Coronavirus outbreak - From China to the World.

[Infidel144]

Covid Patients Testing Positive After Recovery Aren’t Infectious, Study Shows

Researchers are finding evidence that patients who test positive for the coronavirus after recovering aren’t capable of transmitting the infection, and could have the antibodies that prevent them from falling sick again.

Scientists from the Korean Centers for Disease Control and Prevention studied 285 Covid-19 survivors who had tested positive for the coronavirus after their illness had apparently resolved, as indicated by a previous negative test result. The so-called re-positive patients weren’t found to have spread any lingering infection, and virus samples collected from them couldn’t be grown in culture, indicating the patients were shedding non-infectious or dead virus particles.
https://www.bloomberg.com/news/artic...n-t-infectious

And a study out of Singapore:
Covid-19 patients are no longer infectious after 11 days of getting sick even though some may still test positive, according to a new study by infectious disease experts in Singapore.


A positive test “does not equate to infectiousness or viable virus,” a joint research paper by Singapore’s National Centre for Infectious Diseases and the Academy of Medicine, Singapore said. The virus “could not be isolated or cultured after day 11 of illness.”
https://www.bloomberg.com/news/artic...ingapore-study

[Common Soldier]

https://www.healthaffairs.org/doi/fu...aff.2020.00598

I wonder how accurate this study is, and how it should affect policy makers.

The problem is how the study accounted the comorbidity factors, things like diabetes, hypertension and the like that could affect COVID-19 mortality

We know African Americans suffer from higher rates of things like diabetes, more often it is not formally diagnosed in African American. Their "accounting" for comorbidity factors could be off if the underestimated the actual levels of these factors, for example, diabetes, because the patient had never been formally diagnosed for having them.


Or they could be making assumptions about the comorbidity factors levels, assumptions that could be wrong. Determining the levels of these comorbidity factors, and leave opportunity to be manipulated, even subconsciously or deliberately, tonget the results desired. Given how COVID-19 has been politicized

I am not sure how trustworthy the sutdy results will be. Men are dying at a significantly higher rate than women, yet I don't see any studies hinting at bias toward men as the cause. The answers claimed have pretty much proven not correct, for example smoking.





D..

[Common Soldier]

Duplicate.post
.

[B. W.]

Shall we follow the Hydroxychloroquine profit trail and see where it goes also?

Not staking an opinion, just mentioning for the sake of due diligence and impartial commenting...

It's always a good idea to follow the money. I've said many times that it will likely lead you to the truth. The fact remains that Hydroxychloroquiine is cheap and there are many doctors who remain enthusiastic about it use:

https://www.americanthinker.com/blog..._see_this.html

[PointOfViewGun]

It's always a good idea to follow the money. I've said many times that it will likely lead you to the truth. The fact remains that Hydroxychloroquiine is cheap and there are many doctors who remain enthusiastic about it use:

https://www.americanthinker.com/blog..._see_this.html

Cheap doesn't mean not profitable. With president backing it up for mass usage the pharmaceutical companies that produce it will likely make a lot of money over it that they normally would not. Clearly, you're using different standards here.

[sumskilz]

Cheap doesn't mean not profitable. With president backing it up for mass usage the pharmaceutical companies that produce it will likely make a lot of money over it that they normally would not.

The issue is relative. The patent on hydroxychloroquine ran out in 1979, so no one can price it like they have a monopoly. I see here that you can buy it for as little 17 cents per dose.

In contrast, here's an excerpt from an NPR article on Gilead's remdesiver:

Breaking with its usual practices, the Institute for Clinical and Economic Review, or ICER, an influential nonprofit that analyzes drug pricing, issued an expedited report on remdesivir.

"Under normal circumstances, we would be unlikely to do a report when the evidence is this raw and immature," ICER President Steven Pearson said in an interview with NPR. "But it was quite clear that the world is moving at a much quicker pace."

If the price is based just on the cost of making the drug, then a 10-day course of remdesivir should cost about $10, according to the ICER report. (Gilead said results of a recently completed study suggest a five-day course of treatment may be just as effective.)

But if the drug is priced based on the drug's effectiveness, ICER estimates it should cost around $4,500 — assuming the drug is proven to have some benefit on mortality. If it doesn't and the drug only shortens hospital stays, that value-based price goes down to $390...

Rutgers' Carrier said he expects Gilead to set the remdesivir price somewhere between the $10 and $4,500 that ICER estimated. The company has already shown that it can respond to public pressure when it asked the FDA to rescind the orphan drug status it won for remdesivir, he pointed out.

"When you see that $10 figure, that sets a benchmark for a figure that is eminently affordable," Carrier said. Ultimately, he said a price more than $1,000 per treatment course would be unpopular.

Gilead "will be watched very carefully," he said, because of its prior history of pricing. He referred to two other Gilead drugs that drew scrutiny over high price tags. The company charged $1,000 per pill for Sovaldi, a cure for hepatitis C. And its HIV drug Truvada can cost $22,000 per year.

