Coronavirus: How dangerous a threat?

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Here’s some more information on the Henry Ford study vs. the UK’s Recovery study. The Henry Ford study had a total of 2541 patients, with a death rate of 26.4% in controls. The Recovery study

https://www.recoverytrial.net/news/statement-from-the-chief-investigators-of-the-randomised-evaluation-of-covid-19-therapy-recovery-trial-on-hydroxychloroquine-5-june-2020-no-clinical-benefit-from-use-of-hydroxychloroquine-in-hospitalised-patients-with-covid-19

examined a total of 4674 patients, with a death rate of controls of 23.5%. So the control patients in the Ford study did a little worse, but not much. But the Recovery HCQ patients had a 25.7% mortality rate, no improvement at all on controls, while in the Ford study, the patients given HCQ had a mortality rate of only 13%. That's the huge difference in results between these two studies. Why?

To begin, the Recovery study was larger (as Baltimore notes), not just in total subjects, but in those given HCQ, 1542 patients. I'm not sure of the number at Ford, but it must be a lot lower, because there were at least four groups: controls; azithromycin (AZ), an antibiotic; HCQ; and HCQ plus AZ. And very curiously, while the mortality rate of patients given AZ alone was reduced relative to controls (22.4%), with a similar reduction observed for HCQ + AZ (20.1%), the patients given only HCQ had a much lower mortality rate. That really doesn’t make sense. Why would HCQ alone be better than giving it along with an antibiotic which, by itself, also reduced mortality rates? There could be several reasons, but the most likely answer is that the differences in these rates aren’t significant, regardless of what their statistics show. This would be the case if the treatments weren’t random, which in fact they weren’t:

Researchers not involved with the study were critical. They noted that the Henry Ford team did not randomly treat patients but selected them for various treatments based on certain criteria.

"As the Henry Ford Health System became more experienced in treating patients with COVID-19, survival may have improved, regardless of the use of specific therapies," Dr. Todd Lee of the Royal Victoria Hospital in Montreal, Canada, and colleagues wrote in a commentary in the same journal.

"Finally, concomitant steroid use in patients receiving hydroxychloroquine was more than double the non-treated group. This is relevant considering the recent RECOVERY trial that showed a mortality benefit with dexamethasone." The steroid dexamethasone can reduce inflammation in seriously ill patients.
https://edition.cnn.com/2020/07/02/health/hydroxychloroquine-coronavirus-detroit-study/index.html

The bottom line is that the Henry Ford study was retrospective (again, as Baltimore notes), meaning that researchers went back after the fact and looked at the results of various treatments. This is a useful approach, it's a way of mining data that are already there, but it's not as scientifically rigorous as a prospective study, like that at Recovery, where patients are given certain treatments by design at the outset. A retrospective study can't control factors like other treatments, as pointed out in the quotes above. You have to take the subjects as they're given to you.

There’s just one other point I want to make, because it’s almost always ignored in discussions of large scale drug studies: individuals may vary markedly in their response to drugs. There are undoubtedly genetic factors at play. Just as an individual 100 years old may survive C19, while someone 30 years old dies, one individual may gain a benefit to a drug that another does not.

Ryan Padgett, a doctor in his early 40s, became infected while treating some of the earliest cases in Washington state back in March. He was near death, and put on an ECMO machine, that removes the patient’s blood, oxygenates it, and pumps it back in. This is basically a treatment of last resort. Then he was given the drug tocilizubab, which is used to reduce the effects of hyper-immune reactions, or “cytokine storm”. He soon began to improve, and eventually recovered. In a recent interview (some time after the linked article), he said he felt that drug saved his life. Would it help everyone? No. But for this patient in this condition, it seemed to make the difference. And by the way, they also tried HCQ, which didn’t help.

https://www.nytimes.com/2020/04/13/us/coronavirus-doctor-kirkland-padgett.html

Drugs are a matter of playing the percentages. We try to determine whether, on balance, a drug will help or harm someone, but some people may beat the odds, just as they do when they have a relatively mild case when in a high risk group. There may be people who can benefit or have benefitted from HCQ, but the question is whether enough people benefit to balance the negative effects, including increased risk of death. The largest and most rigorous studies that have been carried out indicate that they don't.
 
