Why is chloroquine so controversial?
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.
Comments
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No need for on-patent medicine and a vaccine if a $1/dose generic is effective in treating it.
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Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
It simply means the narrative rejection of chloroquine is political hyperbole, not science.MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
I’d be happy tooMelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.
Severe acute respiratory syndrome (SARS) is an emerging disease that was first reported in Guangdong Province, China, in late 2002. The disease rapidly spread to at least 30 countries within months of its first appearance, and concerted worldwide efforts led to the identification of the etiological agent as SARS coronavirus (SARS-CoV), a novel member of the family Coronaviridae [1]. Complete genome sequencing of SARS-CoV [2,3] confirmed that this pathogen is not closely related to any of the previously established coronavirus groups. Budding of the SARS-CoV occurs in the Golgi apparatus [4] and results in the incorporation of the envelope spike glycoprotein into the virion. The spike glycoprotein is a type I membrane protein that facilitates viral attachment to the cellular receptor and initiation of infection, and angiotensin-converting enzyme-2 (ACE2) has been identified as a functional cellular receptor of SARS-CoV [5]. We have recently shown that the processing of the spike protein was effected by furin-like convertases and that inhibition of this cleavage by a specific inhibitor abrogated cytopathicity and significantly reduced the virus titer of SARS-CoV [6].
Due to the severity of SARS-CoV infection, the potential for rapid spread of the disease, and the absence of proven effective and safe in vivo inhibitors of the virus, it is important to identify drugs that can effectively be used to treat or prevent potential SARS-CoV infections. Many novel therapeutic approaches have been evaluated in laboratory studies of SARS-CoV: notable among these approaches are those using siRNA [7], passive antibody transfer [8], DNA vaccination [9], vaccinia or parainfluenza virus expressing the spike protein [10,11], interferons [12,13], and monoclonal antibody to the S1-subunit of the spike glycoprotein that blocks receptor binding [14]. In this report, we describe the identification of chloroquine as an effective pre- and post-infection antiviral agent for SARS-CoV. Chloroquine, a 9-aminoquinoline that was identified in 1934, is a weak base that increases the pH of acidic vesicles. When added extracellularly, the non-protonated portion of chloroquine enters the cell, where it becomes protonated and concentrated in acidic, low-pH organelles, such as endosomes, Golgi vesicles, and lysosomes. Chloroquine can affect virus infection in many ways, and the antiviral effect depends in part on the extent to which the virus utilizes endosomes for entry. Chloroquine has been widely used to treat human diseases, such as malaria, amoebiosis, HIV, and autoimmune diseases, without significant detrimental side effects [15]. Together with data presented here, showing virus inhibition in cell culture by chloroquine doses compatible with patient treatment, these features suggest that further evaluation of chloroquine in animal models of SARS-CoV infection would be warranted as we progress toward finding effective antivirals for prevention or treatment of the disease.
Results
Preinfection chloroquine treatment renders Vero E6 cells refractory to SARS-CoV infection
In order to investigate if chloroquine might prevent SARS-CoV infection, permissive Vero E6 cells [1] were pretreated with various concentrations of chloroquine (0.1–10 μM) for 20–24 h prior to virus infection. Cells were then infected with SARS-CoV, and virus antigens were visualized by indirect immunofluorescence as described in Materials and Methods. Microscopic examination (Fig. (Fig.1A)1A) of the control cells (untreated, infected) revealed extensive SARS-CoV-specific immunostaining of the monolayer. A dose-dependant decrease in virus antigen-positive cells was observed starting at 0.1 μM chloroquine, and concentrations of 10 μM completely abolished SARS-CoV infection. For quantitative purposes, we counted the number of cells stained positive from three random locations on a slide. The average number of positively stained control cells was scored as 100% and was compared with the number of positive cells observed under various chloroquine concentrations (Fig. (Fig.1B).1B). Pretreatment with 0.1, 1, and 10 μM chloroquine reduced infectivity by 28%, 53%, and 100%, respectively. Reproducible results were obtained from three independent experiments. These data demonstrated that pretreatment of Vero E6 cells with chloroquine rendered these cells refractory to SARS-CoV infection.
