COVID-19 Coronavirus Containment Efforts

[Keith_McClary]

Having family elders live with their children instead of living independently in a far-away state would provide more supervision and support during emergencies.

On the other hand:
Italy's Coronavirus crisis was accelerated because young Italians spend more time with elderly relatives and took illness home from the cities to the countryside, Oxford scientists say

 

[atyy]

The COVID-19 vaccine development landscape
Tung Thanh Le, Zacharias Andreadakis, Arun Kumar, Raúl Gómez Román, Stig Tollefsen, Melanie Saville & Stephen Mayhew
Nature Reviews Drug Discovery, 9 April 2020
https://www.nature.com/articles/d41573-020-00073-5

 

[mfb]

Antibody tests are there

At technologyreview.com
German source

In a particularly affected German town of 12,500 people they tested a representative sample of 1000, the results of 500 are in. 14% had antibodies, 2% had the virus, in total 15% had contact with the virus (that suggests 1% had both the virus and antibodies).
Based on this study the town had a case fatality rate of 0.37%. Calculated back that means 7 deaths in ~1900 infections, so don't interpret too much into that number.

They also outline a process by which social distancing can be slowly unwound, especially given hygienic measures, like handwashing, and isolating and tracking the sick. They think if people avoid getting big doses of the virus—which can happen in hospitals or via close contact with someone infected—fewer people will become severely ill, “while at the same time developing immunity” that can help finally end the outbreak.

Edit: Interestingly, this study shows a very low number of antibodies in some recovered patients with weak symptoms.

 

[atyy]

Interesting preprint about the German situation

https://www.medrxiv.org/content/10.1101/2020.04.04.20053637v1
Estimate of the development of the epidemic reproduction number Rt from Coronavirus SARS-CoV-2 case data and implications for political measures based on prognostics
Authors: Sahamoddin Khailaie, Tanmay Mitra, Arnab Bandyopadhyay, Marta Schips, Pietro Mascheroni, Patrizio Vanella, Berit Lange, Sebastian Binder, Michael Meyer-Hermann

Abstract: The novel Coronavirus SARS-CoV-2 (CoV) has induced a world-wide pandemic and subsequent non-pharmaceutical interventions (NPI) in order to control the spreading of the virus. NPIs are considered to be critical in order to at least delay the peak number of infected individuals and to prevent the health care system becoming overwhelmed by the number of patients to treat in hospitals or in intensive care units (ICUs). However, there is also increasing concern that the NPIs in place would increase mortality because of other diseases, increase the frequency of suicide and increase the risk of an economic recession with unforeseeable implications. It is therefore instrumental to evaluate the necessity of NPIs and to monitor the progress of containment of the virus spreading. We used a data-driven estimation of the evolution of the reproduction number for viral spreading in Germany as well as in all its federal states. Based on an extended infection-epidemic model, parameterized with data from the Robert Koch-Institute and, alternatively, with parameters stemming from a fit to the initial phase of CoV spreading in different regions of Italy, we consistently found that the reproduction number was turned down to a range near 1 in all federal states. We used the latest reproduction number as a starting point for the simulation of epidemic progression and varied the reproduction number, mimicking either release or strengthening of NPIs. Germany is currently, April 3rd, 2020, at the border line of a reproduction number between the scenarios of major immunisation of the population or eradication of the virus. We strongly recommend to keep all NPIs in place and suggest to even strengthen the measures in order to accelerate reaching the state of full control, thus, also limiting collateral damage of the NPIs in time.

 

[chemisttree]

Oh really.
https://www.msn.com/en-us/news/us/more-than-930-coronavirus-cases-in-kc-metro-with-3-new-deaths-tied-to-kck-clusters/ar-BB12lIB6:
https://www.kansas.com/news/coronavirus/article241810656.html#adnrb=900000
https://www.kansascity.com/news/coronavirus/article241863906.html

I'll leave the absurdly obvious conclusion to readers.

