Coronavirus: How dangerous a threat?

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Well, that’s not the way I interpreted scenario 1.



I took that to mean that bats, at least, in high population density could enable this selection. Some bats have an ACE2 sequence that suggests interaction at least with SARS-CoV:

https://www.ncbi.nlm.nih.gov/pubmed/20567988

You seem to believe they are talking about some other species entirely. But they never suggest any species. It would have to be something sold in the wet market. Given that criterion, the high population density (which suggests a relatively small size), and the need for high homology with hACE2, one would think one could narrow it down considerably, but they make no attempt to do so. They throw out this possibility without ever addressing the fact of whether there is actually any species that fulfills all these criteria. If you're going to conclude that another species was more likely than bats, one would think one would suggest what this species is.

To be fair, other authors have suggested possible intermediate species, based on ACE2 homology. These include civets, pigs, ferrets, cats, and some non-human primates. I don't know if any of these animals, other than pigs, are sold in the wet market, and I would think only domestic pigs would have the requisite high population density (swine flu 2?).

https://jvi.asm.org/content/94/7/e00127-20

With regard to the Santa Clara county Ab screening, if I understand the data correctly, they found about 50 people positive for the Ab. That explains why the range is so large. In addition to Baltimore's point about how there may have been a bias for people who either had experienced symptoms, or knew that had been in close contact with others who were, I also wonder about the false positive correction. They say it was based on the manufacturer's data, as well as on 30 Stanford samples, but don't go into details, at least not in what I've seen. A high false positive rate coupled with a relatively small number of total positives could obviously potentially skew the results badly.



Plus the Diamond Princess, Iceland, Vo in Italy, a Chinese study, and Belgium, all of which have estimates of asymptomatics in the range of 50-80%.



Actually, it's 0.011%.

Thanks for sending me that report on the Belgian study. I found it very interesting that < 50% of the symptomatic people were positive. I guess they had some other flu?
They mention pangolins in the sentence before the section you clipped. If it is not clear, natural selection for a bat CoV to pick up the ability to bind a human receptor is not going to happen in a bat. They are already host adapted. A mutation to adapt toward humans would be selected against. If the species barrier between human and bat was low, there would be zoonoses all the time. Bat CoV are classified as bsl2 for a reason. With all due respect, your critiques of a nature peer reviewed article is noted, but you lack the expertise to take your opinion seriously.
 
To pick up where I left off a few days ago: what does getting the USA 'open' again look like? I realize that we can't just look at it as the USA in a bubble, but... If businesses like restaurants can only fill half of their tables at a time, can they make a go of it? If they are only doing half of their old business, beer, vino, booze, dairy, produce, meat, other ag, other (plates, glasses, TP, towels/laundry service...) are only doing half as well. Is that enough to keep thing s above the break even line? Also if businesses are only doing half, are they only bringing back half of their workforce? I'm only talking about restaurants really and it seems difficult at best. What about business that can't be six feet apart (hair salon, dental hygienists...). How do we control the flow of people in and out of a huge facility like a shopping mall so that the stores can get going again without risking starting a C19 spike?

ramble off for now... :eek:
 
If it is not clear, natural selection for a bat CoV to pick up the ability to bind a human receptor is not going to happen in a bat. They are already host adapted. A mutation to adapt toward humans would be selected against.

In the first place, it’s already been reported that SARS-CoV-2 can bind to bat ACE2. This is from a Nature paper published in early February:

ACE2 is known to be a cell receptor for SARS-CoV14. To determine whether 2019-nCoV also uses ACE2 as a cellular entry receptor, we conducted virus infectivity studies using HeLa cells that expressed or did not express ACE2 proteins from humans, Chinese horseshoe bats, civets, pigs and mice. We show that 2019-nCoV is able to use all ACE2 proteins, except for mouse ACE2, as an entry receptor to enter ACE2-expressing cells

https://www.nature.com/articles/s41586-020-2012-7 Zhou, Yank, Feb.3

The Nature Med paper on proximal origin cited this study, but did not refer to it as evidence for SARS-CoV-2 binding to bat ACE2. This might have been because the fluorescent Ab binding they used as evidence was not quantitative, and suggested that SARS-CoV-2 does not interact with bat ACE2 as strongly as with human, civet or pig. But another, more recent study, in Cell, not cited by the Nature Med paper on proximal origin, also found that SARS-Cov-2 was taken up by cells transfected with ACE2, with quantititative results:

https://www.sciencedirect.com/science/article/pii/S0092867420302294?via=ihubHoffman

