This is a very realistic explanation of the disease process of Covid 19. Apparently the New York physicians read the article given the news report today. Ventilators may do more harm than good.
It appears to be a theory from someone anonymous who may not be a medical professional. It is an interesting theory, but where is the data to support it? Where is a medical and scientific analysis by a recognized expert in medical treatment? Thanks for posting it, Ben_C. We need all the info we can get. đź‘Ť
Good question, and the history goes back to SARS. :)
The use of chloroquine to fight it likely came from reviewing the data and research on SARS - as soon as we determined that the virus is basically an iteration of SARS-Cov, hence the name SARS-CoV-2. Thus the research on it goes back to 2005: https://virologyj.biomedcentral.com/a...
While that particular paper was about, basically, killing the virus it does reference the globin binding effect. This is where it is more effective in a sense than it is for malaria because it the mechanism in which it is proposed to cause hypoxia is also the mechanism by which it replicates - and malaria is a bacteria so no double-whammy against it.
Much of the research on this aspect of it is still in "pre-print" status. It will be interesting to see how it shakes out by the time it reaches print status. So far ti does look like this is one of the key differences between sars-cov and sars-cov-2 - the secondary infection mechanism that also interferes with O2 saturation. This is why it is a bit of a surprise, because we initially started trying it from the virus-killing and reproduction inhibiting perspective.
The multiple system infection is not standard, but also not unheard of - SARS and MERS (which had as one of its pathways the renal system) also exhibited these which is why they are/were so different in effect from "regular" CoV (we have a few dozen of them known in humans). The data and research is still early and mostly of the "oh hey, wait a moment" variety, but pretty strong for that phase. Much of the surprise is that most research on chloroquine has been in labs where the effect on preventing reproduction and killing of existing agents is the point - and other effects can't happen. Actually using it in humans is where we're starting to see the "side effect" that is being referenced above.
While the papers are still being worked on, the pathway makes sense and the effects, while surprising, are somewhat obvious in hindsight when you dig into it. I wish I could post more, including links, but I don't want to cause too much reliance on pre-print just yet because key bits can change. That aside, the anti-viral nature of chloroquine is more than enough to justify its use in that capacity and to make "human trials" on the other aspect quite acceptable IMO - we've been using chloroquine since the thirties IIRC and, while the media focuses on its use in malaria treatment, it is also used in many other areas such as lupus.
I will also add that over 80% of critically ill covid-19 cases show lymphopenia, and chloroquine has been found in addressing that in other causes: https://www.pubfacts.com/detail/29772...
However, and one reason I link that one is that there are potential issues that need to be looked at in the context of a widespread usage of it in viral load conditions over longer periods of time. But most fascinating to me in that study is that they used placebos when trialling it on macaques. They used placebos on monkeys. ;)
I read in another article that SARS-CoV2 is 79% genetically related to SARS-CoV and 50% genetically related to MERS. Like you say, hence the designation SARS-CoV2. With the knowledge referenced in your link, there seems to be more than reasonable expectation that the chloroquine treatment could be effective. Good news.
So, how, why, when, and by whom did the name get changed to CoVid-19? This effectively blunts the relationship described by the link between the "novel" virus and possible treatment. And then the suggestion that choloroquine may be effective can be poo-pooed as we have seen. Is the media involved here? Sigh.
The name was t change those are two different but related names. COVID-19 is an acronym (mostly) for the disease (COrona CIrus Diseas 2019) caused by the virus named SARS-CoV-2.
The disease was named first because we didn’t know which corona virus was at fault, just that it was one. You can tell a Corona virus by looking at it in the right microscope. They are named as such due to their crown like appearance.
Thanks. I’m a bit of an odd duck in that in times like this I take solace in immersing myself in the science rather than the news. ;). Then I muster up a bit of hubris and figure others might take some comfort in it as well.
If you only get your info from the talking bobble heads I can see that impression taking hold. But when you look at the actual science instead a very different picture emerges. For example the use of chloroquine isn’t outside of the norm, we’ve known about its anti-viral abilities for about eighty years.