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I am wondering about seasonal flu in the US. Most of the same mitigation measures that are effective for Covid-19 are identical to seasonal influenza..wash your hands,cover your mouth, stay home when you feel ill..avoid large gatherings \social distancing. Curious to know what percentage of the US population is exposed to seasonal flu..looks like it kills between @40-60,000 per year..
US health officials said they estimate that less than @9% of the population has been exposed to Covid-19 w @129,000+ dead..so what are the numbers for the two..exposure:death ratio..
It's something I don't think I see..the % of the population that is infected yearly w flu
 
I disagree. The case count shows a clear and obvious acceleration which looks like a wave to me. What do you think causes waves of pandemics? I am unconvinced waves are caused by mutation of the virus itself. Even earlier in this thread it was pointed out somewhere that when virus mutate usually they become less lethal as ease of spread is inversely proportional to mortality rate - like Ebola outbreaks in Africa.

What causes a rebound is human factors. Like relaxing restrictions too quickly. From what I have read the Spanish flu 2nd and 3rd waves were caused by human factors not virus mutation. Such as troops returning from the war. An equivalent today would be if international flights resumed, the population became complacent on social distancing or other restrictions relaxed too soon. But of course the economic impacts should not be underestimated as this can potentially kill millions too - wars?

We are all at the mercy of scientists around the world feverishly working to develop and test a vaccine or drug that works such as discussed above. The only other option is herd immunity around the world and that could take years and some say immunity isn't possible anyway as has also been discussed here.
Case counts in most states have never stabilized or reduced since the start of this. There are only a handful of states that would even qualify for a second wave. To get a second wave, you would have had to have had a first wave stabilize and start to reduce. 40 to 45 states never experienced this. So we the US outside of handful of states (NY, NJ, RI, Michigan, maybe one or two more in New England) never got close to finishing a first wave. You can't start a 2nd wave when you're still in the middle of a first wave. Most states started reopening while in the middle of the first wave. Basically the stay at home orders were to buy time to find a treatment and hope the treatment would reduce deaths once the reopenings started.
 
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only in German, you can try google translate if you care (it's about long term effects)
I am interested also to find out about any long term negative effects that the virus has on highly healthy people. For example, someone like Novak Djokovic is hardly likely to have his life threatened by covid 19, but will what remains of his professional tennis career be derailed? Well, there are a lot of unanswered questions when it comes to this pandemic.
 
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Apparently, we in the USA are going to be officially told that 'we have to live with it' just days after being officially told that it would soon disappear. Totally normal stuff. For those of you who thought that we would eventually come to our senses and deal with the problem, probably not going to happen any time soon.

Here’s some more information on the Henry Ford study vs. the UK’s Recovery study. The Henry Ford study had a total of 2541 patients, with a death rate of 26.4% in controls. The Recovery study

https://www.recoverytrial.net/news/statement-from-the-chief-investigators-of-the-randomised-evaluation-of-covid-19-therapy-recovery-trial-on-hydroxychloroquine-5-june-2020-no-clinical-benefit-from-use-of-hydroxychloroquine-in-hospitalised-patients-with-covid-19

examined a total of 4674 patients, with a death rate of controls of 23.5%. So the control patients in the Ford study did a little worse, but not much. But the Recovery HCQ patients had a 25.7% mortality rate, no improvement at all on controls, while in the Ford study, the patients given HCQ had a mortality rate of only 13%. That's the huge difference in results between these two studies. Why?

To begin, the Recovery study was larger (as Baltimore notes), not just in total subjects, but in those given HCQ, 1542 patients. I'm not sure of the number at Ford, but it must be a lot lower, because there were at least four groups: controls; azithromycin (AZ), an antibiotic; HCQ; and HCQ plus AZ. And very curiously, while the mortality rate of patients given AZ alone was reduced relative to controls (22.4%), with a similar reduction observed for HCQ + AZ (20.1%), the patients given only HCQ had a much lower mortality rate. That really doesn’t make sense. Why would HCQ alone be better than giving it along with an antibiotic which, by itself, also reduced mortality rates? There could be several reasons, but the most likely answer is that the differences in these rates aren’t significant, regardless of what their statistics show. This would be the case if the treatments weren’t random, which in fact they weren’t:



https://edition.cnn.com/2020/07/02/health/hydroxychloroquine-coronavirus-detroit-study/index.html

The bottom line is that the Henry Ford study was retrospective (again, as Baltimore notes), meaning that researchers went back after the fact and looked at the results of various treatments. This is a useful approach, it's a way of mining data that are already there, but it's not as scientifically rigorous as a prospective study, like that at Recovery, where patients are given certain treatments by design at the outset. A retrospective study can't control factors like other treatments, as pointed out in the quotes above. You have to take the subjects as they're given to you.