So I think the notion that SARS-Cov-2 could not exist in bats because of inability to interact with the bat ACE2 has to be reconsidered. But there are other studies that more directly contradict your statement that a bat coronavirus could not bind to human ACE2. Several such coronaviruses have in fact been reported:

Our findings have important implications for public health. First, they provide the clearest evidence yet that SARS-CoV originated in bats. Our previous work provided phylogenetic evidence of this5, but the lack of an isolate or evidence that bat SL-CoVs can naturally infect human cells, until now, had cast doubt on this hypothesis. Second, the lack of capacity of SL-CoVs to use of ACE2 receptors has previously been considered as the key barrier for their direct spillover into humans, supporting the suggestion that civets were intermediate hosts for SARS-CoV adaptation to human transmission during the SARS outbreak24. However, the ability of SL-CoV-WIV1 to use human ACE2 argues against the necessity of this step for SL-CoV-WIV1 and suggests that direct bat-to-human infection is a plausible scenario for some bat SL-CoVs.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5389864/

This was published in 2013. Three years later, the same group isolated another bat virus, WIV16, that also binds to human ACE2.

https://jvi.asm.org/content/90/6/3253

Another publication, just out in the J. of Virology, aligned the aa sequences of a number of viruses, including SARS-CoV-2, and the W1V1 virus discovered in 2013 (also known as Rs3367). They found the homology between Rs3367 and SARS-CoV-2, in both the total spike protein sequence, the receptor binding domain (RBD), and receptor binding motif (RBM) was slightly higher than for the comparisons with SARS-CoV (2002) and a civet SARS (civets being a prime candidate for an intermediate host).

A phylogenetic tree indicated that SARS-Cov-2 and Rs3367 came from a common ancestor, though with several divergent steps in between. They’re clearly not that closely related. But this analysis shows that the evolutionary process that created the RBD of SARS-Cov-2 could also create other RBDs capable of binding to human ACE2. Clearly--in contrast to your statement to the contrary--natural selection in the bat can result in a virus that can bind to human ACE2. This is obviously not because it's being selected for this, but because--as the Nature Med article notes--there are different paths taken by selection, and some of them could result in a higher affinity for human ACE2. After all, the whole point of postulating an intermediate species like the civet, pangolin, pig, or whatever, is because natural selection in those species can result in a virus that binds human ACE2. Maybe their RBD are closer to this goal, so the selection process doesn't have to take as long, but if it can happen in these species, there really is no reason in principle why it can't occur in a bat.

The authors of this study—again, this was published at about the same time as the Nature Med paper--also concluded that SARS-CoV-2 is capable of recognizing bat ACE2. They also mentioned that their structural studies indicate that a single aa mutation in the SARS-CoV-2 RBD could greatly increase affinity for ACE2 (and thus its deadliness), so it’s possible that a single mutation might also have enabled the jump from bats to humans.

In any case, the authors concluded:

Based on the sequence of ACE2 from Rhinolophus sinicus bats (which can be recognized by bat SARS-CoV strain Rs3367), 2019-nCoV RBD likely also recognizes bat ACE2 as its receptor. Overall, 2019-nCoV likely recognizes ACE2 orthologues from a diversity of species, except for mouse and rat ACE2 (which should be poor receptors for 2019-nCoV)… Thus, bats and other wild animals in and near Wuhan should be screened for both SARS-CoV and 2019-nCoV.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3372174/

The Australian scientist you linked made a similar point about screening bats, and so, though less clearly, did the Nature Med article. With all due respect to the authors of the latter, I think the question of whether SARS-CoV-2 could have been transmitted from bats directly to humans (and consequently, whether the virus could have escaped or leaked from a lab), is still an open one. Important issues in science are rarely settled once and for all by a single study.
 