What has changed in that time is the increasing regulatory state. Fifty years ago we’d have not been bickering over “approved” for treating a disease, we’d have simply used it. This compound has been used for antiviral purposes for nearly a century. That isn’t throwing things at the wall to see what sticks.
The press isn’t telling you that because Trump talks about it favorably. Instead they ignore the decades of it being used as an antiviral and focus on it being used to treat malaria. It lets them go “hurrdurr malaria is a bacteria you scrub”.
Really, it is the press and politicians throwing stuff at the wall to see what sticks. The scientists are methodical and focused.
If that were true it would act more like carbon monoxide poisoning which also prevents the red blood cells from taking up oxygen. You wouldn't see the massive inflammation, hear the cracking in the lungs etc., that are characteristic of the serious caes.
Yes and no, and IIRC CO poisoning is mentioned n there. It is still a virus that triggers the immune system response and produces physical material in the respiratory tract to you'd still see those effects.
Agrees with http://joannenova.com.au/2020/04/urge... I am a great fan of Joanne Nova's web site. She is qualified in micro-biology. Many of the comments are of high caliber, expert and instructive.
Looks interesting, thanks. However I wish she would make statements like this one:
“ Coronavirus it turns out — is a vascular disease as much as lung disease.”
“Coronavirus” is not a disease. It’s one thing for press to screw it up, and another for a microbiologist to do it. It is misleading and confusing. We have about three dozen identified corona viruses and so far o it two of them have shown the ability to infect multiple systems in the human body. While it is correct to point out that the virus SARS-CoV-2 appears able to infect blood cells, it is just as important to point out that it is this particular virus.
Between 15 and 20 percent of “common colds” in the U.S. each year are due to a corona virus (229e to be specific). If you get the press and people believing that “Coronavirus is a blood disease too” you’re going to make things worse. Dumbing down the broad strokes is a terrible idea and something most scientists in the public eye do out of hubris and from being told they have to. It is better to gloss over fine details than to screw up the fundamentals.
Rant over.
The two hypotheses could explain the rumor/appearance of two different strains running through the infected populations. It could come down to bodies that can resist one result but not the other. That is what makes the thankfully rare cases of multi-system infections so dangerous.
It may yet be the case that a small difference does exist in sub strains and that one produces the hypoxia by glomming onto the blood cells and the other by messing with the lungs themselves.
To me though, there is a metric that begs for explanation: the much higher rate of male deaths. I seem to recall that in some locations we are looking at a 70/30 split. If this is true and social factors can be ruled out it could be a huge clue to what is going on in an infection. Sadly with Genderism running rampage these days I doubt we would see many, if any, studies.
TheRealBill- thanks for that. A tricky subject, at least for me, but anyway, what I get from your comments are:
1. Lax terminology adds to confusion, agreed. The type of virus (Coronavirus), within the type this particular virus (SARS-CoV-2), the medical condition suffered by people who get it (COVID-19 aka Wuhu, C-19, etc.)? 2. Explaining observations by assuming not a two-pronged weapon but two different strains. 3. Genderism!
It is indeed a tricky subject, like anything the press is relying on sadly.
Yes, to all of #1 - you got it correctly. Item 2 is where it gets a bit tricky because we are still under a wide range of conditions - most of which are not conducive to a proper analysis. The initial assumptions and claims were that there were two different strains. This is not a common occurrence and most media, being scientifically illiterate or even "anti-literate", glom onto things like "could be" or "is possible". That we have an pair of general conditions emerging could point to two strains but is more likely it is a result of different conditions in a host.
A good way to conceptualize that (and to be clear this is ALL pseudo-scientific hypothesizing for dialectic purposes) imagine that humans have, in they lungs and blood, a set of three consistent ranges of pH - acidity vs alkalinity. Since virus replication is sensitive to pH (this is actually the main way chloroquine works in an anti-viral capacity) if your lungs have a pH level that is beneficial to the virus' reproduction you would be more likely to get lung-sick with it. You could say the same about your blood.
Now imagine, for whatever reason, your serum pH is beneficial to the virus but your lungs no so much. Now imagine that generally speaking most people would fall into the combination of categories mixing those two.
