of USA people not yet old with wrecked are near wrecked or strong on the path to getting a wrecked microbiome and immune system function. The actions taken the last month or two and the ones to be taken by USA individuals may not with the exposure to corona or future exposure to corona or virus going forward will have effects, short, mid, and long term as Baal is considering and articulating.

Getting natural immunity with exposure and those needing vaccine immunity of an effective vaccine is developed is a start, but there has got to be a lot of reckoning on an individual basis of nutrition and how people take care of immune system.

It will be already difficult as whole host of industries are working against this (mostly big-sugar (lots of sugar wrecks microbiome), big-agra/big-chem (refined gmo grain carbs and pesticide residue wrecks microbiome and immune function), big-livestock (added antibiotics wreck our microbiome) , big Tabaco (years and decades of smoking have bad effect on lungs and immune system)... and we will have a lot to get through with the additional burden of this recent wave which will have those short, mid, and long term impact - both from the virus and from the choices of authorities & individuals.

People also can make poor and lazy choices for lifestyle, have an ability to learn how to keep their body working, but economic realities and what is available are factors as well. Nothing is so simple and easily categorized.

Individuals and society/govt will have a lot to figure out going forward.

Baal hit on some of the possible considerations of longer term impact and there are likey more, just from the virus and also the actions/lack of actions from people and govt.

Anyone remember or were around the few hundred thousand US vets who returned from Iraq/Kuwait in 1991... all kind of short, mid, long term baddies all over the place crazy not so easy for docs to understand right away.

 

[rainneverever]

I doubt Economist's NYC stat is right. I've once downloaded confirmed/probable COVID deaths report from NYC. By Apr 13, 6589 confirmed COVID deaths and 3778 probable COVID deaths (COVID on death cert but PCR result pending). From Mar 11-Apr 13, 8184 deaths not to be known as confirmed or COVID deaths.
https://www1.nyc.gov/site/doh/covid/covid-19-data.page

The average monthly deaths in NYC is ~4500 (4000-5000), see the historic graph in this NYT article. The highest numbers were in winter and lowest in summer, so the expected monthly deaths from mid Mar to mid Apr is around average.
https://www.nytimes.com/interactive/2020/04/10/upshot/coronavirus-deaths-new-york-city.html

Edited: Therefore, the excess deaths in NYC from mid Mar to mid Apr is around 6589+3778+8184-4500=14051, total deaths around 6589+3778+8184=18551, total COVID deaths around 10367.

 

[rainneverever]

Several remdesivir trial results are out today! "Remdesivir" was translated into Chinese by many investors as "people's hope", and Bruce Aylward, WHO's expert team head who led investigation in China, said "There is only one drug right now that we think may have real efficacy and that's remdesivir". I think I've discussed previously that antivirals like remdesivir may work at early stage and it may not work for later stage when dyfunction of multiple organs occurs. Now with more trial results, I guess it is time to believe what you believe lol


Double-blinded, placebo-controlled (2:1) trial on 237 severe patients in China
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31022-9/fulltext


Editor’s Pick: In the absence of any known treatment for COVID-19, remdesivir is one of a handful of experimental drugs undergoing clinical trials worldwide. An Article, published in The Lancet, is the first randomised trial of remdesivir and suggests the antiviral drug does not speed recovery from COVID-19 in critically ill patients. However, while not statistically significant, pre-specified secondary outcomes suggest that time to clinical improvement and duration of invasive mechanical ventilation were shorter in people treated with remdesivir.


28-day mortality was similar between the two groups (22 [14%] died in the remdesivir group vs 10 (13%) in the placebo group; difference 1·1% [95% CI −8·1 to 10·3]).


Double-blinded, placebo-controlled trial by NIAID. 1063 patients (not only severe ones according to trial registration info)
https://www.niaid.nih.gov/news-even...esivir-accelerates-recovery-advanced-covid-19


Preliminary results indicate that patients who received remdesivir had a 31% faster time to recovery than those who received placebo (p<0.001). Specifically, the median time to recovery was 11 days for patients treated with remdesivir compared with 15 days for those who received placebo. Results also suggested a survival benefit, with a mortality rate of 8.0% for the group receiving remdesivir versus 11.6% for the placebo group (p=0.059).


Two dose comparison in severe patients by Gilead (no placebo or standard of care control)
https://www.gilead.com/news-and-pre...l-remdesivir-in-patients-with-severe-covid-19

Clinical outcomes varied by geography. Outside of Italy, the overall mortality rate at Day 14 was 7 percent (n=23/320) across both treatment groups, with 64 percent (n=205/320) of patients experiencing clinical improvement at Day 14 and 61 percent (n=196/320) of patients discharged from the hospital.