[Ludicus]

Shall we follow the Hydroxychloroquine profit trail and see where it goes also?

I quote. May 25. Source -Covid Reference, Top articles

A brief (and probably the last) review on hydroxychloroquine and chloroquine.

"A few months ago, lab experiments suggested that hydroxychloroquine (HCQ) and chloroquine (CQ) might have some antiviral effects against SARS-CoV-2 due to an increase in the endosomal pH value which disrupts the virus-cell fusion and some post-entry steps (Wang 2020, Yao 2020). An early enthusiastic mini-review stated “results from more than 100 patients” showed that chloroquine phosphate would be able to alleviate the course of the disease (Gao 2020). Other experts, however, dampened the enthusiasm, pointing out that a benefit of chloroquine would be the first positive signal, after decades of unsuccessful studies conducted in a huge number of acute viral diseases (Touret 2020). On March 17, a preliminary report from Marseille/France appeared to show some benefit in a small non-randomized study on 36 patients (Gautret 2020). Although this work lacked essential standards of data generation and interpretation (Kim 2020), someone’s swanky tweet claiming on March 21 that the combination of HCQ and azithromycin has “a real chance to be one of the biggest game changers in the history of medicine”, attracted world-wide attention and led to tens of thousands of uncontrolled treatments. Moreover, many patients decided against clinical trials of other therapies that would require them to give up chloroquine treatments. This has already prompted serious delays in trial enrolment, muddled efforts to interpret data and endangered clinical research (Ledford 2020). Some countries have stockpiled CQ and HCQ, resulting in a shortage of these medications for those that need them for approved clinical indications.

Only a few weeks later, we are now facing an overwhelming amount of data strongly arguing against any use of both HCQ and CQ.

• The by-far most convincing data were published last Friday, May 22 (Mehra 2020). In this extraordinary multinational registry analysis from 671 hospitals on six continents, 14,888 patients (1,868 received CQ; 3,783 received CQ with azithromycin or clarithromycin; 3,016 received HCQ; and 6,221 received HCQ with a macrolide) were compared to 81,144 control patients who did not receive these drugs. Mortality was higher in all treatment groups than in the controls (18.0-23.8% versus 9.3%) and each treatment regimen was independently associated with an increased risk of in-hospital mortality and with de novo ventricular arrhythmia, especially in the combination groups (4.3-8.1 versus 0.3%). Adjustment for multiple confounding factors, a propensity score matching analysis and a tipping-point analysis (an analysis that shows the effect size and prevalence of an unmeasured confounder that could shift the upper boundary of the CI towards null) did not affect the results. Although the authors concluded that a cause-and-effect relationship between drug therapy and survival should not be inferred and that their data do not apply to the use of any treatment regimen used in the ambulatory, out-of-hospital setting, it is hard to find any argument for any of these strategies. Data do not support the use of these regimens outside randomized clinical trials (RCTs). Researchers who conduct and supervise RCTs should consider whether ongoing recruitment is necessary.

Other key studies arguing against HCQ in recent weeks

1. In an observational study from New York City of 1,376 consecutive hospitalized patients, 811 received HCQ (60% received also azithromycin) (Geleris 2020). After adjusting for several confounders (HCQ patients were more severely ill at baseline), hydroxychloroquine administration was not associated with either a greatly lowered or an increased risk of the composite end point of intubation or death.
2. Another retrospective cohort of 1,438 patients from 25 hospitals in the New York metropolitan region looked at 1,438 patients (Rosenberg 2020). In adjusted Cox models, compared with patients receiving neither drug, there were no significant differences in mortality for patients receiving HCQ + azithromycin, HCQ alone, or azithromycin alone. Cardiac arrest was significantly more likely with HCQ + azithromycin (adjusted OR 2.13).
3. A randomized, Phase IIb clinical trial in Brazil allocated severe COVID-19 patients to receive high-dose CQ (600 mg BID for 10 days) or low-dose CQ (450 mg BID on day 1, QD for 4 days). The DSMB terminated the trial after 81/440 individuals were enrolled (Borba 2020). By day 13 of enrolment, 6/40 patients (15%) in the low-dose group had died, compared with 16/41 (39%) in the high-dose group. Viral RNA was detected in 78% and 76%, respectively.
4. In a retrospective study of 251 patients receiving HCQ plus azithromycin, extreme new QTc prolongation to >500 ms, a known marker of high risk for torsade de pointes, had developed in 23% (Chorin 2020).
5. HCQ does not work as prophylaxis. A case series described 17 lupus patients with COVID-19, among them several severe cases (Mathian 2020). See below (1)
6. Free plasma HCQ concentration achieved with HCQ doses tolerable for humans are probably too low to have any antiviral effects (Fan 2020)".