There is a complete misunderstanding. I reported the numbers for San Marino and New York, not for the whole USA.

My bad, I saw your reference to "whole population", and thought you meant the entire country. But a very high death/total population rate is to be expected in some restricted locales. That does not by itself count as evidence against the Santa Clara Ab test.

Some more studies coming out with claims of very high numbers of infected individuals:

An antibody study reported 64 positives in a “random” sample of 200 in Chelsea, MA. It’s not clear to me whether they went door-to-door in some neighborhood, or approached people on the street, assuming they were allowed to be there. Like the Santa Clara study, it sounds as though there could have been a bias for people who thought they might have had symptoms before, and wanted to confirm this. Chelsea does have a very high case rate, about 2%.

https://www.foxnews.com/science/third-blood-samples-massachusetts-study-coronavirus

Another study, which doesn't sound believable, tested 397 homeless people in Boston, and found 136 positives, all of them asymptomatic. I have to think a lot of them were presymptomatic, but I haven't heard any more about this.

https://www.wbur.org/commonhealth/2020/04/14/coronavirus-boston-homeless-testing

The New England J. of Med. reported that.29/33 of pregnant women who tested positive were asymptomatic. Again, i wonder if some of these women developed symptoms later.

https://www.nejm.org/doi/full/10.1056/NEJMc2009316

Finally, another cruise ship type of situation: 60% of sailors on the USS Theodore Roosevelt who tested positive were asymptomatic. This proportion, though, is consistent with that found in several other studies mentioned here before.

https://www.businessinsider.com/tes...er-sailors-coronavirus-had-no-symptoms-2020-4

I just want to add that, assuming the proportion of asymptomatics is somewhere in the range of 50-75%, the effect of this on morality rates might in effect be cancelled out if number of deaths are underestimated to the same extent. The Economist argues that the most accurate way to estimate number of deaths due to the virus is by comparing rate of deaths this year to an equivalent time period last year. Using this approach, they find that many countries have underestimated their reported deaths by a very large margin:

https://www.economist.com/graphic-detail/2020/04/16/tracking-covid-19-excess-deaths-across-countries

Finally, in an attempt to get an idea of how much effect social distancing might have on the spread of the virus, I came up with these numbers:

From March 1 – March 25, the number of cases in the U.S. doubled on average less than every three days. The total number of cases increased by more than 900 times over this period. The period from March 25 – 28 was the first three day period in which the number of cases did not double, increasing by 81%. Since then, the increase has been lower for every succeeding three day period. It was just 14% for the more recent period, April 15-18.

If the rate of increase from March 1 – 25 had been sustained from March 25 – April 18, the total number of cases would be 62,880,000, about 85 times as great as the actual number. At a mortality rate of just 0.5%, that would correspond to 314,000 deaths, about eight times the current number.

The U.S. is a big, diverse country, and a lot of states were taking independent actions during this time. We can’t say that there was a particular time when strict social distancing rules went into place. Suppose we focus on one state particularly hard hit, Michigan. From March 12 – 30, they reported an increase of cases of more than 540-fold. About a week before the end of this period, the Governor declared a state wide shelter in place order, which has since been extended. From March 30 – April 17, another period of eighteen days, the number of cases increased by just 4.6 times.

If the rate of increase from March 12-30 had been sustained to April 17, we would expect a total number of cases of about 3,520,000, or 117 times the actual current number. Assuming a mortality rate of 0.5%, this would result in about 17,600 deaths, almost eight times the current number.