They didn't explain why Italy is different and why they looked at morality at Day 14 (I guess they are aware that the course of COVID is long): 5-day group 8% (16/200), 10-day group 11% (21/197), outside Italy 7% (23/320), in Italy 18% (14/77)

 

[zeio]

The problem with merely protecting old people is that it focuses on just one thing: deaths occurring in the immediate phase of the Covid-19 disease. I would argue it is a mistake to focus just on excess mortality right at the moment.

There are very good reasons to think that people who survive this, even people nobody would consider old, are going to have long-lasting health issues as a result.

https://www.theguardian.com/society...f-rare-syndrome-in-children-reported-globally

More cases of 'Covid-linked' syndrome in children

Doctors around the world have reported more cases of a rare but potentially lethal inflammatory syndrome in children that appears to be linked to coronavirus infections, Ian Sample and Denis Campbell report.

Nearly 100 cases of the unusual illness have emerged in at least six countries, with doctors in Britain, the US, France, Italy, Spain and Switzerland now reported to be investigating the condition.

...

Many of the children having treatment for the new syndrome have tested positive for coronavirus, but others have not. That could mean that the syndrome is not related to coronavirus, that the children had cleared the virus before they were tested, or that the test missed the infection.

Some doctors suspect the syndrome is a “post-infection inflammatory response” where the immune system overreacts in the wake of an infection. This would suggest that in some children the disease has two phases – the initial infection and a secondary immune response that takes hold later.

 

[Baal]

Several remdesivir trial results are out today! "Remdesivir" was translated into Chinese by many investors as "people's hope", and Bruce Aylward, WHO's expert team head who led investigation in China, said "There is only one drug right now that we think may have real efficacy and that's remdesivir". I think I've discussed previously that antivirals like remdesivir may work at early stage and it may not work for later stage when dyfunction of multiple organs occurs. Now with more trial results, I guess it is time to believe what you believe lol


Double-blinded, placebo-controlled (2:1) trial on 237 severe patients in China
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31022-9/fulltext


Editor’s Pick: In the absence of any known treatment for COVID-19, remdesivir is one of a handful of experimental drugs undergoing clinical trials worldwide. An Article, published in The Lancet, is the first randomised trial of remdesivir and suggests the antiviral drug does not speed recovery from COVID-19 in critically ill patients. However, while not statistically significant, pre-specified secondary outcomes suggest that time to clinical improvement and duration of invasive mechanical ventilation were shorter in people treated with remdesivir.


28-day mortality was similar between the two groups (22 [14%] died in the remdesivir group vs 10 (13%) in the placebo group; difference 1·1% [95% CI −8·1 to 10·3]).


Double-blinded, placebo-controlled trial by NIAID. 1063 patients (not only severe ones according to trial registration info)
https://www.niaid.nih.gov/news-even...esivir-accelerates-recovery-advanced-covid-19


Preliminary results indicate that patients who received remdesivir had a 31% faster time to recovery than those who received placebo (p<0.001). Specifically, the median time to recovery was 11 days for patients treated with remdesivir compared with 15 days for those who received placebo. Results also suggested a survival benefit, with a mortality rate of 8.0% for the group receiving remdesivir versus 11.6% for the placebo group (p=0.059).


Two dose comparison in severe patients by Gilead (no placebo or standard of care control)
https://www.gilead.com/news-and-pre...l-remdesivir-in-patients-with-severe-covid-19

Clinical outcomes varied by geography. Outside of Italy, the overall mortality rate at Day 14 was 7 percent (n=23/320) across both treatment groups, with 64 percent (n=205/320) of patients experiencing clinical improvement at Day 14 and 61 percent (n=196/320) of patients discharged from the hospital.


They didn't explain why Italy is different and why they looked at morality at Day 14 (I guess they are aware that the course of COVID is long): 5-day group 8% (16/200), 10-day group 11% (21/197), outside Italy 7% (23/320), in Italy 18% (14/77)

You beat me to it. The data convinced Fauci, in any case. He said "“It is the first truly high-powered, randomized placebo control trial,” showing a beneficial effect of any drug so far.

And I completely agree with Rain that early vs late are going to probably require different therapeutic strategies. At early stages anti-viral will probably work better. At later stages there is a ton of inflammation, cytokines are going crazy, little clots are forming all over the place, etc.etc.