References
Borba MGS, Val FFA, Sampaio VS, et al. Effect of High vs Low Doses of Chloroquine Diphosphate as Adjunctive Therapy for Patients Hospitalized With Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection: A Randomized Clinical Trial. JAMA Netw Open. 2020 Apr 24;3(4.23):e208857. PubMed: https://pubmed.gov/32330277 . Full-text: https://doi.org/10.1001/jamanetworkopen.2020.8857
Chorin E, Wadhwani L, Magnani S, et al. QT Interval Prolongation and Torsade De Pointes in Patients with COVID-19 treated with Hydroxychloroquine/Azithromycin. Heart Rhythm. 2020 May 11:S1547-5271(20)30435-5. PubMed: https://pubmed.gov/32407884 . Full-text: https://doi.org/10.1016/j.hrthm.2020.05.014
Fan J, Zhang X, Liu J, et al. Connecting hydroxychloroquine in vitro antiviral activity to in vivo concentration for prediction of antiviral effect: a critical step in treating COVID-19 patients. Clin Infect Dis. 2020 May 21:ciaa623. PubMed: https://pubmed.gov/32435791 . Full-text: https://doi.org/10.1093/cid/ciaa623
Gao J, Tian Z, Yang X. Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies. Biosci Trends. 2020 Mar 16;14(1):72-73. PubMed: https://pubmed.gov/32074550 . Full-text: https://doi.org/10.5582/bst.2020.01047
Gautret P, Lagier JC, Parola P, et al. Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial. Int J Antimicrob Agents. 2020 Mar 20:105949. PubMed: https://pubmed.gov/32205204 . Full-text: https://doi.org/10.1016/j.ijantimicag.2020.105949
Geleris J, Sun Y, Platt J, et al. Observational Study of Hydroxychloroquine in Hospitalized Patients with Covid-19. N Engl J Med. 2020 May 7. PubMed: https://pubmed.gov/32379955 . Full-text: https://doi.org/10.1056/NEJMoa2012410
Kim AH, Sparks JA, Liew JW. A Rush to Judgment? Rapid Reporting and Dissemination of Results and Its Consequences Regarding the Use of Hydroxychloroquine for COVID-19. Ann Intern Med 2020. Full-text: https://doi.org/10.7326/M20-1223
Ledford H. Chloroquine hype is derailing the search for coronavirus treatments. Nature Medicine, 24 April 2020. Full-text: https://www.nature.com/articles/d41586-020-01165-3
Mathian A, Mahevas M, Rohmer J, et al. Clinical course of coronavirus disease 2019 (COVID-19) in a series of 17 patients with systemic lupus erythematosus under long-term treatment with hydroxychloroquine. Ann Rheum Dis. 2020 Apr 24. PubMed: https://pubmed.gov/32332072 . Full-text: https://doi.org/10.1136/annrheumdis-2020-217566
Mehra MR, Desai SS, Ruschitzka F, Patel AM. Hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19: a multinational registry analysis. Lancet May 22, 2020 Full-text: https://doi.org/10.1016/S0140-6736(20)31180-6
Rosenberg ES, Dufort EM, Udo T, et al. Association of Treatment With Hydroxychloroquine or Azithromycin With In-Hospital Mortality in Patients With COVID-19 in New York State. JAMA. 2020 May 11. https://pubmed.gov/32392282 . Full-text: https://doi.org/10.1001/jama.2020.8630
Touret F, de Lamballerie X. Of chloroquine and COVID-19. Antiviral Res. 2020 Mar 5;177:104762. PubMed: https://pubmed.gov/32147496 . Full-text: https://doi.org/10.1016/j.antiviral.2020.104762
Wang M, Cao R, Zhang L, et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro. Cell Res. 2020 Mar;30(3):269-271. PubMed: https://pubmed.gov/32020029 . Full-text: https://doi.org/10.1038/s41422-020-0282-0
Yao X, Ye F, Zhang M, et al. In Vitro Antiviral Activity and Projection of Optimized Dosing Design of Hydroxychloroquine for the Treatment of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Clin Infect Dis. 2020 Mar 9. PubMed: https://pubmed.gov/32150618 . Full-text: https://doi.org/10.1093/cid/ciaa237

--------
(1) two cases reported by our university hospital.Post 1637.

"While these two cases do not provide any definite answer to the question of whether antimalarials can prevent COVID-19 or severe disease, they show that, indeed, patients with SLE can develop disease, even if on stable hydroxychloroquine therapy.
The mild disease course should not be attributed to the concomitant antimalarial. Rather, it is likely related to other factors known to be associated with better outcomes, such as female sex and younger age"

-------

Vitamin D deficiency rate is also another likely factor

Who knows...
Vitamin D "deficiency/insufficiency" [25(OH)D < 20 ng/ml] is highly prevalent here. BUT - 1) lab tests are not reliable. 2)There is no evidence of benefit of taking dietary supplementary in chronic diseases. In the general population, the specific indications for Vit D assay testing are not established and Vit.D concentration screening is not recommended.For the majority of the population there is no consistent association between vit.D status and mortality.
Use google translate.From our Centre for Evidence-Based Medicine. Vitamin D in the Prevention of Chronic Diseases: An Evidence Based Analysis (PDF) A Vitamina D na Prevenção de Doenças Crónicas: Uma...2017

------

UK COVID-19 vaccine trial may fail due to...