Just imagine how many cases there would be if they hadn’t prayed away most of the virus.

 

[Ygggdrasil]

There are also multiple strains of Coronavirus so while you may have beaten one strain, there's another right around the corner perhaps not a virulent since you've battled its cousin but still something you can get.

https://www.newscientist.com/articl...are-there-two-strains-and-is-one-more-deadly/

Yeah, I have learned there are reportedly 8 strains of SARS-CoV-2 in the world. We need nine lives!

I think we discussed this earlier in the thread (there should be an informative post by @Ygggdrasil somewhere back there), and this finding is likely over-interpreted (ie. there are two "strains", but the data is not strong enough to support the idea that one is more deadly than the other).

Here is what I have said about the different "strains" of the virus in previous posts:

The paper making the claim about two different strains of the virus has been criticized by other researchers in the field:

An analysis of genetic data from the ongoing COVID-19 outbreak was recently published in the journal National Science Review by Tang et al. (2020) 84. Two of the key claims made by this paper appear to have been reached by misunderstanding and over-interpretation of the SARS-CoV-2 data, with an additional analysis suffering from methodological limitations. [...] Given these flaws, we believe that Tang et al. should retract their paper, as the claims made in it are clearly unfounded and risk spreading dangerous misinformation at a crucial time in the outbreak.

http://virological.org/t/response-to-on-the-origin-and-continuing-evolution-of-sars-cov-2/418

According to the Tang paper, the S and L strains they identify are primarily differentiated by two mutations, one in the orf1ab gene and the other in the ORF8 gene. Neither of these genes are expressed on the surface of the virion, so the mutations will not affect immunity to the virus, and I would expect immunity to one "strain" to confer immunity to the other "strain." The spike protein is the main protein on the surface of the virus, so scientists should monitor mutations in the spike protein to find potential mutations that could affect immunity against the virus.

Regarding the eight "strains" of the virus, the fact that we observe different genotypes because the virus has accrued various mutations, does not mean that these different "strains" of the virus are capable of re-infecting individuals. As an analogy, human individuals differ by ~20 million base pairs, but (as far as we know) all are equally susceptible to the Coronavirus (so to the virus, there is only one strain of human). Only very specific mutations could allow a human to be immune from the virus (e.g. in the case of HIV), and likewise, only very specific mutations in the SARS-CoV-2 virus would allow it to evade immunity in vaccinated individuals.

Thus, many mutations will not have any effect on the virus, and we would mainly care about mutations that affect the behavior of the virus. So far, we have not seem much meaningful change to the viral genome, and the various mutations that differentiate the "strains" (while useful for tracking the spread of the virus) are not expected to affect our immunity to the virus:

Since the start of the pandemic, the virus hasn’t changed in any obviously important ways. It’s mutating in the way that all viruses do. But of the 100-plus mutations that have been documented, none has risen to dominance, which suggests that none is especially important. “The virus has been remarkably stable given how much transmission we’ve seen,” says Lisa Gralinski of the University of North Carolina. “That makes sense, because there’s no evolutionary pressure on the virus to transmit better. It’s doing a great job of spreading around the world right now.”

There’s one possible exception. A few SARS-CoV-2 viruses that were isolated from Singaporean COVID-19 patients are missing a stretch of genes that also disappeared from SARS-classic during the late stages of its epidemic. This change was thought to make the original virus less virulent, but it’s far too early to know whether the same applies to the new one.

https://www.theatlantic.com/science/archive/2020/03/biography-new-coronavirus/608338/
(note: this article from the Atlantic is a great, popular press summary of what we know about how the virus differs from other coronaviruses, and how those differences may lead to its success in spreading across the globe).

Now, that is not to say that the virus won't or cannot mutate to evade immunity. These types of mutations are certainly possible, and people are monitoring virus sequences to monitor for that possibility. Because the immune system recognizes the protein on the surface of the virus (the spike protein), it is very important to monitor changes to the spike protein as these types of mutations do carry the possibility of altering how our immune system recognizes the virus.

