COVID-19 Update

[SigmundChurchill]

For anyone who might be interested, I just wanted to let people know where it is I think we are, and where we might be going with this virus.  I put some thoughts together based on my experience on the front lines, combined with studies I have read, and how they relate to what I am seeing first hand.  I tried to put things in as simple terms as I can, so I apologize in advance if I failed in some areas, and they seem too technical.

A lot of hope is being pinned on vaccines, if we come up with one, it will likely only play a part in defeating this virus. We have never come up with a coronavirus vaccine before, but there has also never been such a huge amount of money being thrown at it either, so who knows?  Even imperfect flu vaccines, still are helpful in that they often cause a less virulent case of the flu in the people who get it, and that might be enough to lower the death tolls as it does with the flu. The majority of people who die from the flu in this country, are the people who did not get vaccinated.  

But the potential problem with a vaccine for a coronavirus, is the possibility of antibody-dependent enhancement (ADE), where a vaccine could make the virus more virulent, rather than less. What happens here, is, say a person has antibodies to coronavirus (which we all do), but not to COVID-19, or to a different strain of COVID-19. COVID-19 docks to the cell membranes on the ACE2 receptors while Antibodies dock to the cells on Fc receptors. So if the antibody binds to the antigen, in this case COVID-19, but since it is a different serotype, it doesn’t kill the virus, and it uses the antibody’s Fc receptors to bind to the cell, and bring it in close proximity to the ACE2 receptors which are more sparse, and now it can enter the cell more easily. In other words, it uses the host’s own immune system against the host. This increases the virulence, and may lead to more severe disease. This may already be happening, even without a vaccine, where it is using our antibodies to other serotypes of coronavirus.

Perfecting treatment may be a better solution than a vaccine, but this involves having a better understanding of the virus than we currently have. One thing I do know, is that the key will not be in eradicating the virus completely, but rather, in keeping it from changing from an upper respiratory infection rather than a lower respiratory infection. It is not the virus itself that is ultimately killing these people. It is the immune response in the lungs (cytokine storm) that is killing them. So treatment will have to come in two forms. Either keeping the virus at bay before it has a foothold in the lower respiratory system, and/or modulating the immune response to the virus once it does get there.

I am not a virologist. I am just a person who manages the sickest of these patients on ventilators all day. So I am seeing patterns, and wondering if these patterns are the key to finding treatments. Why don't we have any children needing ventilators? Is it because their immune system is built to handle new viruses, and mounts a more appropriate response to them? Is the lack of similar viral recognition, and therefor, lack of ADE, responsible? Do they have less ACE2 receptors expression in the lungs than adults? Why am I seeing an overwhelming amount of diabetics on ventilators? Some suggest they are more prone to cytokine storm than the general population. Others suggest they have up-regulation of ACE2 receptors.

There are a lot of reports of hydroxychloroquine working very well on some patients. Hydroxychloroquine, interferes with RNA transcription in viruses, slowing down their ability to replicate. I originally thought that this was the mechanism. But too often, the reports I hear from doctors is that the patients are feeling relief within a matter of hours. That is too quick for this mechanism of action to be the reason. Could it be placebo effect? Possibly. Or could it be that hydroxychloroquine is an immune modulator? It’s immune modulating effects are the reason it works well in autoimmune diseases like Lupus and Rheumatoid Arthritis. Perhaps it is preventing, or calming cytokine storm?

Then there is remdesivir, which I am hearing favorable reports from other doctors. Patients are experiencing relief from fever and shortness of breath after the first infusion. Remdesivir is an antiviral that has been used for Ebola virus in the past. The way it works is that it is an analogue of adenosine. Adenosine is a nucleotide that is part of the virus RNA chain. So instead of inserting adenosine in the RNA chain, the virus is being fooled into inserting remdesivir instead, which causes their termination.