A very interesting interview with Florian Kramer, virologist at Mount Sinai Hospital. In his interview, Krammer comments on the role of immunization, treatments, immunity/group immunity, and the most recent progresses in the development of vaccines. Until the arrival of the coronavirus, a team led by Krammer and Palese have focused their efforts on developing an universal vaccine against influenza, using a novel approach they have developed called chimeric hemagglutinin (cHA). Read the entire Interview- China will have the first vaccine

P. The vaccine is the only way out of this pandemic?
R. Yes. Achieving group immunity involves so many deaths that aspiring to it is immoral

[PointOfViewGun]

The issue is relative. The patent on hydroxychloroquine ran out in 1979, so no one can price it like they have a monopoly. I see here that you can buy it for as little 17 cents per dose.

In contrast, here's an excerpt from an NPR article on Gilead's remdesiver:

Having no patent doesn't changes the story. Companies that do not produce such a drug can not start producing it a moment's notice. It is just a simple fact that companies that are already producing this drug will be far better off when its used in mass.

[B. W.]

Cheap doesn't mean not profitable. With president backing it up for mass usage the pharmaceutical companies that produce it will likely make a lot of money over it that they normally would not. Clearly, you're using different standards here.

As I recall, the doctor in the video said a regime of HCQ cost $16.00. She also claimed it was successful in treating the infection.

I quote. May 25. Source -Covid Reference, Top articles

A brief (and probably the last) review on hydroxychloroquine and chloroquine.

"A few months ago, lab experiments suggested that hydroxychloroquine (HCQ) and chloroquine (CQ) might have some antiviral effects against SARS-CoV-2 due to an increase in the endosomal pH value which disrupts the virus-cell fusion and some post-entry steps (Wang 2020, Yao 2020). An early enthusiastic mini-review stated “results from more than 100 patients” showed that chloroquine phosphate would be able to alleviate the course of the disease (Gao 2020). Other experts, however, dampened the enthusiasm, pointing out that a benefit of chloroquine would be the first positive signal, after decades of unsuccessful studies conducted in a huge number of acute viral diseases (Touret 2020). On March 17, a preliminary report from Marseille/France appeared to show some benefit in a small non-randomized study on 36 patients (Gautret 2020). Although this work lacked essential standards of data generation and interpretation (Kim 2020), someone’s swanky tweet claiming on March 21 that the combination of HCQ and azithromycin has “a real chance to be one of the biggest game changers in the history of medicine”, attracted world-wide attention and led to tens of thousands of uncontrolled treatments. Moreover, many patients decided against clinical trials of other therapies that would require them to give up chloroquine treatments. This has already prompted serious delays in trial enrolment, muddled efforts to interpret data and endangered clinical research (Ledford 2020). Some countries have stockpiled CQ and HCQ, resulting in a shortage of these medications for those that need them for approved clinical indications.

Only a few weeks later, we are now facing an overwhelming amount of data strongly arguing against any use of both HCQ and CQ.

• The by-far most convincing data were published last Friday, May 22 (Mehra 2020). In this extraordinary multinational registry analysis from 671 hospitals on six continents, 14,888 patients (1,868 received CQ; 3,783 received CQ with azithromycin or clarithromycin; 3,016 received HCQ; and 6,221 received HCQ with a macrolide) were compared to 81,144 control patients who did not receive these drugs. Mortality was higher in all treatment groups than in the controls (18.0-23.8% versus 9.3%) and each treatment regimen was independently associated with an increased risk of in-hospital mortality and with de novo ventricular arrhythmia, especially in the combination groups (4.3-8.1 versus 0.3%). Adjustment for multiple confounding factors, a propensity score matching analysis and a tipping-point analysis (an analysis that shows the effect size and prevalence of an unmeasured confounder that could shift the upper boundary of the CI towards null) did not affect the results. Although the authors concluded that a cause-and-effect relationship between drug therapy and survival should not be inferred and that their data do not apply to the use of any treatment regimen used in the ambulatory, out-of-hospital setting, it is hard to find any argument for any of these strategies. Data do not support the use of these regimens outside randomized clinical trials (RCTs). Researchers who conduct and supervise RCTs should consider whether ongoing recruitment is necessary.