These stats seem to indicate that social distancing has had an enormous impact on the spread of the virus. However, limits of testing may also factor in. E.g., as far as I know, the U.S. is testing at most about 150,000 people a day. The positivity rate--the % who test positive--is about 20%, reflecting the fact that tests tend to target people most likely to be infected. This means that a maximum of about 30,000 positives might be detected daily. As it happens, the daily increase in positives in the U.S. has been bouncing around this number for much of this month. A similar case can be made forMichigan, where one might expect a maximum of about 600 cases detected a day.
 
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Sometime next week we should get the information from Gilead about the results from their multiple tests for Remdesivir, which is the drug that many are hopeful is truly working even close to what has been reported. If those reports are close to accurate it's possible this drug will be going into mass testing and possibly an emergency approval. Even if this is approved it won't be a miracle drug as it is not a pill it's a drip and thus has to be used in a place like a hospital or a clinic. If the reports are anywhere near close to reality and we do end up with this one approved, we will still need another drug that does work for Covid-19 for less severe patients. Having multiple options would be a big help in getting countries opened back up.


As for antibody testing, here is some information done in Los Angeles. USC and the LA dept of health and human services is doing a study. This is the report from USC:
 
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As for antibody testing, here is some information done in Los Angeles. USC and the LA dept of health and human services is doing a study. This is the report from USC:

From the article:

Based on the results of the first round of testing, the research team estimates that approximately 4.1% of the county’s adult population has an antibody to the virus. Adjusting this estimate for the statistical margin of error implies about 2.8% to 5.6% of the county’s adult population has an antibody to the virus — which translates to approximately 221,000 to 442,000 adults in the county who have been infected. That estimate is 28 to 55 times higher than the 7,994 confirmed cases of COVID-19 reported to the county at the time of the study in early April.

Sounds very much like what the Santa Clara study found, which I suppose gives the latter a little more credibility. Still flies in the face of so many studies of the virus itself, with a few exceptions I mentioned in the previous post.

Was the sample random?

With help from medical students from the Keck School of Medicine of USC, USC researchers and public health officials conducted drive-thru antibody testing on April 10 and 11 at six sites. Participants were recruited via a proprietary database that is representative of the county population. The database is maintained by LRW Group, a market research firm.

Did they pick each one randomly, or was anyone on some larger list allowed to volunteer? Not clear to me.

Edit:

OK, here's some more information, indicating it was the latter:

To find participants in the Los Angeles County study, researchers used a random sample of email addresses and telephone numbers of residents to invite people to participate in what they said would be a Covid-19 survey.
The scientists set limits on participation, based on factors like ethnicity and age, in an effort to ensure the sample represented the county’s population. About 1,100 people signed up to be tested.

https://www.nytimes.com/2020/04/21/health/coronavirus-antibodies-california.html

Finally, as with the S.C. study, a relatively small absolute number of people actually tested positive--only 45. This means a high false positive rate could skew results badly, though this would have been thoroughly addressed at the outset. But more important, if people volunteered, it wouldn't take a lot of individuals who had good reason to think they had the virus before--if not from symptoms, from the people they were in contact with--to weight the results. Again, the researchers are claiming they weeded out these people with questionnaires.

One thing for sure: studies like these add fuel to those arguing that the virus is no more deadly than the seasonal flu. But before I'll believe that, I'll want to see these data reconciled with virus testing that says differently.
 
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The high false positives seems to be a huge problem with the current antibody tests. For those to be helpful we need them to be much more accurate.

We also now have reports that the first Covid-19 death in the US was actually in the San Fransisco Bay area on February 6th.

 
I'm linking you to an article I find truly disingenuous:

It argues that strategies like the one in New Zealand should have been installed in other countries. It totally 'forgets' a number of things:
  • New Zealand is an island, is not a transport hub and has a low population density
  • It installed the measures after they had been in place elsewhere, so it's not as if they acted early
  • Measures in other countries are as strict or more strict than in NZ (or Australia)

In most western countries, where tens of thousands of people come in and out every day, the infection was much too widespread to 'crunch' the virus. Look at Italy and Spain: incredibly far-reaching lock-downs, yet still several thousand new cases every day. Pointing to NZ as example completely ignores several realities. There are too many poorly reasoned opinions in the press these days.
 