A greater concern is some of the research mentioned by @mfb suggesting that some fraction of people with mild COVID-19 infections have very low levels of antibodies against the virus after recovery.

 

[kyphysics]

That's likely to be a bad idea. See this:

someone needs to get this info. to that doctor then

 

[kyphysics]

Edit: Interestingly, this study shows a very low number of antibodies in some recovered patients with weak symptoms.

a.) SOME antibodies are better than none, though, right?
b.) Would that mean you'd need to recover from a severe case of COVID-19 to get LOTS of antibodies?
c.) If you recovered from a weak case and have few antibodies, does that mean you'd not necessarily be able to fight off the virus again if exposed?

I know we're still early in data collection/analysis and any answers may just be preliminary or speculative, but still asking anyways.

 

[atyy]

a.) SOME antibodies are better than none, though, right?
b.) Would that mean you'd need to recover from a severe case of COVID-19 to get LOTS of antibodies?
c.) If you recovered from a weak case and have few antibodies, does that mean you'd not necessarily be able to fight off the virus again if exposed?

I'm not sure, but the post-recovery antibody level has also been discussed in the context of using convalescent plasma for treatment, where it makes sense that one would need high antibody levels. Interestingly, this review says that in other diseases, there may be non-neutralizing antibodies that contributed to recovery.

"The latter study highlights a challenge in using convalescent sera, namely, that some who recover from viral disease may not have high titers of neutralizing antibody (23). Consistent with this point, an analysis of 99 samples of convalescent sera from patients with SARS showed that 87 had neutralizing antibody, with a geometric mean titer of 1:61 (3). This suggests that antibody declines with time and/or that few patients make high-titer responses. It is also possible that non-neutralizing antibodies are produced that contribute to protection and recovery, as described for other viral diseases (24–26)."

 

[Keith_McClary]

Flow analyses to validate SARS-CoV-2 protective masks
About distance rules, mouth-nose protection, particle filtering respiratory protection, filter materials and mask manufacturing

Christian J. Kähler, Rainer Hain University of the Bundeswehr Munich Institute of Fluid Mechanics and Aerodynamics Werner-Heisenberg-Weg 39 85577 Neubiberg Germany

 

[mfb]

The global official death toll (sum of the official numbers) exceeded 100,000. The real value is probably quite a bit higher. The US death toll reached Italy's number.
1.7 million confirmed cases, rising at 100,000 per day.

A report that some mutations in humans might provide some resistance against the disease:
https://www.researchgate.net/publication/340461531_Structural_Variations_in_Human_ACE2_may_Influence_its_Binding_with_SARS-CoV-2_Spike_Protein

Most ACE2 variants showed similar binding affinity for SARS‐CoV‐2 spike protein as observed in the complex structure of wild type ACE2 and SARS‐CoV‐2 spike protein. However, ACE2 alleles, rs73635825 (S19P) and rs143936283 (E329G) showed noticeable variations in their intermolecular interactions with the viral spike protein. In summary, our data provide structural basis of potential resistance against SARS‐CoV‐2 infection driven by ACE2 allelic variants.

 

[bhobba]

New Zealand and Australia both report falling numbers of new cases. It is possible to stop this virus early on if the countries act fast enough.

The government in Aus put in our current restrictions about mid March, which are somewhere between level 2-3, but are being tweaked all the time so now we probably are at level 3. When this was bought in all commentators, including me at the time, thought we would be at level 4 (ie total lockdown) in a few days. It didn't happen. It is now thought we imposed them just in a nick of time. We still have people ignoring it, but the police are increasingly clamping down hard on violations - so much so quite a few people say they sometimes are silly eg someone fishing in a tinny away from anyone. I think over time we will get better at when to strongly enforce the rules, and when to be more lenient. But in general experts are optimistic here in Aus:
https://www.abc.net.au/news/2020-04...ns-on-the-cusp-of-slowing-paul-kelly/12141050

Thanks
Bill

 

[kyphysics]

https://www.bloomberg.com/news/arti...uld-be-ready-in-six-months-times?srnd=premium
Coronavirus Vaccine Could Be Ready in Six Months: Times

A vaccine against the Coronavirus could be ready by September, according to a scientist leading one of Britain’s most advanced teams.