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Thinking that I f asking this question means the Science is too robust for your understanding?MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
I hate the drink, but lots of folks should be thankful for chloroquine...it led to the drink Gin and Tonic.
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HoustonHusky said:
I hate the drink, but lots of folks should be thankful for chloroquine...it led to the drink Gin and Tonic.
https://www.youtube.com/watch?v=DI3yXg-sX5c
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https://forbes.com/sites/alexledsom/2020/05/10/hydroxychloroquinenumber-of-prescriptions-explode-in-france/#1c7f96e5180f
Prescriptions are higher than ever! -
I honestly don't get what the big deal is. It's 'script only, so people can't run out & get it. It might work, and maybe more likely doesn't work. TDS is skrong. -
Are they showing Trump’s pressers in France? Maybe during the Jerry Lewis movie marathons.RaceBannon said:https://forbes.com/sites/alexledsom/2020/05/10/hydroxychloroquinenumber-of-prescriptions-explode-in-france/#1c7f96e5180f
Prescriptions are higher than ever! -
The media doesn’t want it to work. Most stories say: Trump says “without evidence” that it might work. I remember when they said: Trump accuses Obama administration of spying, “without evidence”..... whoopsie poopsie!GrundleStiltzkin said:
I honestly don't get what the big deal is. It's 'script only, so people can't run out & get it. It might work, and maybe more likely doesn't work. TDS is skrong. -
Some evidence shows it works (with zinc), some show it doesn't. The process of sorting through that has a name.MikeDamone said:
The media doesn’t want it to work. Most stories say: Trump says “without evidence” that it might work. I remember when they said: Trump accuses Obama administration of spying, “without evidence”..... whoopsie poopsie!GrundleStiltzkin said:
I honestly don't get what the big deal is. It's 'script only, so people can't run out & get it. It might work, and maybe more likely doesn't work. TDS is skrong.It's SCIENCE
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Those are not your words. I accuse you of plagiarism.MikeDamone said:
I’d be happy tooMelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.
Severe acute respiratory syndrome (SARS) is an emerging disease that was first reported in Guangdong Province, China, in late 2002. The disease rapidly spread to at least 30 countries within months of its first appearance, and concerted worldwide efforts led to the identification of the etiological agent as SARS coronavirus (SARS-CoV), a novel member of the family Coronaviridae [1]. Complete genome sequencing of SARS-CoV [2,3] confirmed that this pathogen is not closely related to any of the previously established coronavirus groups. Budding of the SARS-CoV occurs in the Golgi apparatus [4] and results in the incorporation of the envelope spike glycoprotein into the virion. The spike glycoprotein is a type I membrane protein that facilitates viral attachment to the cellular receptor and initiation of infection, and angiotensin-converting enzyme-2 (ACE2) has been identified as a functional cellular receptor of SARS-CoV [5]. We have recently shown that the processing of the spike protein was effected by furin-like convertases and that inhibition of this cleavage by a specific inhibitor abrogated cytopathicity and significantly reduced the virus titer of SARS-CoV [6].
Due to the severity of SARS-CoV infection, the potential for rapid spread of the disease, and the absence of proven effective and safe in vivo inhibitors of the virus, it is important to identify drugs that can effectively be used to treat or prevent potential SARS-CoV infections. Many novel therapeutic approaches have been evaluated in laboratory studies of SARS-CoV: notable among these approaches are those using siRNA [7], passive antibody transfer [8], DNA vaccination [9], vaccinia or parainfluenza virus expressing the spike protein [10,11], interferons [12,13], and monoclonal antibody to the S1-subunit of the spike glycoprotein that blocks receptor binding [14]. In this report, we describe the identification of chloroquine as an effective pre- and post-infection antiviral agent for SARS-CoV. Chloroquine, a 9-aminoquinoline that was identified in 1934, is a weak base that increases the pH of acidic vesicles. When added extracellularly, the non-protonated portion of chloroquine enters the cell, where it becomes protonated and concentrated in acidic, low-pH organelles, such as endosomes, Golgi vesicles, and lysosomes. Chloroquine can affect virus infection in many ways, and the antiviral effect depends in part on the extent to which the virus utilizes endosomes for entry. Chloroquine has been widely used to treat human diseases, such as malaria, amoebiosis, HIV, and autoimmune diseases, without significant detrimental side effects [15]. Together with data presented here, showing virus inhibition in cell culture by chloroquine doses compatible with patient treatment, these features suggest that further evaluation of chloroquine in animal models of SARS-CoV infection would be warranted as we progress toward finding effective antivirals for prevention or treatment of the disease.
