Coronavirus

[jerry33]

Real world you might have more than 10000 units of coronavirus hanging around. You don't need to up the temperature though, you could do two 15 minute cycles back to back and that would kill more virus than a single cycle.

It's all a matrix of heat over time. Increase the temp and you can do it for less time to get the same effect but you also increase damage to items in the car that are susceptible to heat and aren't viruses. Increase the time at the same temp and it's more effective but doesn't expose materials in the car to the higher temps.

True. The concern is that if you only kill most of them, will you create a strain of heat resistant virus?

 

[NicoV]

Belgium is transitioning from a period of (much) more than normal deaths, to a less than normal number of deaths: Ondersterfte na weken van oversterfte

This seems to be a common effect after an epidemic as weak people that would have died anyway in the near future, died early because of the pandemic.

 

[AlanSubie4Life]

Belgium is transitioning from a period of (much) more than normal deaths, to a less than normal number of deaths: Ondersterfte na weken van oversterfte

This seems to be a common effect after an epidemic as weak people that would have died anyway in the near future, died early because of the pandemic.

Suspect it may be some other cause, like continued caution and lack of complete resumption of normal activity.

Why do I say that? Because the average years of life lost turns out to be about 11 years (will depend on the details of the population, but that’s close enough). So certainly it will reduce future mortality, but that reduction in future death will be spread over quite a long time period - on average about 10 years.

 

[dfwatt]

True. The concern is that if you only kill most of them, will you create a strain of heat resistant virus?

In a word no.

 

[dhanson865]

Someone messaged me and said that using 7 day buckets for the data can be manipulated, so I'm doing another version of the graph with a 4 day moving average to split the difference between the single day source data and a weekly view that I wanted to look at.

In my original comparison we entered phase one at 30 new cases per week and exited phase one at 60 cases per week. His complaint was that is cherry picking since shifting the numbers by 2 days makes that comparison 26 vs 31.

The moving average was 6 at the start of the phase 1 reopening and was at 9.75 at the end of the phase 1 reopening. Not double, but clearly an increase.

 

[Doggydogworld]

Belgium is transitioning from a period of (much) more than normal deaths, to a less than normal number of deaths: Ondersterfte na weken van oversterfte

This seems to be a common effect after an epidemic as weak people that would have died anyway in the near future, died early because of the pandemic.

There may be some "harvesting effect", but IMHO it's more due to the lockdowns (which are still partly in place). Euromomo shows a sharp decline in deaths among kids when the lockdowns started, indicating a decline in non-COVID deaths (accidents, flu, etc.). This decline in non-COVID deaths would logically apply across all age groups, but was more than offset by COVID deaths in older age brackets. As COVID deaths decline the non-COVID decline becomes visible across more age groups.

Where did you find the data for "all other causes combined" for Spain? A very quick calculation for the US came to a roughly similar result, at least by order of magnitude, using unverified numbers though. And I don't quite understand why that calculation would involve calculating age groups separately. That only seems to invite avoidable errors.

I didn't have data for Spain. It was an order-of-magnitude comparison, and mortality vs age group doesn't vary that dramatically among developed countries. I saw a chart in a "just a flu" article which compared age-stratified IFR to all-cause mortality. The article was crap so I didn't save a link, but I checked enough points on the chart using US data to verify it was legit. I seems like a good way to present COVID death risk.

FWIW, the 18,722 and 26,744 came from this report. I don't read Spanish, but 26,744 is in Table 2 and 18,722 in Table 3.

 

[dfwatt]

Having trouble wrapping my head around the molecular mechanism on statins. ACE inhibitors I could see a potential mechanism (note - that is NOT a treatment recommendation at this time from me).

It's a puzzle box for sure.