Sarah Gilbert, professor of vaccinology at Oxford University, told The Times on Saturday that she is “80% confident” the vaccine would work, and could be ready by September. Experts have warned the public that vaccines typically take years to develop, and one for the Coronavirus could take between 12 to 18 months at best.

In the case of the Oxford team, however, “it’s not just a hunch, and as every week goes by we have more data to look at,” Gilbert told the London newspaper.

Thoughts from the crew here?

 

[Astronuc]

https://www.bloomberg.com/news/arti...uld-be-ready-in-six-months-times?srnd=premium
Coronavirus Vaccine Could Be Ready in Six Months: Times
Thoughts from the crew here?

http://www.ox.ac.uk/news/2020-02-07-oxford-team-begin-novel-coronavirus-vaccine-research

The Jenner Institute at the University of Oxford has agreed a contract with Italian manufacturer Advent Srl to produce the first batch of a novel Coronavirus vaccine for clinical testing.

The vaccine ‘seed stock’ is currently being produced at the University’s Clinical Biomanufacturing Facility, and will be transferred to Advent who will initially produce 1,000 doses for the first clinical trials of the vaccine, ChAdOx1 nCoV-19.

More importantly,

The vaccines are produced using a safe version of an adenovirus; another virus that can cause a common cold-like illness. The adenovirus has been modified so that it cannot reproduce within the body, and the genetic code to provide instructions for making the Coronavirus Spike protein . . .

The body then forms antibodies to the Spike protein.

 

[bhobba]

Thoughts from the crew here?

We are in uncharted waters here. The testing of the Oxford vaccine is being done here in Aus at the CSIRO's Geelong facility. Interestingly UQ's vaccine testing is being done in Holland. Everyone involved in this is doing everything they can to shorten it. We hear that it will take 12 to 18 months and even that is unprecedented. Well not quite - the Swine Flu Vaccine was developed from 14 May 2009 to November 2009. What is unprecedented is a vaccine in such a short period of time we do not yet have a vaccine for the type of pandemic virus - in this case the Coronovirus. We have been developing vaccines against the Flu for yonks. So we will have to take the 80% estimate as an informed 'guess' from someone on the front lines. The UQ vaccine is timelined for 18 months since it was started in January - but have stated they have consistently beaten their timelines and are hopeful it will be available in mass quantities end of the year - a bit after the Oxford effort. My guess is these people are working around the clock, they are true heroes, and are obviously enthused about what they are doing - they must be to maintain morale. There could be some 'overexubrance' going on. That said it's still encouraging.

I firmly believe, and Australia has shown its possible, if we hold the course we can control the outbreak until we get the vaccine. It is now estimated here, in Aus, only 2.2% of the population will eventually get it - I have posted where some expert thinks we could even wipe it out by getting R0 less than 1 - personally I think that is over optimistic. That's better than the Flu - and we have a vaccine for that - which varies from 3%-11% of the population. So keep the faith - we know how to control this thing - the math is well known - and we will triumph.

Thanks
Bill

 

[mfb]

I don't know what causes the difference but the trends in Australia and NZ look much better than in Europe. Yes, many countries have a downwards trend, but it's a really slow trend. At this rate the healthcare system can handle it but it means we need very long lockdowns unless something else reduces the spread. That will come with many other problems.

The US consistently reports ~30,000 new cases per day now (graph). At 20% positive tests they are still missing many cases. New Jersey has 58,000 positive tests and 62,000 negative tests... New York has 180,000 positive and 260,000 negative tests (tables by state)).