Other key studies arguing against HCQ in recent weeks

1. In an observational study from New York City of 1,376 consecutive hospitalized patients, 811 received HCQ (60% received also azithromycin) (Geleris 2020). After adjusting for several confounders (HCQ patients were more severely ill at baseline), hydroxychloroquine administration was not associated with either a greatly lowered or an increased risk of the composite end point of intubation or death.
2. Another retrospective cohort of 1,438 patients from 25 hospitals in the New York metropolitan region looked at 1,438 patients (Rosenberg 2020). In adjusted Cox models, compared with patients receiving neither drug, there were no significant differences in mortality for patients receiving HCQ + azithromycin, HCQ alone, or azithromycin alone. Cardiac arrest was significantly more likely with HCQ + azithromycin (adjusted OR 2.13).
3. A randomized, Phase IIb clinical trial in Brazil allocated severe COVID-19 patients to receive high-dose CQ (600 mg BID for 10 days) or low-dose CQ (450 mg BID on day 1, QD for 4 days). The DSMB terminated the trial after 81/440 individuals were enrolled (Borba 2020). By day 13 of enrolment, 6/40 patients (15%) in the low-dose group had died, compared with 16/41 (39%) in the high-dose group. Viral RNA was detected in 78% and 76%, respectively.
4. In a retrospective study of 251 patients receiving HCQ plus azithromycin, extreme new QTc prolongation to >500 ms, a known marker of high risk for torsade de pointes, had developed in 23% (Chorin 2020).
5. HCQ does not work as prophylaxis. A case series described 17 lupus patients with COVID-19, among them several severe cases (Mathian 2020). See below (1)
6. Free plasma HCQ concentration achieved with HCQ doses tolerable for humans are probably too low to have any antiviral effects (Fan 2020)".

References
Borba MGS, Val FFA, Sampaio VS, et al. Effect of High vs Low Doses of Chloroquine Diphosphate as Adjunctive Therapy for Patients Hospitalized With Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection: A Randomized Clinical Trial. JAMA Netw Open. 2020 Apr 24;3(4.23):e208857. PubMed: https://pubmed.gov/32330277 . Full-text: https://doi.org/10.1001/jamanetworkopen.2020.8857
Chorin E, Wadhwani L, Magnani S, et al. QT Interval Prolongation and Torsade De Pointes in Patients with COVID-19 treated with Hydroxychloroquine/Azithromycin. Heart Rhythm. 2020 May 11:S1547-5271(20)30435-5. PubMed: https://pubmed.gov/32407884 . Full-text: https://doi.org/10.1016/j.hrthm.2020.05.014
Fan J, Zhang X, Liu J, et al. Connecting hydroxychloroquine in vitro antiviral activity to in vivo concentration for prediction of antiviral effect: a critical step in treating COVID-19 patients. Clin Infect Dis. 2020 May 21:ciaa623. PubMed: https://pubmed.gov/32435791 . Full-text: https://doi.org/10.1093/cid/ciaa623
Gao J, Tian Z, Yang X. Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies. Biosci Trends. 2020 Mar 16;14(1):72-73. PubMed: https://pubmed.gov/32074550 . Full-text: https://doi.org/10.5582/bst.2020.01047
Gautret P, Lagier JC, Parola P, et al. Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial. Int J Antimicrob Agents. 2020 Mar 20:105949. PubMed: https://pubmed.gov/32205204 . Full-text: https://doi.org/10.1016/j.ijantimicag.2020.105949
Geleris J, Sun Y, Platt J, et al. Observational Study of Hydroxychloroquine in Hospitalized Patients with Covid-19. N Engl J Med. 2020 May 7. PubMed: https://pubmed.gov/32379955 . Full-text: https://doi.org/10.1056/NEJMoa2012410
Kim AH, Sparks JA, Liew JW. A Rush to Judgment? Rapid Reporting and Dissemination of Results and Its Consequences Regarding the Use of Hydroxychloroquine for COVID-19. Ann Intern Med 2020. Full-text: https://doi.org/10.7326/M20-1223
Ledford H. Chloroquine hype is derailing the search for coronavirus treatments. Nature Medicine, 24 April 2020. Full-text: https://www.nature.com/articles/d41586-020-01165-3
Mathian A, Mahevas M, Rohmer J, et al. Clinical course of coronavirus disease 2019 (COVID-19) in a series of 17 patients with systemic lupus erythematosus under long-term treatment with hydroxychloroquine. Ann Rheum Dis. 2020 Apr 24. PubMed: https://pubmed.gov/32332072 . Full-text: https://doi.org/10.1136/annrheumdis-2020-217566
Mehra MR, Desai SS, Ruschitzka F, Patel AM. Hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19: a multinational registry analysis. Lancet May 22, 2020 Full-text: https://doi.org/10.1016/S0140-6736(20)31180-6
Rosenberg ES, Dufort EM, Udo T, et al. Association of Treatment With Hydroxychloroquine or Azithromycin With In-Hospital Mortality in Patients With COVID-19 in New York State. JAMA. 2020 May 11. https://pubmed.gov/32392282 . Full-text: https://doi.org/10.1001/jama.2020.8630
Touret F, de Lamballerie X. Of chloroquine and COVID-19. Antiviral Res. 2020 Mar 5;177:104762. PubMed: https://pubmed.gov/32147496 . Full-text: https://doi.org/10.1016/j.antiviral.2020.104762
Wang M, Cao R, Zhang L, et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro. Cell Res. 2020 Mar;30(3):269-271. PubMed: https://pubmed.gov/32020029 . Full-text: https://doi.org/10.1038/s41422-020-0282-0
Yao X, Ye F, Zhang M, et al. In Vitro Antiviral Activity and Projection of Optimized Dosing Design of Hydroxychloroquine for the Treatment of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Clin Infect Dis. 2020 Mar 9. PubMed: https://pubmed.gov/32150618 . Full-text: https://doi.org/10.1093/cid/ciaa237

