It’s blowing up. The so called protestors, as was very obvious, were a major factor. The interesting thing is hospitalizations. I was had a lunch meeting with the person that runs Covid response on the tech side for USC. She asked me to guess how many total cases there were in all 3 hospitals. I guessed 350. Real number? 6.
In this paper, we employ the natural experimental setting created by the U.S. protests precipitated by George Floyd’s tragic death to document the causal impact of social distancing measures on the spread of SARS-CoV-2. Using a DID analysis, in which the treatment effect corresponds to the onset of the protests and the treatment group corresponds to the counties in which protests reportedly took place, we document a country-wide increase of more than 3·06 cases per day, per 100,000 population, following the onset of the protests, and a further increase of 1·73 cases per day, per 100,000 population, in the counties in which the protests took place. Relative to the average number of new COVID-19 cases per day during the week preceding the onset of the protests, this represents a 61·2% country-wide increase in COVID-19 cases, and further 34·6% increase in the protest counties.Well, we now have two papers (neither peer-reviewed yet) analyzing the same data (even through the same date, 6/20), in theory, coming to different conclusions. I don't have the time to go through them, but the one red flag for me on the paper you cited was that US cases were completely flat (using 7-day moving averages, below) from 5/27 (the day before the protests started) to 6/14, while the paper talks about measurable case increases per day for the US. If there were a true spike, since cases manifest themselves with symptoms in about 5 days, one would've expected to see cases rising easily within 5-10 days, but instead there were no increases for 18 days. This was followed by a 21% increase in US cases from 6/14 to 6/20, which is the overall increase from 5/27 to 6/20, so where do they get the 61% countrywide increase from, overall? The math is just not adding up there, unless I'm missing something.
https://www.nber.org/papers/w27408....xsZ91jyO89-5DuB9b7Fze1-_t08Ng4yxXRi0IYvCgjQMQ
Saying it twice doesn't make it any more convincing. Looking at the actual US cases per day, there was zero case growth from 5/27 to 6/14, followed by a 21% increase from 6/14 to 6/20, which is completely inconsistent with a 61% increase from 5/27 to 6/20, as reported in this paper.
assuming the numbers from the NE are not being manipulated
All the contrarians here said the NE was exagerating deaths and cases, now they are hiding them? Always a conspiracy no matter what.
Interesting coincidence that a paper came out today in Cell addressing many of these same questions on this mutation that were discussed in the Scripps paper first talked about on 6/10 (the Cell paper was submitted on 4/29 and I think was discussed back then, but can't find it). Anyway, this paper dives more deeply into evolution of the virus's mutation and less on the cell-level infectivity that the Scripps paper focused more on. It seems pretty clear from the Cell paper that this G614 strain (the one with a glycine amino acid substituted for an aspartic acid on the spike protein) from Europe that hit NY/NJ is more highly transmissible in the real world (not just in vitro), as this strain has become more prevalent even in locations that were originally seeing only the D614 strain, i.e., it out-competed it (as per the graphic).
The good news, still, is that both strains appear to be equally deadly to individuals, although the bad news is that clearly a strain that is more transmissible will likely impact and kill more people (even if not a higher percentage of infected people). The other piece of good news is that the authors of both papers believe that an antibody treatment or vaccine would likely work for both strains, as they're not different enough to change that (unlike flu, which mutates much faster than this virus, which is why a new vaccine is needed every year). Both papers are linked below.
https://www.cell.com/action/showPdf?pii=S0092-8674(20)30820-5
https://www.scripps.edu/_files/pdfs/news-and-events/The D614G mutation in the SARS-CoV-2 spike protein reduces S1.pdf
Remember the arm of the Brazillian study that was dosing 1200mg and halted? The Recovery trial knew of this episode in Brazil and continued a similar dosing strategy.If they "murdered" them, they didn't do a very good job, as the mortality rates for the HCQ and control arms were statistically the same. And chloroquine, which is almost identical to hydroxychlorioquine, is used to treat amoebic dysentery and HCQ is generally considered safer than CQ, which is why doctors went much more for HCQ for COVID, realizing higher doses would likely be better for trying to knock out the virus. So my guess is Landray was simply comparing the amount of the CQ base dosed in AD for CQ and using that for HCQ, since the two molecules are so similar (HCQ just has an OH group where CQ has an H - the rest is identical) - at worst he misspoke slightly. And dosing HCQ at about 2X the usual level is not unusual in a situation like this
https://www.drugs.com/dosage/chloroquine.html#Usual_Adult_Dose_for_Amebiasis
In addition, there were other HCQ studies with similar high doses that didn't raise any particular red flags, including this one that used a "loading dose of 1200 mg daily for three days followed by a maintenance dose of 800 mg daily for the remaining 2 or 3 weeks of treatment," which is linked below. Sounds almost identical to the Recovery trial. Mortality wasn't being looked at in this trial (which was deemed ineffective for HCQ), but if they were murdering patients, presumably they would have noticed. You and the HCQ army haven't convinced me that the Recovery study was problematic in any way.