In my experience with the sickest patients, on ventilators, neither of these drugs prevents them from dying. At the beginning, we were putting anyone with low oxygen saturation on ventilators, because under normal circumstances, that is what saves the life of a person when their oxygen saturation becomes critically low. But the presentation of this virus is so different than what we see under “normal circumstances”, that we don’t immediately put them on ventilators anymore. We use high flow oxygen, and let them breath on their own, until a point where they are breathing at an unsustainable rate, and gasping, where they will definitely die soon without a ventilator. Some of the patients end up not getting to this point, and get better without the ventilator, but most of the patients that look like they need a ventilator before the high flow oxygen, end up needing one after the high flow oxygen too. So in these patients that are on ventilators, the drugs dont save them. They are too far gone. The only thing that seems to save them is youth, and the general health of the patient before they were infected. But even young and healthy patients die, just at a lower rate. Who knows, maybe the rate would be higher for these patients without the drugs, but even so, they die at an abysmal rate.

Then there are the plasma studies, which show promise. The plasma of patients that have recently recovered has antibodies that should match well with other COVID-19 patients. These studies have just begun, and it requires time to find donors. I am hoping this works well enough to save even the ventilated patients, because from what I have seen, nothing else works on them.

[benfica_77]

@SigmundChurchill Thank you very much for this post. I really appreciate your informed opinion on the matter. I can appreciate what you see is mostly anecdotal but it helps shape and frame where we are at in this battle. We need more posts like this!! 

I have read that this virus is mutating at an exponential rate and that due to these mutations that there is a possibility of re-infection? What's your thoughts on that? 

Also again on the same line of thinking regarding mutations.....do you think that it can mutate itself into a less deadly version?? 

It's really interesting that time and time again when I read about living a long healthy life, minimizing inflammation is a key component. It seems it's playing a factor here again with the cytokine storm you are mentioning.  

Your post was a great balance of keeping things not too technical. Only had to ask the Mrs. (soon to be veterinarian) a couple terms!

Again thanks for the post Mr. Siglo VI !!  

[bsubtown]

@SigmundChurchill
Can you speak at all to your experience with those diabetes patients. In particular I'm interested in knowing if you're seeing a difference in type 1 and type 2 and then BMI's particularly in the type 2 patients correlating at all with more severe cases.
Awesome info. Thanks

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[BoliDan]

Thanks, Elliot. Intersting stuff. I cant imagine how stressful this must be for you, your colleagues and familes. Stay well, see ya in the herf.

[SigmundChurchill]

20 minutes ago, benfica_77 said:

@SigmundChurchill Thank you very much for this post. I really appreciate your informed opinion on the matter. I can appreciate what you see is mostly anecdotal but it helps shape and frame where we are at in this battle. We need more posts like this!! 

I have read that this virus is mutating at an exponential rate and that due to these mutations that there is a possibility of re-infection? What's your thoughts on that? 

Also again on the same line of thinking regarding mutations.....do you think that it can mutate itself into a less deadly version?? 

It's really interesting that time and time again when I read about living a long healthy life, minimizing inflammation is a key component. It seems it's playing a factor here again with the cytokine storm you are mentioning.  

Your post was a great balance of keeping things not too technical. Only had to ask the Mrs. (soon to be veterinarian) a couple terms!

Again thanks for the post Mr. Siglo VI !!  

You’re welcome.  As far as mutation, there are now 3 strains that we know about.  Strain A, strain B, and strain C, which can be traced to different parts of the world.  For example, in Wuhan, the original strain (Strain A) has been overtaken by strain B, while in the USA and Australia, it is still Strain A, and in Europe, it is mostly strain B, with a couple of countries showing strain C to be dominant.

Because it is so contagious, it as more opportunity to mutate.  A mutation in a virus is not like the mutations in, say, natural selection.  Meaning, there is no intelligence to a virus mutation.  It is merely an accident.  It can make the virus less virulent, more virulent, or it can be of equal virulence.

Yes, the inflammation, or cytokine storm is interesting because it is not seeming to happen in children.  And as I said, that is likely because their immune system, which is still accustomed to seeing new viruses, is putting out an appropriate immune response.  This is where ADE (or lack of it in their case) might be playing a role.