 

[Astronuc]

New signs suggest Coronavirus was in California far earlier than anyone knew
https://www.latimes.com/california/...rus-deaths-signs-of-earlier-spread-california
LA Times reports that it appears that SARS-Cov-2 was circulating in San Francisco area well before March, possibly since December. Two people returning from Wuhan to Santa Clara County tested positive a week before federal approval of emergency testing for the disease on February 4. In this thread, the death on March 4 of a passenger from the Grand Princess (man developed symptoms during period February 11-21 on the cruise) was reported as the first death in California (Placer County), and a second death (70-year old man found deceased at home) occurred on March 6, but that was not publicly announced. A woman who died on March 9 of COVID-19 had become ill by February 20. This woman lived off the same main road about 4 miles as the second from the second fatality.

Stanford's virology laboratory had been looking at 2800 samples collected since January and is finding positive indications of coronavirus.

http://med.stanford.edu/news/all-ne...d-samples-to-track-early-spread-of-virus.html

CNN reported on Why New York appears to be hit so hard by coronavirus
https://www.cnn.com/2020/04/11/opinions/new-york-hit-hard-coronavirus-sepkowitz/index.html

The state's total of 181,026 cases, as of April 11, is higher than Spain's (161,852 cases) and Italy's (152,271), countries with populations many times larger than New York. Of the 20,389 deaths in the United States, 8,627, or 42%, have occurred in New York. Its mortality rate is 4.7%, compared with 3.4% in the rest of the country, and New York City and its suburban counties — Nassau, Suffolk, Westchester and Rockland — are responsible for 93% of the statewide case count. Furthermore, in New York City, the Covid-19 death rate is about 6% higher than most countries.

Mortality rate is based on reported positive cases. Deaths and positive cases are under-reported. CNN reports, "A caution on numbers: Counting cases and mortality rates is difficult because most counting is done by county or borough or parish rather than city, and city of residence may differ from city of diagnosis or death. Even so, New York City is off the charts." Same problem applies to NY state and other states.

Population density explanation may explain some of the difference, but not all of it. New York's densest borough is Manhattan, while relatively sprawling Queens sits at fourth out of five. But Queens has more than twice the cases and twice the rate of cases as Manhattan.

 

[bhobba]

I don't know what causes the difference

My guess, and it's just that, is two factors. Going hard ASAP. We went hard just in a nick of time. And testing and tracing constantly. The US, Italy etc did not go hard enough initially, but seem to be levelling off now - deaths are a lagging indicator. I think they will bring it under control eventually, test and trace very vigorously like we do, then it's just a matter of time until the vaccine - it's coming. In Australia we get 1500-3000 deaths each year from the flu - and we have a vaccine for that - we have about 50-60 so far from the Coronavirus. So when under control, like here, and I believe other countries will eventually be able to do the same, it's not the apocalypse some have predicted. The apocalypse is in the economy, but resisting lifting the restrictions too early, must, and I emphasize must, be resisted. Regardless how bad we get hit economically we can recover. Still some do not seem to get it. Just as an example this Easter people were not allowed to travel except for essential purposes - getting a flu shot, buying food etc. Going to your holiday house over Easter is obviously not essential travel. Yet some are complaining - they have no right to do that to them (in fact they do - the number of armchair constitutional lawyers posting is amazing) and get this one - we want a rebate on our rates since we can't visit them. You have to wonder at their priorities - you really do.

Thanks
Bill

 

[kyphysics]

I don't know what causes the difference but the trends in Australia and NZ look much better than in Europe.

The US consistently reports ~30,000 new cases per day now (graph). At 20% positive tests they are still missing many cases. New Jersey has 58,000 positive tests and 62,000 negative tests... New York has 180,000 positive and 260,000 negative tests (tables by state)).

Could the Australia and NZ difference be attributed to the weather theory: heat, humidity, and sunshine make for lower survival rates of the virus outside of hosts? I know the science is up for debate right now. But, with Australia and NZ having been in summer/warmer weather, maybe that was a difference? Plus, I had read much of Australia's outbreak came from foreign travelers (meaning perhaps people were coming back with it from colder climates).