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Here's a very informative link that briefly summarizes some of the recent antibody tests:

https://www.sciencemag.org/news/202...ount-coronavirus-infections-may-be-unreliable

It begins with the first one, the German study that found 14% (or 15%, adding in some estimated negatives without antibodies) of the population of a town positive

Streeck and his colleagues claimed the commercial antibody test they used has “more than 99% specificity,” but a Danish group found the test produced three false positives in a sample of 82 controls, for a specificity of only 96%. That means that in the Heinsberg sample of 500, the test could have produced more than a dozen false positives out of roughly 70 the team found.

More than a dozen, indeed. That rate would produce 18 false positives. That would reduce the rate to 10.4%, and the proportion of asymptomatics to 62% (65% with that correction). That’s again within the 50-75% range that many virus tests have reported.

What about the Santa Clara study? Well, if you’re into conflicts of interest, there’s this juicy tidbit:

On the day the preprint posted, co-author Andrew Bogan—a venture capitalist with a molecular biology Ph.D.—published an op-ed in The Wall Street Journal asking, “If policy makers were aware from the outset that the Covid-19 death toll would be closer to that of seasonal flu … would they have risked tens of millions of jobs and livelihoods?” He did not disclose his role in the study.

Other criticisms of the study we’ve discussed here, including a possible bias for people more likely to have had the virus, and questions about false positives. With regard to the latter, only 50 people in the study actually tested positive, so if the false positive rate were only 1%, which doesn’t seem outrageous, two-thirds of the positives would be false. A false positive rate of 1.5% would wipe out all the true positives. I guess we can only say for sure that the false positive rate was no higher than that!

It also turns out that the researchers who ran the S.C. study also participated in the LA test. Same antibody test. So the same criticisms that apply to the one apply to the other.

There’s yet another antibody study, carried out by the Netherlands on blood donors, that found 3% of the subjects positive. That translates to almost twenty times as many people who have been infected as the actual case numbers.

Not mentioned in this link, but Sweden has also carried out an antibody test on blood donors, and found 11% were positive. That would project to more than 1 million cases in the country, more than 70 times the actual number. The researchers claim that there are no false positives, but many false negatives, i.e., that the 11% is an underestimate. Based on numbers like this, and modeling, one Swedish researcher is predicting herd immunity for the Stockholm area within a month. Sweden is particularly worth watching, because they have had an unusually loose policy, basically telling citizens to function on the honor system, not restricting their movements. But it seems that Swedes have been acting not that differently from people in countries with stricter policies, because the economy is taking a big hit.

https://spectator.us/swedish-experiment-paying-off/

Finally, this is too juicy not to mention, particularly on a bike forum. Many people here will have heard of Chris Cuomo, CNN anchor and brother of the Governor of NY. Chris tested positive at the end of March, but less than two weeks later was seen with his wife (who later also tested positive) and some others outside of a property that he owns but where he does not live. A cyclist who happened to be in the vicinity recognized Cuomo and told him he was breaking his own brother's self-isolation rule. Cuomo responded by calling him a "jackass loser fat-tire biker", and apparently threatening him. Cuomo later complained that his fame doesn't allow him to tell other people to go to hell.

https://nypost.com/2020/04/14/long-island-bicyclist-verbally-attacked-by-chris-cuomo-fires-back/
 
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This was posted on The Guardian's live corona page:
(the source is not really impartial though)

Some blood tests being marketed to tell people if they have ever had Covid-19 are a “disaster”, Roche chief executive, Severin Schwan, said on Wednesday, as he prepares to launch the Swiss drugmaker’s own antibody test in May.
In developing its test, Schwan said, Roche scrutinised some existing products now on offer but rejected them as unreliable in determining if somebody has actually ever had the disease.
“It’s a disaster. These tests are not worth anything, or have very little use,” Schwan told reporters on a conference call on the Basel-based company’s first-quarter results. “Some of these companies, I tell you, this is ethically very questionable to get out with this stuff.”
 