Some clues in this paper on the

Pleiotropic Effects of Statins on the Vascular Tissue

Abstract
The statins are lipid-lowering agents that act by inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme is responsible for the conversion of HMG-CoA to mevalonate. Products of mevalonate metabolism are critical for several cellular processes of eukaryotic cells, and inhibition of the mevalonate pathway by statins has pleiotropic effects. It has been reported that statins inhibit the migration and proliferation of vascular smooth cells (VSMCs), reduce interleukin-6 expression in VSMCs, improve endothelium-dependent vasomotion, and inhibit the expression of plasminogen activator inhibitor-1 and matrix metalloproteinases in endothelial cells. These effects of statins are independent of plasma cholesterol level, and are completely blocked by exogenous mevalonate and some isoprenoids. These findings suggest that statins exert direct antiatherosclerotic effects on the vascular wall beyond their effects on plasma lipids.

Several of its indirect targets (particularly IL-6) are upregulated in COVID-19, or by the renin-angiotensin system, so it may counter some effects of COVID19 infection. There was that most interesting chart in the Lancet paper on odds ratios around HCQ combos that shown statin use having a somewhat protective odds ratio.

here'a another piece that notes anti-inflammatory effects on vascular wall.
But all of this is a far cry still from RCT evidence showing a positive effect in COVID19.

 

[KenC]

Just saw this headline: Ford's police SUVs will heat up to 133 degrees to disinfect the interior - CNN

What do you think, should Teslas have a COVID Sterilization Mode?

So, just park your car in the sun, and don't turn on overheat protection, and you're set.

 

[shinytop]

Overheat protection only works for 12 hours after you put the car in park. During this stay at home my X goes days without driving. Checking yesterday afternoon about 3 PM the interior of the car was reporting 155 degrees.

 

[N5329K]

Useful vaccine tracker here:
COVID-19 vaccine tracker

 

[dfwatt]

Just saw this headline: Ford's police SUVs will heat up to 133 degrees to disinfect the interior - CNN

What do you think, should Teslas have a COVID Sterilization Mode?

In a word, no.

 

[Norbert]

FWIW, the 18,722 and 26,744 came from this report. I don't read Spanish, but 26,744 is in Table 2 and 18,722 in Table 3.

Yes, I have seen it. This is a different report, not from the study itself. As far as I can tell, they are published by the same website ("mscbs" apparently "Ministerio de Sanidad"), but the study was done by "Instituto de Salud Carlos III", whereas the report with the death numbers (which you linked here) is titled to be by "Centro de Coordinación de Alertas y Emergencias Sanitarias".

So any calculation or table showing both (infection level and death numbers, or IFR) together has been created by someone else, who combined the study with other data. The problem isn't so much the data itself (although it lacks time-of-death lag), but it seems that this hasn't always been done in a good way, in one case (not the one you quoted) apparently in a very misleading way (making more than one significant error in the same direction). So be very careful with any report or claim about that study that includes death numbers or an IFR estimate. (Including my own, of course.)

 

[SVMike]

And the fourth problem is that hospitals were also pulling that zero-inventory crap, keeping only enough supplies to last until the next shipment, and when the next shipment didn't come, they were screwed. I mean, I'm exaggerating a little bit here, but not by nearly as much as I wish I were.

In December I had an unscheduled dentist visit (crown came off). I was brought to an extra room in the back, not the front area I normally was treated in. I walked by a long hallway covered floor to ceiling on both sides with 6" deep shelves full of masks and gloves...all for an office of ~10 dentists. I asked why such a stockpile? The dentist said -- just in case.

 

[SVMike]

Somehow, we’re fine printing thousands of dollars for everyone, but can’t seem to get the necessary masks to everyone.

The Treasury should buy some elastic and attach to each side of a dollar bill

 

[SVMike]

I am under the impression that we don’t yet have proof that having had COVID gives you immunity for very long.

Proof?

I'm not a doctor. But we can do simulations and projections from other viruses. But actual proof requires people who have recovered actually living and not getting reinfected for the time duration that we want to see immunity for.

 

[SVMike]

I'm thinking of the ones that get between the material and in cracks that don't get the full temperature. There could be quite a lot of those.