[FireMedic]

20 minutes ago, bsubtown said:

@SigmundChurchill
Can you speak at all to your experience with those diabetes patients. In particular I'm interested in knowing if you're seeing a difference in type 1 and type 2 and then BMI's particularly in the type 2 patients correlating at all with more severe cases.
Awesome info. Thanks

Sent from my Pixel 3 XL using Tapatalk
 

I know you didn't ask me but I'll throw in what I'm seeing in the field. I have ran calls on both types 1 and 2 and have seen a wide range of BMI in both types. My experience has been that the real indicator is overall health. I had a patient at the beginning of this that coded shortly after transport, was in the ICU for the last 3 weeks, placed on dialysis because of kidney failure but is starting to recover slowly. Age, and overall health have been a bigger factor out here anyway. Disclaimer I don't deal with the patient long term but do check on their status everyday, their success rate is my success rate. I'm sure @SigmundChurchill will be able to be more eloquent, I'm just a knuckle dragging hose monkey. Stay safe

[SigmundChurchill]

49 minutes ago, bsubtown said:

@SigmundChurchill
Can you speak at all to your experience with those diabetes patients. In particular I'm interested in knowing if you're seeing a difference in type 1 and type 2 and then BMI's particularly in the type 2 patients correlating at all with more severe cases.
Awesome info. Thanks

Sent from my Pixel 3 XL using Tapatalk
 

We are seeing both, but a lot more Type II diabetics.  That could be because there are a lot more type II diabetics in the population, or it could be because type II diabetics are usually obese compared to type I diabetics.  And obesity definitely plays a role in this disease.  Most (but not all) of the patients that are on ventilators, with no pre-existing conditions, and not elderly, are either obese, morbidly obese, or at the very least, clinically overweight.  And that goes for most of the diabetics too.

Type I diabetics, their islet cells (cells that secrete insulin) were seen as foreign and have been destroyed by their immune system.  The islet cells are dependent on angiotensin converting enzyme 2 (ACE2), to secret insulin.  The virus gets into the cells of our body through the ACE2 receptors, not just in the pancreas, but in the lungs and other organs.  Both, lack of insulin (type I diabetes), and insulin resistance (type II diabetes), lead the body to create more ACE2 receptors.  So that may be the link.

[SigmundChurchill]

20 hours ago, FireMedic said:

I know you didn't ask me but I'll throw in what I'm seeing in the field. I have ran calls on both types 1 and 2 and have seen a wide range of BMI in both types. My experience has been that the real indicator is overall health. I had a patient at the beginning of this that coded shortly after transport, was in the ICU for the last 3 weeks, placed on dialysis because of kidney failure but is starting to recover slowly. Age, and overall health have been a bigger factor out here anyway. Disclaimer I don't deal with the patient long term but do check on their status everyday, their success rate is my success rate. I'm sure @SigmundChurchill will be able to be more eloquent, I'm just a knuckle dragging hose monkey. Stay safe

This is correct.  The few people that survive this stage of the disease are the ones that are younger and otherwise healthy.  

I would even say, a young person with well controlled hypertension, who gets aerobic exercise every day, has a better chance than an older, sedentary person.  Assuming the hypertensive person wasn’t treating their hypertension with ACE inhibitors.  People on ACE inhibitors for hypertension have upregulated the ACE2 receptors in their body, in order to counteract the ACE inhibition from the drug.

[barry12321]

@SigmundChurchillThanks for taking the time to put these thoughts together.  Very informative and offers a clearer perspective.  Hard to decipher anything from the media these days.

[MigsG]

Thanks for sharing your experience and thoughts with us here, Elliot. I appreciated reading this.  Here's hoping you continue to stay well-protected as you help people in dire need.  

[SigmundChurchill]

47 minutes ago, Lrabold89 said:

@SigmundChurchillso in terms of protection...i have a newborn who i have to take to get shots and and an ultrasound..what is the best way for us to stay protected being that we have to go take care of this ? is this disease something you can catch from simply breathing it in ? thank you!

 

You can catch it from simply breathing in, but for that to happen, it has to be aerosolized and in the air.  Under normal circumstances, this is not the case.  If someone is coughing in the room you are standing in before you get there, it is possible.  I read about an entire church choir getting COVID-19 during a choir practice, but I would imagine that belting out gospel songs could fill the room with it.  But under normal circumstances, staying more than 6 feet away and having a short conversation with no coughing or sneezing involved, would not be a likely scenario where you would get it.

1.  Personally, I would call the pediatrician’s office and find out what precautions they are taking.  For example, I would not want to be sitting in a waiting room full of patients.  I would hope they would have a system set up that avoids this during this particular time.  If not, I would wonder if this is really the right pediatrician for me.