It would be reasonable then, in this imaginary scenario, to see different results from the same virus with no mutation at all. If you have + blood and - lungs, you could see, theoretically, the hypoxic reaction. If you have - blood and + lungs, you could instead see the "more traditional" lung infection. You could carry that further and imagine that +blood and +lung is the worst combination and the -/- could mean a cough, some hacking, maybe a small fever or not, and you move on. Sadly, people in today's media find that to be too much of a concept to either understand or convey. So they go with "ZOMG muh virus is mutating".
On #3, yeah, sadly. I have zero doubt that if it were reversed it would be plastered everywhere, movies made, and a ribbon color dedicated to "raising awareness" of how the virus is somehow sexist (and the Patriarchy knew it so they delayed doing anything cuz ... patriarchy!).
Didja notice the people who die are on ventilators? Just found out by BFF may have had this crap in November and my granddaughter may have had it in January. Awaiting results. They fully recovered. My BFF is 72 and granddaughter is 25.
The use of chloroquine to fight it likely came from reviewing the data and research on SARS - as soon as we determined that the virus is basically an iteration of SARS-Cov, hence the name SARS-CoV-2. Thus the research on it goes back to 2005: https://virologyj.biomedcentral.com/a...
While that particular paper was about, basically, killing the virus it does reference the globin binding effect. This is where it is more effective in a sense than it is for malaria because it the mechanism in which it is proposed to cause hypoxia is also the mechanism by which it replicates - and malaria is a bacteria so no double-whammy against it.
Much of the research on this aspect of it is still in "pre-print" status. It will be interesting to see how it shakes out by the time it reaches print status. So far ti does look like this is one of the key differences between sars-cov and sars-cov-2 - the secondary infection mechanism that also interferes with O2 saturation. This is why it is a bit of a surprise, because we initially started trying it from the virus-killing and reproduction inhibiting perspective.
The multiple system infection is not standard, but also not unheard of - SARS and MERS (which had as one of its pathways the renal system) also exhibited these which is why they are/were so different in effect from "regular" CoV (we have a few dozen of them known in humans). The data and research is still early and mostly of the "oh hey, wait a moment" variety, but pretty strong for that phase. Much of the surprise is that most research on chloroquine has been in labs where the effect on preventing reproduction and killing of existing agents is the point - and other effects can't happen. Actually using it in humans is where we're starting to see the "side effect" that is being referenced above.
While the papers are still being worked on, the pathway makes sense and the effects, while surprising, are somewhat obvious in hindsight when you dig into it. I wish I could post more, including links, but I don't want to cause too much reliance on pre-print just yet because key bits can change. That aside, the anti-viral nature of chloroquine is more than enough to justify its use in that capacity and to make "human trials" on the other aspect quite acceptable IMO - we've been using chloroquine since the thirties IIRC and, while the media focuses on its use in malaria treatment, it is also used in many other areas such as lupus.
I will also add that over 80% of critically ill covid-19 cases show lymphopenia, and chloroquine has been found in addressing that in other causes: https://www.pubfacts.com/detail/29772...
However, and one reason I link that one is that there are potential issues that need to be looked at in the context of a widespread usage of it in viral load conditions over longer periods of time. But most fascinating to me in that study is that they used placebos when trialling it on macaques. They used placebos on monkeys. ;)
So, how, why, when, and by whom did the name get changed to CoVid-19? This effectively blunts the relationship described by the link between the "novel" virus and possible treatment. And then the suggestion that choloroquine may be effective can be poo-pooed as we have seen. Is the media involved here? Sigh.
The disease was named first because we didn’t know which corona virus was at fault, just that it was one. You can tell a Corona virus by looking at it in the right microscope. They are named as such due to their crown like appearance.
What has changed in that time is the increasing regulatory state. Fifty years ago we’d have not been bickering over “approved” for treating a disease, we’d have simply used it. This compound has been used for antiviral purposes for nearly a century. That isn’t throwing things at the wall to see what sticks.