https://www.medrxiv.org/content/10.1101/2020.04.10.20060558v2
Here is how I believe they got the numbers they did:Well, we now have two papers (neither peer-reviewed yet) analyzing the same data (even through the same date, 6/20), in theory, coming to different conclusions. I don't have the time to go through them, but the one red flag for me on the paper you cited was that US cases were completely flat (using 7-day moving averages, below) from 5/27 (the day before the protests started) to 6/14, while the paper talks about measurable case increases per day for the US. If there were a true spike, since cases manifest themselves with symptoms in about 5 days, one would've expected to see cases rising easily within 5-10 days, but instead there were no increases for 18 days. This was followed by a 21% increase in US cases from 6/14 to 6/20, which is the overall increase from 5/27 to 6/20, so where do they get the 61% countrywide increase from, overall? The math is just not adding up there, unless I'm missing something.
https://www.nber.org/papers/w27408....xsZ91jyO89-5DuB9b7Fze1-_t08Ng4yxXRi0IYvCgjQMQ
Not that similar. The Brazilian study was chloroquine, not hydroxychloroquine and chloroquine is generally known to be more toxic than hydroxychloroquine, plus that dosing was 30% greater than the HCQ dosing in Recovery (12 g total in Brazilian study vs. 9.2 g total in the Recovery trial, not the 9.6 g you posted: it's 2 g the first 24 hours, then 0.8 g/day for 9 days).
Remember when Numbers said if HCQ worked we would have known it as it was used heavily in hospitals from late March to mid-April? I guess we now know it does work. Study covered period from 3/13 to 4/17.
You are wrong.
There are two studies out now. The Ford study and a NYC hospital study showing 46% mortality reduction by HCQ.
BTW, NYC hospital study shows HCQ patients had 46% reduction in mortality.
https://link.springer.com/article/10.1007/s11606-020-05983-z#MOESM1
Supplementary Table 6. The results of univariate Cox proportional hazard regression models.
Hazard ratio (95% CI) P value
Hydroxychloroquine use
0·54 (0·39-0·74) < 0·001
"It takes two to three weeks after infection for a person to be in critical condition or to die, so death curves generally follow along behind infection curves, something like one to two weeks delayed," Benjamin Neuman, chair of biological sciences at Texas A&M University-Texarkana, told Business Insider.
Usually, the dose at 24 hours is considered the start of the next day's dose. I've seen it reported most places as 2 g. And besides are you going to hang your hat on a difference of 0.4 g, when you've been wrong about most of the rest of this discussion? You are wrong on the lethal dose of 4 g of HCQ, as per the paper I shared and that the cumulative dose is deadly, you were wrong on implying the Brazilian study was HCQ, when it was actually CQ, plus you said they were using similar dosing when they were not (the Brazilian study dosed 30% higher than the Recovery trial), and you've yet to acknowledge that the Chinese study used significantly greater dosing of HCQ, cumulatively, than Recovery, without any apparent major toxicity/mortality issues, so your sensationalist comments about "murdering" patients are completely inappropriate. Also, CQ, which is very closely related to HCQ is used in ameobic dysentery, so the author could've easily been referring to that.
The one thing we agree on on this is that it would be nice to see the paper with all the details. Given the Chinese study with doses as high (higher, cumulatively), I still see no issue with the Recovery dosing. I can't comment on what was published or removed from any websites, since I haven't seen them and docs are often changed after protocols change (HCQ being removed from Recovery).
I never implied Brazillian study was using HCQ. I never said 0.4g was going to make a difference. I was correcting your mistaken statement.