There’s just one other point I want to make, because it’s almost always ignored in discussions of large scale drug studies: individuals may vary markedly in their response to drugs. There are undoubtedly genetic factors at play. Just as an individual 100 years old may survive C19, while someone 30 years old dies, one individual may gain a benefit to a drug that another does not.

Ryan Padgett, a doctor in his early 40s, became infected while treating some of the earliest cases in Washington state back in March. He was near death, and put on an ECMO machine, that removes the patient’s blood, oxygenates it, and pumps it back in. This is basically a treatment of last resort. Then he was given the drug tocilizubab, which is used to reduce the effects of hyper-immune reactions, or “cytokine storm”. He soon began to improve, and eventually recovered. In a recent interview (some time after the linked article), he said he felt that drug saved his life. Would it help everyone? No. But for this patient in this condition, it seemed to make the difference. And by the way, they also tried HCQ, which didn’t help.

https://www.nytimes.com/2020/04/13/us/coronavirus-doctor-kirkland-padgett.html

Drugs are a matter of playing the percentages. We try to determine whether, on balance, a drug will help or harm someone, but some people may beat the odds, just as they do when they have a relatively mild case when in a high risk group. There may be people who can benefit or have benefitted from HCQ, but the question is whether enough people benefit to balance the negative effects, including increased risk of death. The largest and most rigorous studies that have been carried out indicate that they don't.
'individuals may vary markedly in their response to drugs'

Amen. So can genetically identical individuals due to epigenetics. If people want neat and tidy answers, biomedical research is not the field to work in. That CNN article actually does a good job of explaining some conflicts, but 99% of the people taking victory laps on Twitter never read past the headline. My favorite part is the hospital CEO contorting into a pretzel claiming that this new study doesn't conflict with the prior trials. It is just 'nuanced data'. Oh-kayyyy guy.....good talk.
 
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A recent study published in Cell concludes that a new, more infectious version of the virus has now taken over:

A global study has found strong evidence that a new form of the coronavirus has spread from Europe to the US. The new mutation makes the virus more likely to infect people but does not seem to make them any sicker than earlier variations of the virus, an international team of researchers reported Thursday.

"It is now the dominant form infecting people," Erica Ollmann Saphire of the La Jolla Institute for Immunology and the Coronavirus Immunotherapy Consortium, who worked on the study, told CNN.

"This is now the virus."
The new version seems to multiply faster in the upper respiratory tract -- the nose, sinuses and throat -- which would explain why it passes around more easily, the researchers said.

But tests on 1,000 hospitalized coronavirus patients in Britain showed those infected with the new version did not fare any worse than those who caught the original strain…

"All the results agreed that the G form was three to nine times more infectious than the D form," he added. "We now had experimental evidence that supported, in part, what Bette was seeing in her analysis of the sequences across the globe -- the G form had a fitness advantage in terms of infectivity."
https://edition.cnn.com/2020/07/02/health/coronavirus-mutation-spread-study/index.html?fbclid=IwAR0CN4HnXGvNvhd8tMKQOWSq0rCnQcoc4EUxfSwhiMvT_h_iDrsd35CY2nQ

A little biochemistry lesson. G614 refers to the fact that there is a glycine residue (G) at position 614, vs. D614, where there is an aspartic acid (D) residue. Glycine is coded for by the three nucleotide bases GGX, where X can be any of the four bases, G, C, A or U (an example of redundant coding). Aspartic acid is coded for by GAC or GAU. So a mutation of the A to G would result in changing the code from aspartic acid to glycine.

Why is the new form more infectious? Aspartic acid has a negative charge, and is slightly larger, or bulkier, than glycine. Removing that negative charge, and/or making the amino acid less bulky, may improve the interaction of the spike protein, where the amino acid is located, with the host cell in humans, allowing the virus to bind with greater affinity, and thus increase the probability of entering the cell. Though the mutation occurs in a region of the spike protein that does not actually contact the cell, it still may have an effect on that region, particularly as the region is between the contact area and another portion of the virus critical to cell entry. Still another possibility, raised by a couple of studies in which the G614 was created artificially in the lab, and used to infect cells in culture, is that the mutation reduces premature cleavage of the spike protein. After contact with the cell, the spike does have to be cleaved as part of the process of entering the cell, but if that cleavage occurs prior to contact, the attachment process is disrupted.