Why? Because infected people cough onto their hands and stick their fingers into these cracks?
Or the germs crawl into cracks to stay safe from the heat?

Given the tiny percentage of transmission that is from surfaces as opposed to airborne, this may be Much Ado for a little benefit.

How about cracking the windows and turning on the fan for 2 minutes?

 

[Norbert]

Someone messaged me and said that using 7 day buckets for the data can be manipulated, so I'm doing another version of the graph with a 4 day moving average to split the difference between the single day source data and a weekly view that I wanted to look at.

In my original comparison we entered phase one at 30 new cases per week and exited phase one at 60 cases per week. His complaint was that is cherry picking since shifting the numbers by 2 days makes that comparison 26 vs 31.

The moving average was 6 at the start of the phase 1 reopening and was at 9.75 at the end of the phase 1 reopening. Not double, but clearly an increase.

View attachment 546748

I'm not so sure about that. With a lot of ups and down, there are always problems one way or the other.

If I look at the 4 day moving average, and do an additional interpolation in my mind, I'd think the first value should be around 3.5, and the second around 7. (Although the second depends on how it will continue.)

That's still double.

The main problem is that you have an exceptional upswing at the end, and not enough data to tell if that's an outlier or the beginning of a real trend.

I haven't used 7 day buckets very much yet, but they seem promising to me. If you have the option and patience (or software), it might be worth trying to move the cut off points between the buckets. But in this case you can tell it is still difficult to make a judgement because the 7 day buckets still have a lot of up and down. So you might think of using 14-day buckets in this case, starting at the end going backwards. That will probably show a much more even picture, but not answer your question of what to make of the upswing at the end.

However you do it, I think the problem is in this case you need future data to evaluate the upswing-or-not at the end.

EDIT: If you take your 7 day buckets and combine them into 14 days buckets, starting at the end, you get this sequence:
48, 47, 24, 30.5, 42.5.
This is much smoother, but if you move the cut off points, it probably wouldn't go as low as 24. That may or may not be better. It still suggests a strong incline in the last 6 weeks

 

[linux-works]

How about cracking the windows and turning on the fan for 2 minutes?

uhm, phrasing?

 

[Norbert]

NPR article about Indiana study, mentioned by Carl Bergstrom on twitter:
Carl T. Bergstrom on Twitter

The story: Antibody Tests Point To Lower Death Rate For The Coronavirus Than First Thought

It references the Indiana study announcement: IU, ISDH release preliminary findings about impact of COVID-19 in Indiana: News at IU: Indiana University

The two relevant passages:

After analyzing these test results, IUPUI public health researchers determined that during the last week of April, 1.7 percent of participants tested positive for the novel coronavirus and an additional 1.1 percent tested positive for antibodies -- bringing the estimated population prevalence of the virus in the state to 2.8 percent, or approximately 186,000 Hoosiers who were actively or previously infected as of May 1, Menachemi said.

IUPUI scientists estimate the infection-fatality rate for the novel coronavirus in Indiana to be 0.58 percent, making it nearly six times more deadly than the seasonal flu, which has an infection-fatality rate of 0.1, according to the U.S. Centers for Disease Control and Prevention.

Suspecting that they didn't use any death lag, I checked the official death numbers here: ISDH - Novel Coronavirus: Novel Coronavirus (COVID-19)

For May 1, the number is 1,177. However even 1,177 / 186,000 is already 0.63%. So their IFR estimate is lower even without considering death lag.

The number for May 16 is 1,692, resulting in 0.91%. Add just a few probable deaths, let alone excess deaths, and it is over 1%.

 

[deonb]

It doesn't need to be perfect. It takes a measurable dose of virus (several hundred particles) to cause an infection, so killing most of them (e.g. 99%) is just as effective as killing all of them.

I never understood the virtue of that. The same goes for Clorox - killing "99%" of virusses.

A single sneeze contains about 200 million viral particles. If you kill 99% of them there are still 2 million left. It takes just a few thousand to make you sick. So...