Speculative question based on speculative/inconclusive science. Still, it's an area I'd like to hear more of if possibly relevant. We won't know until summer here in the U.S. But, lab studies have shown that heat does seem to affect the virus.

 

[kyphysics]

"The seasonality of flu and other respiratory viruses has been known for hundreds of years, if not thousands," says Akiko Iwasaki, a professor of immunobiology at the Yale University School of Medicine. "During the winter months, we tend to have a surge in the cases of respiratory infection, including the influenza viruses."

There are a number of factors that contribute to why the flu arrives in the winter, but Iwasaki says the primary factor is the relative humidity of the air. In winter, the drop in the amount of water vapor in the cold, dry air makes it easier for viruses to become airborne.

We can only hope!

This makes what Iwasaki calls the "perfect setting" for respiratory viruses to transmit.

"When you cough or sneeze or even talk, you're generating these droplets that are coming out of your mouth," she says. "And some of them, if you're infected, will contain virus particles. In very arid conditions, those particles lose the water vapor and they become airborne." This allows the virus to persist in the air for a long time, much longer than in summer.

Of course, she's talking about traditional cold and flu viruses that have been studied for years.

The question is whether the new Coronavirus will also behave this way.

Iwasaki thinks so.

There's some debate in the article - it's worth looking at.

 

[bhobba]

Could the Australia and NZ difference be attributed to the weather theory: heat, humidity, and sunshine make for lower survival rates of the virus outside of hosts?

We have the case of Greenland:
https://en.wikipedia.org/wiki/2020_coronavirus_pandemic_in_Greenland

My guess is in the worst hit countries the virus was circulating longer than originally thought and the response was not vigorous when it was found to be circulating. In Aus the first case was in January and we took action virtually immediately. All along we have taken early and hard action. Plus constant and full tracing. Here in Aus when we trace we find only something like 1% have it, but in other countries it was something like 9% indicating it had been spreading longer and/or the tracing was not as though.

Yes summer will help, but I do not think its the major cause.

Thanks
Bill

 

[chemisttree]

I’d like to be optimistic about a vaccine but we don’t have a single vaccine for any of the coronaviruses that humans get. Perhaps we should put our money on zinc and hydroxychloroquine?

 

[bhobba]

I’d like to be optimistic about a vaccine but we don’t have a single vaccine for any of the coronaviruses that humans get. Perhaps we should put our money on zinc and hydroxychloroquine?

Maybe, we will have to see.

Thanks
Bill

 

[wukunlin]

Could the Australia and NZ difference be attributed to the weather theory: heat, humidity, and sunshine make for lower survival rates of the virus outside of hosts? I know the science is up for debate right now. But, with Australia and NZ having been in summer/warmer weather, maybe that was a difference? Plus, I had read much of Australia's outbreak came from foreign travelers (meaning perhaps people were coming back with it from colder climates).

With regards to NZ, the summers of Auckalnd in my experience is barely hotter than the winters of Taiwan and Southern China, so I'm still skeptical about the weather theory. I think NZ closing its borders rather swiftly and implemented quarantines contributed to the mitigation of the virus the most, together with being quite isolated from the rest of the world and having a low population density.

 

[kyphysics]

We have the case of Greenland:
https://en.wikipedia.org/wiki/2020_coronavirus_pandemic_in_Greenland

My guess is in the worst hit countries the virus was circulating longer than originally thought and the response was not vigorous when it was found to be circulating. In Aus the first case was in January and we took action virtually immediately. All along we have taken early and hard action. Plus constant and full tracing. Here in Aus when we trace we find only something like 1% have it, but in other countries it was something like 9% indicating it had been spreading longer and/or the tracing was not as though.

Yes summer will help, but I do not think its the major cause.

Thanks
Bill

Greenland is interesting. It's population is 56,000-ish. If I'm not mistaken, the geography and physical layout of cities is spread out. It's much easier to coordinate a program of action, presumably, for a smaller sized population than with a larger one. And if there are natural geographic or city-scape features that promote distance between humans, then presumably that helps slow/prevent the spread as well.