One can imagine someone being exposed to a very tiny amount of virus, not enough to trigger cell entry if the virus is the earlier form, but now enough if the virus is the more recent form. Or perhaps the earlier form enters, but not in as many cells as with the more recent form, so the person, while infected, has a lower viral load to spread to others. The link notes that the new form seems to multiply faster in the upper respiratory tract. This would not be because of any enhanced replication process within the cell, but simply because more cells get infected with it. Other factors may determine if the virus infects the lower respiratory tract, which leads to more serious symptoms.

This is speculation on my part, but the bottom line, based on empirical evidence, is that the new form of the virus doesn’t increase severity of symptoms. And that makes sense, because if it did, infected people would be less likely to spread it, or spread it as much. From the point of view of the virus, the healthier the individual is, the more and longer the virus will be spread.

But that 3-9 x more infectious claim should be taken with a grain of salt. That seems to be based on cell culture studies, which aren't necessarily representative of the situation with people. Certainly it doesn't mean that the number of people on average that an infected person passes the virus to is going to be increased by that amount. If that were the case, just about everyone would become infected quite soon.
 
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A recent study published in Cell concludes that a new, more infectious version of the virus has now taken over:





https://edition.cnn.com/2020/07/02/health/coronavirus-mutation-spread-study/index.html?fbclid=IwAR0CN4HnXGvNvhd8tMKQOWSq0rCnQcoc4EUxfSwhiMvT_h_iDrsd35CY2nQ

A little biochemistry lesson. G614 refers to the fact that there is a glycine residue (G) at position 614, vs. D614, where there is an aspartic acid (D) residue. Glycine is coded for by the three DNA bases GGX, where X can be any of the four nucleotide bases, G,C,A or T (an example of redundant coding). Aspartic acid is coded for by GAC or GAT. So a mutation of the A to G would result in changing the code from aspartic acid to glycine.

Why is the new form more infectious? Aspartic acid has a negative charge, and is slightly larger, or bulkier, than glycine. Removing that negative charge, and/or making the amino acid less bulky, may improve the interaction of the spike protein, where the amino acid is located, with the host cell in humans, allowing the virus to bind with greater affinity, and thus increase the probability of entering the cell. One can imagine someone being exposed to a very tiny amount of virus, not enough to trigger cell entry if the virus is the earlier form, but now enough if the virus is the more recent form. Or perhaps the earlier form enters, but not in as many cells as with the more recent form, so the person, while infected, has a lower viral load to spread to others. The link notes that the new form seems to multiply faster in the upper respiratory tract. This would not be because of any enhanced replication process within the cell, but simply because more cells get infected with it. Other factors may determine if the virus infects the lower respiratory tract, which leads to more serious symptoms.

This is speculation on my part, but the bottom line, based on empirical evidence, is that the new form of the virus doesn’t increase severity of symptoms. And that makes sense, because if it did, infected people would be less likely to spread it, or spread it as much. From the point of view of the virus, the healthier the individual is, the more and longer the virus will be spread.
Well hopefully this means that any treatment developed will work for both strains and that any vaccine that actually works will work for both strains.
 
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And - back in Japan - according to the article the higher numbers are "partly due to increased testing among nightlife workers in Kabukicho/Ikebukuro".
"70% in their 20s & 30s... but despite the spike the number of serious cases is declining" the gvt are saying.
 
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Well hopefully this means that any treatment developed will work for both strains and that any vaccine that actually works will work for both strains.
It's a good point you raise: will vaccines already developed towards the earlier version work on this one? Since most vaccines are directed towards the spike protein, the likely answer is many may not work as well, and in fact, the authors of one cell culture study calculated, on a theoretical basis, that this mutation would reduce affinity of at least some vaccines for the virus. However, there's a lot of room to work on the spike protein, so probably some vaccines will not be affected. This could reduce the pool of viable candidates, though.
 
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It's a good point you raise: will. vaccines already developed towards the earlier version work on this one? Since most vaccines are directed towards the spike protein, the likely answer is many may not work as well, and in fact, the authors of one cell culture study calculated, on a theoretical basis, that this mutation would reduce affinity of at least some vaccines for the virus. However, there's a lot of room to work on the spike protein, so probably some vaccines will not be affected. This could reduce the pool of viable candidates, though.
According to this article (posted below) it appears that the mutation is what was going through Italy and then New York. If it hasn't mutated since then, then it's very possible that at least part of the vaccines they are working on are actually for the mutated version and not the original version. It's also possible if they have been checking samples of people from both the east and west coasts in the US it could be at least a few of the vaccines in development are attempting to work against both strains. I've read previously that the version of Covid that first showed up in both California and Washington (state) was the original strain while the one that showed up in New York was the Italian strain.