Some human context; much like the report I posted on rural Washington


What I’ve seen is that the lethality rate of Covid is lower than Sars or Mers but that, as discussed, the infection mechanism is much more aggressive and fluid.

@jm, As you probably know, reopening is going to happen/is happening on a state to state level. Some, let's say, being more responsible than others. There are proposals out there (and I think practices in place) that are going to require service people to wear masks and gloves with purchases being made off apps. Is this sustainable for restaurants? Probably not all, but some, if not many. It wouldn't be one of the worst things to come out of this situation (in the US especially) if food production, availability and distribution became more localized and specialized. Such a transformation would ultimately benefit the health of those most susceptible and minimize working conditions that multiply the virus. A couple of weeks ago after the initial lockdown I rode past two "essential" deliveries of cases of soda from Coca-Cola trucks double parked in the bus lane across from some of the crowded housing projects (where diabetes and respiratory problems are something of a probably birth right by this point) in one of the most afflicted zip codes in the city. I won't bother enumerating all the levels of historical cynicism, ignorance dysfunction in that vignette.

As has been discussed a few times, a lot of this will probably come down to testing and while the federal govt. may issue guidelines, it's likely going to be down to governors and local community leaders to vet the testing policies they want to see implemented and ask the federal government to assist with procuring on scale. Short of a sharing of information and a global agreement on acceptable criteria or threshholds and test methods (as what, overseen by WHO? That's not going to happen) it's probably going to end up a patchwork in the short term with the greatest emphasis being placed on sheltering the vulnerable and screening anyone who comes into contact or works with them and a greater regulation of childrens' environments. Part of what leaders and other public figures don't really want to admit is that we're leaving behind a world of institutions and their autonomy (or illusions of autonomy) or of profiteering from information accumulation and control and entering into one where life itself becomes an open air laboratory. And this is part of the chaos that we're seeing play out: where there are all sorts of competing interests and competencies.
 
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In the first place, it’s already been reported that SARS-CoV-2 can bind to bat ACE2. This is from a Nature paper published in early February:



https://www.nature.com/articles/s41586-020-2012-7 Zhou, Yank, Feb.3

The Nature Med paper on proximal origin cited this study, but did not refer to it as evidence for SARS-CoV-2 binding to bat ACE2. This might have been because the fluorescent Ab binding they used as evidence was not quantitative, and suggested that SARS-CoV-2 does not interact with bat ACE2 as strongly as with human, civet or pig. But another, more recent study, in Cell, not cited by the Nature Med paper on proximal origin, also found that SARS-Cov-2 was taken up by cells transfected with ACE2, with quantititative results:
SARS CoV2 is not the virus that jumped across the species barrier, Merckx. That is the point that you are not understanding. A bat coronavirus jumped into some other species and evolved into SARS CoV2. The most likely course of events was that it jumped into an intermediate species like pangolins or civets that were kept at high density. Put a virus in a new host, especially one jammed together at high density, and you have a perfect recipe for natural selection of new traits. (See also: Bird Flu) So that mostly innocuous bat CoV is now a real potential human pathogen. There is no selective pressure in bats.
So I think the notion that SARS-Cov-2 could not exist in bats because of inability to interact with the bat ACE2 has to be reconsidered.
It will be in competition with host adapted bat CoV, so it would be selected against. Saying it can interact ignores the affinity of any potential interaction. Protein- protein interactions are common in biology. Needless to say that no competition experiments were performed. Getting viruses to infect transformed tissue culture cells is a much lower barrier than infecting humans.
With all due respect to the authors of the latter, I think the question of whether SARS-CoV-2 could have been transmitted from bats directly to humans (and consequently, whether the virus could have escaped or leaked from a lab), is still an open one.
That is what scenario 2 in the paper expressly analyzed. But the evolution of the progenitor virus would occur in humans, not the bat. The fact that there is no single example you can show that widespread infection of a bat CoV happened from direct infection strongly speaks against the possibility. You can argue with the evolutionary virologists all you want, but that doesn't make your arguments make any sense. Nor does any of our arguments preclude your lab scenario. Read what we are saying. Jump from an intermediate species is the 'most likely' course of events based on the genetic evidence. It is not the only one.
 