--------
(1) two cases reported by our university hospital.Post 1637.

"While these two cases do not provide any definite answer to the question of whether antimalarials can prevent COVID-19 or severe disease, they show that, indeed, patients with SLE can develop disease, even if on stable hydroxychloroquine therapy.
The mild disease course should not be attributed to the concomitant antimalarial. Rather, it is likely related to other factors known to be associated with better outcomes, such as female sex and younger age"

-------

Who knows...
Vitamin D "deficiency/insufficiency" [25(OH)D < 20 ng/ml] is highly prevalent here. BUT - 1) lab tests are not reliable. 2)There is no evidence of benefit of taking dietary supplementary in chronic diseases. In the general population, the specific indications for Vit D assay testing are not established and Vit.D concentration screening is not recommended.For the majority of the population there is no consistent association between vit.D status and mortality.
Use google translate.From our Centre for Evidence-Based Medicine. Vitamin D in the Prevention of Chronic Diseases: An Evidence Based Analysis (PDF) A Vitamina D na Prevenção de Doenças Crónicas: Uma...2017

------

A very interesting interview with Florian Kramer, virologist at Mount Sinai Hospital. In his interview, Krammer comments on the role of immunization, treatments, immunity/group immunity, and the most recent progresses in the development of vaccines. Until the arrival of the coronavirus, a team led by Krammer and Palese have focused their efforts on developing an universal vaccine against influenza, using a novel approach they have developed called chimeric hemagglutinin (cHA). Read the entire Interview- China will have the first vaccine

I would be willing to bet that you will never see a study that confirms a cheap treatment for Covid-19. Now, you can do whatever you like. But me, I'm taking vit-c, zinc, and Vit-d3 supplements daily. Maybe I'll get lucky and not get sick.

[sumskilz]

Who knows...

As I understand it, there are issues with accurate screening, but it's probably safe to say African-Americans generally have lower average vitamin D levels in the US.

I was thinking along the lines of this:

Genetic cause of disparity in COVID-19 deaths?

A second goal of Chatham and Cron’s study is to obtain genetic samples that will be sequenced to determine if patients who experience cytokine storm syndrome harbor mutations associated with enhanced IL-1-beta responses or perforin pathway mutations. This genetic evaluation eventually could be used to identify patients at high risk for cytokine storm syndrome.

Unfortunately, the distribution of some of these mutations in the population is unequal, Chatham noted. And that could explain part of the reason why African Americans have been disproportionately affected by COVID-19. Genetic polymorphisms associated with enhanced IL-1 production are present in about 40% of African Americans but only 6% of Caucasians,” Chatham said.

And this:

The role of Vit D in regulating the immune system has been supported by multiple studies[11]. Vit D can suppress cytokine production by simultaneously boosting the innate immune system (thus reducing the viral load) and decreasing the overactivation of the adaptive immune system to immediately respond to the viral load. Some researchers have suggested the potential role of Vit D in suppressing cytokine storm during the 1918- 1919 viral influenza pandemic[12]. Moreover, the role of Vit D in enhancing immune response in flu and previous coronaviruses has been suggested[11,13]. It is this ability of Vit D in suppressing cytokine production[14,15]that motivated our focus on Vit D deficiency and its association with severe COVID-19.

To the best of our knowledge, no randomized blinded experiment has yet reported Vit D status and cytokine levels in patients with COVID-19. In spite of this, it is still possible to investigate the association between Vit D status and unregulated inflammation and cytokine production leading to severe COVID-19 based on a potential link between Vit D deficiency and C-reactive proteins (CRP)[16].

CRPs are produced primarily in the liver in response to inflammation to minimize damage to tissues from autoimmunity, infection, and other causes. The inflammatory cells’ ability to convert Vit D metabolites into calcitriol (the active form of Vit D) and to express the nuclear receptor of Vit D suggests a potential inverse association between CRP and Vit D, which is also supported by epidemiological studies[17,18]. Early studies have shown that calcitriol treatment attenuates both CRP and inflammatory cytokines (CD4(+) IFN-γ) in hemodialysis patients[19]. Researchers have proposed that calcitriol modulates cytokine levels (such as TNF-α and IL-1β) through the intercellular role of calcium[20,21]. Here we combine Vit D and CRP data from NHANES, 2009-2010 dataset[22] with clinical data from COVID-19 patients[23] to investigate the potential role of Vit D in regulating inflammation and cytokine production leading to severe COVID-19 across different countries. We partially address some of the concerns regarding association between Vit D and other risk factors of COVID-19 A-CMR including heart disease, diabetes, age, and obesity in each country via regression analysis.