The press isn’t telling you that because Trump talks about it favorably. Instead they ignore the decades of it being used as an antiviral and focus on it being used to treat malaria. It lets them go “hurrdurr malaria is a bacteria you scrub”.
Really, it is the press and politicians throwing stuff at the wall to see what sticks. The scientists are methodical and focused.
http://joannenova.com.au/2020/04/urge...
I am a great fan of Joanne Nova's web site. She is qualified in micro-biology.
Many of the comments are of high caliber, expert and instructive.
“ Coronavirus it turns out — is a vascular disease as much as lung disease.”
“Coronavirus” is not a disease. It’s one thing for press to screw it up, and another for a microbiologist to do it. It is misleading and confusing. We have about three dozen identified corona viruses and so far o it two of them have shown the ability to infect multiple systems in the human body. While it is correct to point out that the virus SARS-CoV-2 appears able to infect blood cells, it is just as important to point out that it is this particular virus.
Between 15 and 20 percent of “common colds” in the U.S. each year are due to a corona virus (229e to be specific). If you get the press and people believing that “Coronavirus is a blood disease too” you’re going to make things worse. Dumbing down the broad strokes is a terrible idea and something most scientists in the public eye do out of hubris and from being told they have to. It is better to gloss over fine details than to screw up the fundamentals.
Rant over.
The two hypotheses could explain the rumor/appearance of two different strains running through the infected populations. It could come down to bodies that can resist one result but not the other. That is what makes the thankfully rare cases of multi-system infections so dangerous.
It may yet be the case that a small difference does exist in sub strains and that one produces the hypoxia by glomming onto the blood cells and the other by messing with the lungs themselves.
To me though, there is a metric that begs for explanation: the much higher rate of male deaths. I seem to recall that in some locations we are looking at a 70/30 split. If this is true and social factors can be ruled out it could be a huge clue to what is going on in an infection. Sadly with Genderism running rampage these days I doubt we would see many, if any, studies.
A tricky subject, at least for me, but anyway, what I get from your comments are:
1. Lax terminology adds to confusion, agreed.
The type of virus (Coronavirus), within the type this particular virus (SARS-CoV-2), the medical condition suffered by people who get it (COVID-19 aka Wuhu, C-19, etc.)?
2. Explaining observations by assuming not a two-pronged weapon but two different strains.
3. Genderism!
Yes, to all of #1 - you got it correctly. Item 2 is where it gets a bit tricky because we are still under a wide range of conditions - most of which are not conducive to a proper analysis. The initial assumptions and claims were that there were two different strains. This is not a common occurrence and most media, being scientifically illiterate or even "anti-literate", glom onto things like "could be" or "is possible". That we have an pair of general conditions emerging could point to two strains but is more likely it is a result of different conditions in a host.
A good way to conceptualize that (and to be clear this is ALL pseudo-scientific hypothesizing for dialectic purposes) imagine that humans have, in they lungs and blood, a set of three consistent ranges of pH - acidity vs alkalinity. Since virus replication is sensitive to pH (this is actually the main way chloroquine works in an anti-viral capacity) if your lungs have a pH level that is beneficial to the virus' reproduction you would be more likely to get lung-sick with it. You could say the same about your blood.
Now imagine, for whatever reason, your serum pH is beneficial to the virus but your lungs no so much. Now imagine that generally speaking most people would fall into the combination of categories mixing those two.
It would be reasonable then, in this imaginary scenario, to see different results from the same virus with no mutation at all. If you have + blood and - lungs, you could see, theoretically, the hypoxic reaction. If you have - blood and + lungs, you could instead see the "more traditional" lung infection. You could carry that further and imagine that +blood and +lung is the worst combination and the -/- could mean a cough, some hacking, maybe a small fever or not, and you move on. Sadly, people in today's media find that to be too much of a concept to either understand or convey. So they go with "ZOMG muh virus is mutating".
On #3, yeah, sadly. I have zero doubt that if it were reversed it would be plastered everywhere, movies made, and a ribbon color dedicated to "raising awareness" of how the virus is somehow sexist (and the Patriarchy knew it so they delayed doing anything cuz ... patriarchy!).