Results
Preinfection chloroquine treatment renders Vero E6 cells refractory to SARS-CoV infection
In order to investigate if chloroquine might prevent SARS-CoV infection, permissive Vero E6 cells [1] were pretreated with various concentrations of chloroquine (0.1–10 μM) for 20–24 h prior to virus infection. Cells were then infected with SARS-CoV, and virus antigens were visualized by indirect immunofluorescence as described in Materials and Methods. Microscopic examination (Fig. (Fig.1A)1A) of the control cells (untreated, infected) revealed extensive SARS-CoV-specific immunostaining of the monolayer. A dose-dependant decrease in virus antigen-positive cells was observed starting at 0.1 μM chloroquine, and concentrations of 10 μM completely abolished SARS-CoV infection. For quantitative purposes, we counted the number of cells stained positive from three random locations on a slide. The average number of positively stained control cells was scored as 100% and was compared with the number of positive cells observed under various chloroquine concentrations (Fig. (Fig.1B).1B). Pretreatment with 0.1, 1, and 10 μM chloroquine reduced infectivity by 28%, 53%, and 100%, respectively. Reproducible results were obtained from three independent experiments. These data demonstrated that pretreatment of Vero E6 cells with chloroquine rendered these cells refractory to SARS-CoV infection. -
MelloDawg said:
Those are not your words. I accuse you of plagiarism.MikeDamone said:
I’d be happy tooMelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.
Severe acute respiratory syndrome (SARS) is an emerging disease that was first reported in Guangdong Province, China, in late 2002. The disease rapidly spread to at least 30 countries within months of its first appearance, and concerted worldwide efforts led to the identification of the etiological agent as SARS coronavirus (SARS-CoV), a novel member of the family Coronaviridae [1]. Complete genome sequencing of SARS-CoV [2,3] confirmed that this pathogen is not closely related to any of the previously established coronavirus groups. Budding of the SARS-CoV occurs in the Golgi apparatus [4] and results in the incorporation of the envelope spike glycoprotein into the virion. The spike glycoprotein is a type I membrane protein that facilitates viral attachment to the cellular receptor and initiation of infection, and angiotensin-converting enzyme-2 (ACE2) has been identified as a functional cellular receptor of SARS-CoV [5]. We have recently shown that the processing of the spike protein was effected by furin-like convertases and that inhibition of this cleavage by a specific inhibitor abrogated cytopathicity and significantly reduced the virus titer of SARS-CoV [6].
Due to the severity of SARS-CoV infection, the potential for rapid spread of the disease, and the absence of proven effective and safe in vivo inhibitors of the virus, it is important to identify drugs that can effectively be used to treat or prevent potential SARS-CoV infections. Many novel therapeutic approaches have been evaluated in laboratory studies of SARS-CoV: notable among these approaches are those using siRNA [7], passive antibody transfer [8], DNA vaccination [9], vaccinia or parainfluenza virus expressing the spike protein [10,11], interferons [12,13], and monoclonal antibody to the S1-subunit of the spike glycoprotein that blocks receptor binding [14]. In this report, we describe the identification of chloroquine as an effective pre- and post-infection antiviral agent for SARS-CoV. Chloroquine, a 9-aminoquinoline that was identified in 1934, is a weak base that increases the pH of acidic vesicles. When added extracellularly, the non-protonated portion of chloroquine enters the cell, where it becomes protonated and concentrated in acidic, low-pH organelles, such as endosomes, Golgi vesicles, and lysosomes. Chloroquine can affect virus infection in many ways, and the antiviral effect depends in part on the extent to which the virus utilizes endosomes for entry. Chloroquine has been widely used to treat human diseases, such as malaria, amoebiosis, HIV, and autoimmune diseases, without significant detrimental side effects [15]. Together with data presented here, showing virus inhibition in cell culture by chloroquine doses compatible with patient treatment, these features suggest that further evaluation of chloroquine in animal models of SARS-CoV infection would be warranted as we progress toward finding effective antivirals for prevention or treatment of the disease.