The Possible Role of Vitamin D in Suppressing Cytokine Storm and Associated Mortality in COVID-19 Patients

In plain language:

Backman and his team were inspired to examine vitamin D levels after noticing unexplained differences in COVID-19 mortality rates from country to country. Some people hypothesized that differences in healthcare quality, age distributions in population, testing rates or different strains of the coronavirus might be responsible. But Backman remained skeptical.

"None of these factors appears to play a significant role," Backman said. "The healthcare system in northern Italy is one of the best in the world. Differences in mortality exist even if one looks across the same age group. And, while the restrictions on testing do indeed vary, the disparities in mortality still exist even when we looked at countries or populations for which similar testing rates apply.

"Instead, we saw a significant correlation with vitamin D deficiency," he said.

By analyzing publicly available patient data from around the globe, Backman and his team discovered a strong correlation between vitamin D levels and cytokine storm -- a hyperinflammatory condition caused by an overactive immune system -- as well as a correlation between vitamin D deficiency and mortality.

"Cytokine storm can severely damage lungs and lead to acute respiratory distress syndrome and death in patients," Daneshkhah said. "This is what seems to kill a majority of COVID-19 patients, not the destruction of the lungs by the virus itself. It is the complications from the misdirected fire from the immune system."

This is exactly where Backman believes vitamin D plays a major role. Not only does vitamin D enhance our innate immune systems, it also prevents our immune systems from becoming dangerously overactive. This means that having healthy levels of vitamin D could protect patients against severe complications, including death, from COVID-19.

"Our analysis shows that it might be as high as cutting the mortality rate in half," Backman said. "It will not prevent a patient from contracting the virus, but it may reduce complications and prevent death in those who are infected."

Backman said this correlation might help explain the many mysteries surrounding COVID-19, such as why children are less likely to die. Children do not yet have a fully developed acquired immune system, which is the immune system's second line of defense and more likely to overreact.

"Children primarily rely on their innate immune system," Backman said. "This may explain why their mortality rate is lower."

EDIT:

Having no patent doesn't changes the story.

It certainly does, competition has already brought the prices of HCQ extremely low. In contrast, a company like Gilead can charge hundreds or several thousand dollars for a single patented treatment and the only choice is to buy or not buy, because you can't get it from anyone else.

[Genava]

Gilead has pledged to donate around 1.5 million doses of remdesivir, about 40% of which is going to the U.S. government. But not all of the remaining 60% of supply has been allocated. The biotech is reportedly increasing its U.S. donation to about 940,000 doses by June.

https://www.fiercepharma.com/pharma/...al-opportunity

[sumskilz]

https://www.fiercepharma.com/pharma/...al-opportunity

Well, that's cool of them. That's 600,000 to the US government, at 11 doses per course, that would be enough to treat 54,545 people, but that is a small percentage of the current active cases and a tiny percentage of the US population as a whole. After that, how much would it cost?

According to the article:

The Institute for Clinical and Economic Review recently found remdesivir would be cost-effective at $28,670 if the analysis used as a benchmark the common $100,000 per incremental quality-adjusted life-year gained. But the U.S. drug cost watchdog argued that $50,000/QALY should be applied to remdesivir during a public health emergency. After that calculation, ICER pegged a reasonable price at $4,460.

For Dickinson, using a tighter threshold for remdesivir seemed unreasonable when the typical standard is $100,00/QALY. The company is running its own cost-savings analysis for hospitals that will be used to inform final pricing, Porges noted.

Dickinson suggested that the cost to manufacture remdesivir is “an order of magnitude greater than” the $10 per 10-day course ICER used in its report, Porges said. Nevertheless, the SVB Leerink analyst expects Gilead would still be able to make money abiding by the $4,460-per-course price. High profit margins might be out of reach at that level, but all eyes are on the drug’s affordability, the analyst noted.

So $4,460 per person for the rest of us is evidently a bargain.

[PointOfViewGun]

As I recall, the doctor in the video said a regime of HCQ cost $16.00. She also claimed it was successful in treating the infection.

EDIT:
It certainly does, competition has already brought the prices of HCQ extremely low. In contrast, a company like Gilead can charge hundreds or several thousand dollars for a single patented treatment and the only choice is to buy or not buy, because you can't get it from anyone else.

Nope. A drug that is to be used frequently for a long periods of time by a vast portion of the public will generate a lot of profit regardless of how low the price is.