Just a guess.

I would't think to completely invalidate the weather theory based on Greenland. It seems weather is just one factor. Geography and city-scape spacing...population size...earlier preventative measures (testing and tracing) all probably have a big impact too (if not more possibly?).

 

[mfb]

I’d like to be optimistic about a vaccine but we don’t have a single vaccine for any of the coronaviruses that humans get. Perhaps we should put our money on zinc and hydroxychloroquine?

There was no need for a vaccine for any Coronavirus so far. 4 of them just cause a common cold. SARS was stopped before vaccine development progressed much, MERS never evolved to spread well among humans.
Zinc and hydroxychloroquine and many others are attempts to treat the disease, and they are not very promising so far. That's very different from a vaccine.

My guess, and it's just that, is two factors. Going hard ASAP. We went hard just in a nick of time. And testing and tracing constantly. The US, Italy etc did not go hard enough initially, but seem to be levelling off now - deaths are a lagging indicator. I think they will bring it under control eventually, test and trace very vigorously like we do, then it's just a matter of time until the vaccine - it's coming.

It's going down faster because it's on a lower level overall so there is more effort per case? That would be very useful for Europe. We'll see.

Globally there are about 60 million deaths per year, or 160,000 per day.
By confirmed deaths COVID-19 killed 7000 per day in the last days, or 4% of all deaths. The actual number will be higher due to some dead people who don't get tested and governments that under-report numbers. If this rate would be sustained over the whole year it would be one of the leading causes of deaths (graphs of other causes).
As comparison: Road accidents are responsible for ~2% of all global deaths.

 

[chemisttree]

There was no need for a vaccine for any Coronavirus so far. 4 of them just cause a common cold. SARS was stopped before vaccine development progressed much, MERS never evolved to spread well among humans.
Zinc and hydroxychloroquine and many others are attempts to treat the disease, and they are not very promising so far.

Perhaps you could adjust your thinking?




$20 per patient to treat sounds very promising to me.

 

[peanut]

Experimental drug remdesivir showed promise in an early analysis (not a randomized control trial); clinical improvement observed in 36 out of 53 (68%).

All received remdesivir for up to 10 days on a compassionate use basis, a program that allows people to use unapproved medicines when no other treatment options are available. Over 18 days, 68% of the patients improved, with 17 of the 30 patients on mechanical ventilation being able to get off the breathing device. Almost half of the patients studied were ultimately discharged, while 13% died.

Several large scale clinical trials are underway to evaluate the benefit of remdesivir for COVID19. One conducted in China could report results end April / early May. Another, sponsored by the US National Institutes of Health, has enrolled patients rapidly as the virus spread throughout the country.

Remdesivir, a broad-spectrum antiviral, is viewed by researchers and doctors as one of the most promising agents against SARSCoV2, the Coronavirus that causes COVID-19, to enter human trials to date. In lab studies conducted prior to the outbreak on numerous compounds, researchers found the drug had potent activity against a wide variety of coronaviruses similar to the new coronavirus.

 

[kyphysics]

False Negatives Raise Doctors' Doubts About Coronavirus Tests
A surprising number of patients have obvious symptoms but still test negative, say doctors

https://www.bloomberg.com/news/arti...est-results-raise-doctors-doubts?srnd=premium

False-negative results from Coronavirus tests are becoming an increasing concern, say doctors trying to diagnose patients and get a grip on the outbreak, as a surprising number of people show up with obvious symptoms only to be told by the tests that they don’t have the disease.

While still more research is necessary to determine the true prevalence of such false-negative results, experts agree that the problem is significant. False negatives not only impede the diagnosis of disease in individual patients and an accurate understanding of the extent of its proliferation, but also risk patients who think they aren't ill further spreading the virus.

This is interesting. Not sure how to take it.