Results
Preinfection chloroquine treatment renders Vero E6 cells refractory to SARS-CoV infection
In order to investigate if chloroquine might prevent SARS-CoV infection, permissive Vero E6 cells [1] were pretreated with various concentrations of chloroquine (0.1–10 μM) for 20–24 h prior to virus infection. Cells were then infected with SARS-CoV, and virus antigens were visualized by indirect immunofluorescence as described in Materials and Methods. Microscopic examination (Fig. (Fig.1A)1A) of the control cells (untreated, infected) revealed extensive SARS-CoV-specific immunostaining of the monolayer. A dose-dependant decrease in virus antigen-positive cells was observed starting at 0.1 μM chloroquine, and concentrations of 10 μM completely abolished SARS-CoV infection. For quantitative purposes, we counted the number of cells stained positive from three random locations on a slide. The average number of positively stained control cells was scored as 100% and was compared with the number of positive cells observed under various chloroquine concentrations (Fig. (Fig.1B).1B). Pretreatment with 0.1, 1, and 10 μM chloroquine reduced infectivity by 28%, 53%, and 100%, respectively. Reproducible results were obtained from three independent experiments. These data demonstrated that pretreatment of Vero E6 cells with chloroquine rendered these cells refractory to SARS-CoV infection.
-
CDC issued a memo saying those on chloroquine needed to be in the hospital to take it and monitored fore a rare heart rhythm it can cause. I believe they just pulled that. But hey it wasn't just because trump said it works.
Proven to work in early stages. Doesn't work on vet patients. -
The spike glycoprotein is a type I membrane protein that facilitates viral attachment to the cellular receptor and initiation of infection, and angiotensin-converting enzyme-2 (ACE2) has been identified as a functional cellular receptor of SARS-CoV [5]. We have recently shown that the processing of the spike protein was effected by furin-like convertases and that inhibition of this cleavage by a specific inhibitor abrogated cytopathicity and significantly reduced the virus titer of SARS-CoV [6].
I just want the processing of the spike protein to be effected so I can be right! -
spike protein superiority guy
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There is science which casts doubt on it as well and the narrative rejection you see in the mainstream news at times contains that science. Some say you can take it and improve. Some say it doesn’t have the impact Trump suggests. Neither are made up studies. This is how scientific method works. The fringe websites will always be political in nature.GrundleStiltzkin said:
It simply means the narrative rejection of chloroquine is political hyperbole, not science.MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
Pretty much what I’m saying. Stop attaching a political tag & figure it out. @ScottAdams had a good point yesterday, if it was a miracle drug we’d probably know by now. But as a dangerous alternative, I just don’t understand the kerfuffle.MelloDawg said:
There is science which casts doubt on it as well and the narrative rejection you see in the mainstream news at times contains that science. Some say you can take it and improve. Some say it doesn’t have the impact Trump suggests. Neither are made up studies. This is how scientific method works. The fringe websites will always be political in nature.GrundleStiltzkin said:
It simply means the narrative rejection of chloroquine is political hyperbole, not science.MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
Level headed, I can get on board. Damning chloroquine into oblivion because of a negative study would be like doing the same to all prescription drugs you see on TV because the side effects you hear of at the end include “suicidal thoughts.”GrundleStiltzkin said:
Pretty much what I’m saying. Stop attaching a political tag & figure it out. @ScottAdams had a good point yesterday, if it was a miracle drug we’d probably know by now. But as a dangerous alternative, I just don’t understand the kerfuffle.MelloDawg said:
There is science which casts doubt on it as well and the narrative rejection you see in the mainstream news at times contains that science. Some say you can take it and improve. Some say it doesn’t have the impact Trump suggests. Neither are made up studies. This is how scientific method works. The fringe websites will always be political in nature.GrundleStiltzkin said:
It simply means the narrative rejection of chloroquine is political hyperbole, not science.MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
I’d say that www.ncbi.nlm.nih.gov isn’t a fringe website.MelloDawg said:
There is science which casts doubt on it as well and the narrative rejection you see in the mainstream news at times contains that science. Some say you can take it and improve. Some say it doesn’t have the impact Trump suggests. Neither are made up studies. This is how scientific method works. The fringe websites will always be political in nature.GrundleStiltzkin said:
It simply means the narrative rejection of chloroquine is political hyperbole, not science.MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
The amount of deceptive and inaccurate reporting on this drug has been off-the-charts. Media personalities were mocking it as "completely ineffective" i.e., only idiots would believe it worked at all, while some people were actually and demonstrably benefitting from it.GrundleStiltzkin said:
I honestly don't get what the big deal is. It's 'script only, so people can't run out & get it. It might work, and maybe more likely doesn't work. TDS is skrong.