 
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RE: Long-term battle:
I don't know how many of you use Twitter, but @DaniOliver describes her horrific 90 day battle with C19.
my morning..two sips of coffee ,hung 4 bifold closet doors and started reading the first part of my daily news..Dani Oliver can lead an early morning viewer to some intriguing places..Dani Oliver photography took 15 minutes of looking at things I hadn't previously seen. Cool.
Dirt I didn't expect that a Covid recap using tweets was going to be uplifting..I was right. The descriptions of the experience up to now are pretty ucking scary.
there is a common thread in a majority of the personal recounts I have read that commonality is disappointment. I have watched and read half a dozen or more things on the 1918 Spanish flu and the emotions and opinions again have similarity. I really feel like the last 2 weeks in America are the ground work for what is ahead and in my opinion it's lots more suffering,sickness and death. To be disappointed in anybody for not having the magic bullet after @6-7 months is unrealistic and that level of expectation is wide spread and is from the absolute top to bottom.
The first super effective steps are in place..generally cleaning everything,limited movements,and mindfulness when movements are necessary..ordering out food daily or multiple trips to the store per week w the kids in the car is not mindful. But the vivid examples of not using your mind at all..not social distancing and using a mask..
So trashing the CDC may be easy but the guidelines that they gave have basis in an effective strategy..wash your hands,stay covered and limit exposure to people,places and things..
Vaccines are great but we have to get there..and everyone sitting in the computer keyboard backseat saying "are we there yet!!!" Is normal I guess but the answer is still the same.. " we are not close,I will tell you when we get there "
I think in the public sphere if folks think anything that they say is contributing to a motivational pressure on government or companies to hurry the uck up..that's silly..
And on the other side of the American coin..a forth of all deaths..no strategy and the message yesterday..just deal with it, go out and walk between the rain drops has science based people in a head on collision with the group that is encouraging older citizens to damn the torpedoes and just die quietly
 
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Since I posted this morning I walked the dog, and had a great dirt ride. Both of those give me time to think (although I must admit that a lot of my ride was spent without much thought...my brain needs that).

C19 "mutating": I think that there is probably a semantic discussion to be had here because by pure definition it just means change, but most people think of it as a drastic change I think. There seems to be no doubts that C19 has several 'variations' , but my understanding is that there isn't much difference. It makes sense that the one in NYC (or Italy, etc.) was too aggressive and died with its hosts/victims. What we are seeing now isn't a mutation as much as a slightly different variation(s) that seems to be better at keeping itself, and therefore its hosts/victims, alive I think (that doesn't mean that more aggressive version aren't still with us). I agree with those that C19 affects each person differently and treatments/therapies will work the same. Those with more understanding feel free to add/subtract/correct.

As I shared, the Boise mayor signed a mask mandate. There were people marching on city hall yesterday to protests of course. There was lots of "its a free country" which is cover for "I'm selfish", and one guy offered proof of his selfishness by adding "its a free country so I'm free to not wear a mask, and you are free to stay home". HMM, so your freedom to spread C19 means that I am not free to leave my home...is that lost on you?...it probably is. Sure, if you like the sound of "its a free country" chant it all you want, but remember that we have laws and rules to protect each other from each other. For example we have speed limits. Is this guy going to argue that its a free country and he can drive as fast as he wants and if you don't like being run over by him stay home? He probably is.

Leaders complaining that they don't need input from medical experts because the experts have been 'wrong all along'. First of all, the experts haven't really been too far off especially considering that this is a novel virus. I also understand that anti-science, and plt*cs are a driving factor, but come on man you haven't really listened to the experts anyway so now saying it out loud is hollow. It reminds me of the cartoon from the late '90s when obesity was really blowing up: a very large man was talking to his doctor about felling poor and being tired all of the time. After some discussion and tests, the doctor recommended that the guy stop smoking, reduce alcohol, eat healthier, exercise, and reduce body fat. The next few panels show the guy gorging on junk food, drinking, smoking, passed out... At his six month check up he is mad at the doctor because he still isn't feeling well.
 