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Sometime next week we should get the information from Gilead about the results from their multiple tests for Remdesivir, which is the drug that many are hopeful is truly working even close to what has been reported. If those reports are close to accurate it's possible this drug will be going into mass testing and possibly an emergency approval. Even if this is approved it won't be a miracle drug as it is not a pill it's a drip and thus has to be used in a place like a hospital or a clinic. If the reports are anywhere near close to reality and we do end up with this one approved, we will still need another drug that does work for Covid-19 for less severe patients. Having multiple options would be a big help in getting countries opened back up.


As for antibody testing, here is some information done in Los Angeles. USC and the LA dept of health and human services is doing a study. This is the report from USC:
Maybe, but maybe not. I was my mom's home health care after her recent neck surgery and twice a day I hooked her up to antibiotic drips. After 10 days she started doing it on her own. There's no reason a C19 treatment (drip) couldn't be done the same way. Patients would only need to be at the clinic to get the picc line in, and then later to get it removed.
 
Still chewing up normal pro level training..interview by Uran and others..and the announcement that most experts see having the Tour d France as great public health risk. I don't see anything absolute so in my view..currently I think that there could be a way to conduct many sporting events using masks and social distancing.
I hope bike racing makes it through this.
Kids baseball and soccer games may finally give parents the bad guy that they hoped for!! Not sitting through an entire game and having the virus to blame..
And for young kids soccer nothing works anyway..you tell them here is your position..let's say right wing..the whistle blows and all players from both teams converge on the ball..often the goal tender included..so social distancing ain't gonna happen..
There are restaurants here that are open w tables @6ft apart.
Going into the store is done using number tags..the store employee working as a doorman gives out @10 number tags and until one comes back you can't go in..they wipe off the number and hand it to you..
Also people from San Diego,Tijuana and Mexicali are coming to Ensenada ,hearing that because they only have @7 cases medical care is easier than big cities..now proof of residency is required. I have copies of water,sewer,electric and two bank payments. As a non-profit Mexican citizen not certain that I will not have to stay in San Diego until southern travel restrictions are lifted..
This also presents serious health problems for me,because w my new road shoes,MP3 player loaded and 2 pairs of Pearl Azumi bibs my excuses for daily training will be over.
if any of you see what looks like Santa Claus doing short out of the saddle intervals,please only make mental notes..seeing me train hard is right up there with Big Foot doing motorpacing or hill repeats..a rare sighting
 
Maybe, but maybe not. I was my mom's home health care after her recent neck surgery and twice a day I hooked her up to antibiotic drips. After 10 days she started doing it on her own. There's no reason a C19 treatment (drip) couldn't be done the same way. Patients would only need to be at the clinic to get the picc line in, and then later to get it removed.

It's between a 5 to 10 day treatment. It sounds like it needs monitoring to know how much you actually get before they stop it.
 
Cuomo said he gave NY results to the White House yesterday. Neither side is plumping them. So...,

There are other reports out there that are non-positive at best. Or anecdotal in terms of symptom management at a very mild level.
We can always wait for the South Dakota clinical trial. I have a good feeling about that one. I think the anecdotal consensus is that really sick patients are not helped at all. There might be some benefit to those that are less sick and/or get early intervention. But those are also the ones who probably would recover on their own. I think Fauci has been cool on this since the outset because he has gotten more complete information than has been made public.
 
It's between a 5 to 10 day treatment. It sounds like it needs monitoring to know how much you actually get before they stop it.
Each one of my mom's med balls was a precise amount, and we/they did a blood check every five days to determine the dosage for the next five days. She was on that for 22 days.

The question is, do the labs have the capacity to produce the med balls for home treatment.
 
More first hand accounts from the early days in Wuhan and conflicted attitudes and lines of information


 
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