On the one hand, it's disturbing that testing can potentially lead to lots of false negatives. On the other hand, if it's true that many actual carriers test negative (how many? - no one may know), then perhaps the real fatality rate is lower? And, additionally, perhaps many more people have immunity than we think?

I really hope we can get immunity test out soon. Perhaps many more people have already been infected than we know and have survived with immunity.

Thoughts?

 

[peanut]

False Negatives Raise Doctors' Doubts About Coronavirus Tests
A surprising number of patients have obvious symptoms but still test negative, say doctors

https://www.bloomberg.com/news/arti...est-results-raise-doctors-doubts?srnd=premium
This is interesting. Not sure how to take it.

On the one hand, it's disturbing that testing can potentially lead to lots of false negatives. On the other hand, if it's true that many actual carriers test negative (how many? - no one may know), then perhaps the real fatality rate is lower? And, additionally, perhaps many more people have immunity than we think?

I really hope we can get immunity test out soon. Perhaps many more people have already been infected than we know and have survived with immunity.

Thoughts?

WHO has specifically warned about the improper use and interpretation of tests, particularly lateral flow IgM/IgG assays (these are the blood tests that look like pregnancy tests and require a drop of blood). The only thing WORSE than NO TEST is a BAD TEST, which will give people a false sense of security and may increase their risk of contracting disease.

 

[Vanadium 50]

New signs suggest Coronavirus was in California far earlier than anyone knew

Certainly the California experience is different from the rest of the county. However, when the first case was has become extremely politicized for reasons I don't entirely understand.

New York's densest borough is Manhattan, while relatively sprawling Queens sits at fourth out of five. But Queens has more than twice the cases and twice the rate of cases as Manhattan.

New York reports where the hospitalization or death occurred, not the place of residence. This explains why Rockland and Westchester counties are apparently being hit the hardest. They have a slightly high fraction of hospitals than NYC, but you know what they have a lot of? Nursing homes.

Even so, if someone lives in Queens and works in Manhattan, where should the case be charged? Indeed, what exactly is population? The daytime population of Manhattan is 4 million, even though only 1.6M people live there.

Illinois has statistics based on ZIP code of residence. I aggregated by county (I am too cheap to buy the demographics by ZIP code) and in some cases city. Roughly, each order of magnitude in population is a factor of 1500 cases per million. It appears to be somewhat non-linear with a trend above the curve for the largest cities.

One very interesting feature is that nearby population density matters. Aurora, Naperville and Rockford are comparably sized. Aurora and Naperville are close enough for people to commute to Chicago, and they have a case rate per million about 950. Rockford really is not, and it's at 350.

 

[bhobba]

Interestingly, just watching 60 minutes now, the new worry is people are basically doing the right thing, but will over time get sick of it so it may not remain controlled. This worries a lot of people, especially the police. The feeling is we need the vaccine end of this year, early next year. There were interviews with a number of vaccine experts and they are optimistic. But if it does not happen things can get bad, really bad. Another is the dumb situation with water here in Aus - we have tons of it actually in many key growing areas, but can't touch it. It's tied very much up with politics and not suitable for discussion here. The only thing I want to mention is if we need the water to prevent food shortages the situation will become quite interesting.

Thanks
Bill

 

[chemisttree]

Is a potential food shortage due to not growing enough locally or not having enough workers available to process and distribute it?

 

[bhobba]

Is a potential food shortage due to not growing enough locally or not having enough workers available to process and distribute it?

Simply, for political reasons, we have tons of water passing by many fertile growing areas that the growers are not allowed to use. Allow them to use it, and everything else is in place to grow a lot more food locally that is now imported. But the imports are drying up due to Coronovirus.

Thanks
Bill

 

[Keith_McClary]

when the first case was has become extremely politicized for reasons I don't entirely understand

I guess it's like wildfires, they blame whosever utility pole blew down and sparked it. (Rather than thinking: "Hey, we're living in a tinderbox that will inevitably go up in flames.")