As the world looks on..the data is there for the US..@20-30 million w the virus.
Test to identify the sick,get them isolated and under aggressive ever advancing treatments. Then the rest of the population can w reckless abandoned and motivation seldom seen..rebuild the country,house by house..our citizens young and old..the unborn deserve an intelligent scientific approach to the duration that the pandemic affects us..
over 130,000 dead..we need to work together on this scared independence day..
Faith based solutions to a world wide pandemic don't appear as a sound solution..
 
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Here’s some more information on the Henry Ford study vs. the UK’s Recovery study. The Henry Ford study had a total of 2541 patients, with a death rate of 26.4% in controls. The Recovery study

To begin, the Recovery study was larger (as Baltimore notes), not just in total subjects, but in those given HCQ, 1542 patients. I'm not sure of the number at Ford, but it must be a lot lower, because there were at least four groups: controls; azithromycin (AZ), an antibiotic; HCQ; and HCQ plus AZ. And very curiously, while the mortality rate of patients given AZ alone was reduced relative to controls (22.4%), with a similar reduction observed for HCQ + AZ (20.1%), the patients given only HCQ had a much lower mortality rate. That really doesn’t make sense. Why would HCQ alone be better than giving it along with an antibiotic which, by itself, also reduced mortality rates? There could be several reasons, but the most likely answer is that the differences in these rates aren’t significant, regardless of what their statistics show. This would be the case if the treatments weren’t random, which in fact they weren’t:
The answer is in the original paper
https://www.ijidonline.com/article/S1201-9712(20)30534-8/fulltext
"The combination of hydroxychloroquine + azithromycin was reserved for selected patients with severe COVID-19 and with minimal cardiac risk factors. "

So all things being equal you would expect the combination treatment to be worse
https://edition.cnn.com/2020/07/02/health/hydroxychloroquine-coronavirus-detroit-study/index.html

The bottom line is that the Henry Ford study was retrospective (again, as Baltimore notes), meaning that researchers went back after the fact and looked at the results of various treatments. This is a useful approach, it's a way of mining data that are already there, but it's not as scientifically rigorous as a prospective study, like that at Recovery, where patients are given certain treatments by design at the outset. A retrospective study can't control factors like other treatments, as pointed out in the quotes above. You have to take the subjects as they're given to you.
I would not call this a retrospective study. The treatment regimes appear to be planned in advance. But (in common with many covid studies) it is not randomised. I think the reporting of this study looks fair. They have shown the possible biases between the treatment groups. One significant difference is that the "no treatment" group is older. That alone is reason to be sceptical about the conclusions (although to be fair there are other differences between the treatment groups which are not in favour of HCQ)
 
A bigger issue is the difference in dexamethasone use between the two groups given what we know about its benefit for severe Covid. No matter what you call it, it is inferior to the Recovery trial and will not change policy. Chloroquine will be shelved until the next viral outbreak.
 
The answer is in the original paper
https://www.ijidonline.com/article/S1201-9712(20)30534-8/fulltext
"The combination of hydroxychloroquine + azithromycin was reserved for selected patients with severe COVID-19 and with minimal cardiac risk factors. "
IOW, as I guessed, the study was not random. Each group was not treated the same other than for the drug being studied. That's what not being random means.

I would not call this a retrospective study. The treatment regimes appear to be planned in advance. But (in common with many covid studies) it is not randomised.
The authors themselves refer to it as a retrospective study. They also use the term "observational", which, in this context, is basically synonymous with retrospective. Yes, there was some design in advance, they didn't just look at patients they knew nothing about before. But the design was constrained by the situation. I suppose you could call it a hybrid study, not purely retrospective.

Meanwhile, at least ten Secret Service agents have tested positive in the last two weeks. The CDC may want to consider a separate category in its records.

A recent study in Germany reports that about 80% of people not/never infected with SARS-CoV-2 nevertheless have some T-cell mediated immunity to the virus. They believe this is from previously having been infected with a relatively harmless coronavirus responsible for common colds. This could possibly be a factor accounting for why some people fight off this virus much more quickly and easily than others of about the same age and health. Go out and catch a cold!

https://www.researchsquare.com/article/rs-35331/v1
 
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Also, its important to note that 60K is the worst year(s), most years are under 40K.
And...the 45 million infected is based on symptoms, the number could be much higher; and those numbers were achieved with no restrictions at all. They would be far lower if there was mask wearing, social distancing, not to mention lockdowns..

OTOH, nearly half of Americans get an annual flu shot. This should protect them, as well as reduce the risk of catching the virus for those who aren't vaccinated.
 
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