[sumskilz]

Nope. A drug that is to be used frequently for a long periods of time by a vast portion of the public will generate a lot of profit regardless of how low the price is.

Okay sure, I said "relative". What will make more money? A drug that costs $16 per course or a drug that will cost $4,460 per course? It's not even close, even if remdesivir really does cost $100 per course to manufacture.

[tgoodenow]

But with the number of UK coronavirus cases dropping every day, there may not be enough people to test it on, according to the institute's director Professor Adrian Hill.

He told The Sunday Telegraph: "It's a race against the virus disappearing, and against time. We said earlier in the year that there was an 80% chance of developing an effective vaccine by September.

"But at the moment, there's a 50% chance that we get no result at all. We're in the bizarre position of wanting COVID to stay, at least for a little while."

https://www.google.com/amp/s/news.sk...rking-11993739

So now we’re worried about enough people with the disease to test the vaccine?

[tgoodenow]

Edit: double post please delete

[PointOfViewGun]

Okay sure, I said "relative". What will make more money? A drug that costs $16 per course or a drug that will cost $4,460 per course? It's not even close, even if remdesivir really does cost $100 per course to manufacture.

Definitely the drug that costs 16 dollars. You clearly don't know a funny little thing called elasticity of demand. A drug that costs 4,460$ will only reach relatively very few patients, meanwhile the cheap drug can bought by tens of millions frequently. Expensive one provide a good profit margin while the cheap one provides a very good profit in absolute terms.

[Ludicus]

.The Possible Role of Vitamin D in Suppressing Cytokine Storm and Associated Mortality in COVID-19 Patients

Speculation, but let's wait and see.
More, CEBM - Oxford. On behalf of the Oxford COVID-19 Evidence Service Team
Centre for Evidence-Based Medicine, Nuffield Department of Primary Care Health Sciences
University of Oxford

May 2020
Vitamin D: A rapid review of the evidence for treatment or prevention of COVID-19

an overview of systematic reviews of vitamin D for all non-skeletal conditions suggests that vitamin D2 or D3 supplementation has no important clinical effect on most conditions, including chronic inflammation, strengthening the hypothesis that low vitamin D status is a consequence of ill health, rather than its cause.[21]
We found no clinical evidence that vitamin D supplements are beneficial in preventing or treating COVID-19. We would need evidence from well-masked randomized trials to determine if there are effects, before recommending vitamin D3 supplements for treating or preventing COVID-19 infection.

[sumskilz]

Definitely the drug that costs 16 dollars. You clearly don't know a funny little thing called elasticity of demand. A drug that costs 4,460$ will only reach relatively very few patients, meanwhile the cheap drug can bought by tens of millions frequently. Expensive one provide a good profit margin while the cheap one provides a very good profit in absolute terms.

Actually nobody would buy the more expensive drug if both were perceived to be effective, so if you held exclusive rights to the more expensive drug, it would be imperative to thoroughly discredit the inexpensive drug. At that point, you could then adjust your price up or down to maximize profits with whichever strategy you like, because there would be no competition. That might explain why a company like Novartis would be sponsoring trials of hydroxychloroquine alongside trials of their own patented drug, while their research director publicly scoffs at hydroxychloroquine proponents in the role of an unbiased expert without mentioning the conflict of interest. That doesn't make him wrong, but it's the type thing that makes me suspicious about some of the trials that seem to be designed to be destined to fail based on the proposed mechanism and known side effects. That said, I won't be surprised if most potential treatments (including HCQ) turn out to offer little to no benefit.

[Ludicus]

That might explain why a company like Novartis would be sponsoring trials of hydroxychloroquine

I use their antiangiogenics therapies.I was not aware of that....Frankly.
I am always skeptical of the value of unnecessary vitamin supplements. Half of all Americans and Europeans take vitamin supplements on a regular basis. I still remember when Linus Pauling, Nobel Prize in Chemistry claimed that vitamin C prevents and alleviates the episodes of the common cold. In 1970, Pauling published Vitamin C and the Common Cold, urging the public to take high doses of Vit C.. a complete nonsense. In another paper, Vitamin C, the Common Cold and the Flu,he promised to ward off a predicted swine flu pandemic.!!!! Vit C. sales quadrupled. At least 15 studies have now shown that vitamin C doesn't treat the common cold but Pauling refused to believe it, continuing to promote vitamin C and urged doctors to give cancer patients massive doses of vitamin C. So, cancer researchers decided to test Pauling's theory, and they concluded "We were unable to show a therapeutic benefit of high-dose vitamin C.", and then Pauling claimed that claimed that vitamin C worked only if cancer victims had received no prior chemotherapy!!!
Next, he claimed that vitamin C, when taken with massive doses of vitamin A and E and vitamin E as well as selenium and beta-carotene , could treat virtually every disease known to man, including AIDS.
Long live to Linus Pauling Institute!
Linus Pauling Institute | Discovering How to Live Longer