 

[NextLevel]

One of the guys I like to listen to, David Diamond, who became a speaker on cholesterol because of the problems he saw with the lipid heart disease hypothesis, always liked to mention that most of the processes that caused heart disease raised clotting factors. Since a little knowledge can be a dangerous thing, I wonder whether this virus/disease is raising clotting factors by raising inflammation or doing so through a different mechanism and if so what mechanism... maybe a healthy person can resist but someone with really high clotting just gets the organ damage etc...

 

[rainneverever]

High D-dimer level in blood was discussed by front line doctors early on and they regarded it as one of the indicators of poor prognosis.

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30566-3/fulltext published on Mar 11
The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage

https://www.medpagetoday.com/infectiousdisease/covid19/85577
Endothelial damage and subsequent clotting is common in severe and critical COVID-19 coronavirus, which may have implications for treatment, Chinese clinicians said at a webinar co-sponsored by the Chinese Cardiovascular Association and American College of Cardiology. (youtube video https://youtu.be/CjEhV68GcD8 Mar 19)
"Clots in the small vessels of all organs, not only the lungs but also including the heart, the liver, and the kidney," were described by Bin Cao

Bin Cao is the principle investigator who led remdesivir trial and lopinavir–ritonavir trial in China.
BTW, lopinavir–ritonavir (anti-HIV drug) trial was on severe patients. The mortality of control here was much worse than remdesivir trial control group. One can argue that the subjects from each trial do not reflect the infected population (sampling bias).
https://www.nejm.org/doi/full/10.1056/NEJMoa2001282
The 28-day mortality was numerically lower in the lopinavir–ritonavir group than in the standard-care group for either the intention-to-treat population (19.2% vs. 25.0%; difference, −5.8 percentage points; 95% CI, −17.3 to 5.7) or the modified intention-to treat population (16.7% vs. 25.0%; difference, −8.3 percentage points; 95% CI, −19.6 to 3.0)

In terms of the molecular mechanisms why clotting happened in COVID, as I previously said, basic research can definitely provide answers. Not now. Most labs are closed now And without molecular mechanisms, clinicians still should watch D-dimer level and consider anticoagulant drugs (I know some front line doctors in US do).

 

[Baal]

One of the guys I like to listen to, David Diamond, who became a speaker on cholesterol because of the problems he saw with the lipid heart disease hypothesis, always liked to mention that most of the processes that caused heart disease raised clotting factors. Since a little knowledge can be a dangerous thing, I wonder whether this virus/disease is raising clotting factors by raising inflammation or doing so through a different mechanism and if so what mechanism... maybe a healthy person can resist but someone with really high clotting just gets the organ damage etc...

I think it is too early to know. However a very likely mechanism is that the virus infects some of the endothelial cells that form the inner layer of the blood vessels and which typically express ACE-2, a known receptor for SARS-CoV-2. In this hypothesis the virus usually enters the body through the respiratory tract and certainly infects type II pneuomocytes but also enters adjacent microvasculature and infects endothelial cells (especially in the pulmonary vasculature, but also throughout the body). This produces a lesion in the endothelial layer that in turn can result in activation of clotting mechanisms. The fact that endothelial damage can lead to thrombosis is well known, normally a healthy endothelium secretes factors that inhibit clotting, but damaged or dysfunctional endothelial cells stop doing that. (It is a bit more complex than this but you get the idea). Endothelial dysfunction also causes the arterioles and venuoles contract. One thing that is attractive about this idea is that in large measure the main complications of diabetes are also seen first in endothelium (this is what produces the microvascular complications that lead to blindness, heart attacks and strokes, as well as sometimes necessitating amputations in the periphery). The kidney disease caused by diabetes is also microvascular in nature but probably involves other cells more than the endothelial cells. This could explain why these types of patients do much worse in the short run. Some of the weird skin lesions people are seeing in Covid-19 look a lot like diabetic vascular disease to me.

This idea can also partially explain some of the weird features of Covid-19 (the fact that it is not really a classical ARDS in a lot of patients). Instead there is a lot of so-called "silent hypoxemia" where the lungs have good mechanical properties but gas exchange is impaired, so patients seem to breathe ok but have crazy low blood oxygen.

A lot of critical care docs are now infusing the really sick patients with as much of various anticoagulants (e.g.) heparin as the patients can tolerate. Endothelial involvements suggests several other things that might help too.

Here is a paper in Lancet showing SARS-CoV-2 particles in endothelial cells of Covid-19 patients.

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30937-5/fulltext