I read very few articles that said it flat out didn't work, but instead read many, many articles and studies that said it was potentially dangerous to anyone with heart problems or taking meds for blood pressure, arrhythmia, irregular heartbeat, etc., so it wasn't "recommended." That's not the same thing as banning it or suggesting it was malpractice to prescribe it, but that didn't matter at all to the mainstream media. It was all about crushing any optimism coming from the White House or anyone who saw a potential path through the crisis.
The Media wants this crisis to last until the election so the Left can beat Trump. It couldn't be more obvious, and at this point, you pretty much know the media personalities are lying if their lips are moving. Yes, it really has gotten that bad. -
So not for my dog?Sledog said:CDC issued a memo saying those on chloroquine needed to be in the hospital to take it and monitored fore a rare heart rhythm it can cause. I believe they just pulled that. But hey it wasn't just because trump said it works.
Proven to work in early stages. Doesn't work on vet patients. -
Heads up. You can get it off label in a 5 lb bucket down at Pool Barn
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You are correct, that was not political in nature. I imagine I could find a .gov website which has an opposite set of findings. Science is exciting!MikeDamone said:
I’d say that www.ncbi.nlm.nih.gov isn’t a fringe website.MelloDawg said:
There is science which casts doubt on it as well and the narrative rejection you see in the mainstream news at times contains that science. Some say you can take it and improve. Some say it doesn’t have the impact Trump suggests. Neither are made up studies. This is how scientific method works. The fringe websites will always be political in nature.GrundleStiltzkin said:
It simply means the narrative rejection of chloroquine is political hyperbole, not science.MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds. -
Leftists can't assess risk. That's why people are still stuck in lockdown mode.GrundleStiltzkin said:
Pretty much what I’m saying. Stop attaching a political tag & figure it out. @ScottAdams had a good point yesterday, if it was a miracle drug we’d probably know by now. But as a dangerous alternative, I just don’t understand the kerfuffle.MelloDawg said:
There is science which casts doubt on it as well and the narrative rejection you see in the mainstream news at times contains that science. Some say you can take it and improve. Some say it doesn’t have the impact Trump suggests. Neither are made up studies. This is how scientific method works. The fringe websites will always be political in nature.GrundleStiltzkin said:
It simply means the narrative rejection of chloroquine is political hyperbole, not science.MelloDawg said:
Could you elaborate? You seem to understand the science of what was said in this abstract.MikeDamone said:Seems it’s worth a very serious look.
BUT TRUMP SAID IT!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232869/
Background
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.
For someone over the age of 60, the probability of dying from COVID is X%, the odds of dying from chloroquine is Y%.
If X > Y, take chloroquine.
If Y > X, don't take chloroquine.
It's fucking maff. So somebody else explain it to the Dazzler.
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RaceBannon said:
https://forbes.com/sites/alexledsom/2020/05/10/hydroxychloroquinenumber-of-prescriptions-explode-in-france/#1c7f96e5180f
Prescriptions are higher than ever!