2.  That said, wear a mask.  When you call the pediatrician, in addition to the asking about the waiting room, ask their opinion about putting a mask on the baby too.  My experience with this disease has been only with adults so I will defer to them.

3.  Very important.  After you touch the doorknob to enter the building, do not touch your face.  Do not touch the baby.  At that point, consider your hands to be contaminated.  So you can open the door to the office, use the pen to sign in or fill out forms or touch whatever else needs to be touched, but dont touch your face or the baby’s face until you wash your hands with soap for at least 20 seconds, and then water.  Now your hands are not contaminated until you touch something else in the office, in which case you have to wash again.  I would also bring Purell or something like it.  It is likely you will have to touch doorknobs to get out of the building, and you will want to clean your hands in the parking lot before contaminating your car door handle, steering wheel, and anything else in the car that you touch.

3.5.  The other option is rubber gloves.  But keep in mind that while the gloves are protecting your hands, the outside of the gloves still carry the virus.  So while the gloves are on, don't touch your face or the baby.  Then you still have to wash your hands after taking off the gloves because just the act of taking them off, often inadvertently causes you to touch your skin with the outside of the glove.

I know it sounds kind-of crazy, and a lot to remember, so, welcome to my world, 80 hours a week for the past month and a half.?

 And remember, we unconsciously touch our faces 23 times per hour (more when we smoke our cigars).  Just be conscious of it.

 

[Rhinoww]

@SigmundChurchill thank you for sharing your experiences. I imagine it is hard to come to a place like this, where we all escape our daily grind a bit, and dive back into what must be a very draining work day.
 

I can only speak for myself but you have helped me better understand the science and frankly the need to maintain good physical conditioning particularly in times like these. 
 

thanks for taking the time to share your thoughts and synthesizing your research. Incredibly helpful. 
 

 

[ElJavi76]

Amazing read all the way thru. Looking forward to the day the medical community and scientist can pin this thing down. It's caused way too much loss and heartache. 

To all of our medical staff, doctors, nurses, first responders, etc... God speed. Please stay safe. You're risking your health for the sake of strangers, and there's nothing more noble than that. Thank you all, and thank you to your families for sharing such brilliant individuals with the world.

We could never repay you!

[saintsmokealot]

@SigmundChurchill Thank you for this write up and the updates throughout this ordeal not to mention being on the front lines.

[Rrm7284]

Great thread, much appreciated! One of the most informative reads I’ve seen in the topic.

[Habana Mike]

Thanks! Knowledge and insight help immensely.

[Konablacksand]

SigmundChurchill makes some very nice points and I applaud him and others like him who are treating the most critical and severe cases of SARS-CoV2 infections while putting themselves in a precarious position. While I agree with some of the high level opinions, there are some technical aspects that are a bit misconstrued specifically with the physiology of how Coronaviruses invade healthy host cells. Coronavirus do attach to the ACE2 receptor sites of human host cells through the mechanism of the S protein "spikes" which attach to ACE2 receptors, at that point, the virus produces an enzyme which deactivates the host cell immune response (MDA5 receptor) essentially "blocking" the alarm system which triggers an immune response, thus  allowing the virus' fusion peptides to attach itself to the host cell encode its RNA into the host cell in order to replicate itself. The use of ACE2 inhibitors to treat Covid-19 infections is dicey since ACE2 inhibitors trigger the production of more cellular ACE2 recpetors which then can cause more viruses to attach to more host cells and increasing replication. The hope for a vaccine is a long shot since most vaccines use live attenuated viruses but as Sigmund pointed out, we create Flu vaxes each year and none of them are even 90% effective (I used to mfg FluVirin at Novartis from 2000-2005 and I NEVER received a flu shot nor will I) Fatalities every flu season are not directly proportional to those not receiving flu vaccine but rather due to age, pre-existing medical conditions and susceptibilty to co-infections such as pneumonia. Creation of vaccines using surface protein antigens are rarely effective (harvesting a virus' surface proteins without the virus itself attached and using this to create an antigenic response in the immune system). I had worked with gp120 and gp41 surface proteins of HIV for a company that tried to create a HIV vaccine back in 2000. In addition I have worked in the manufacture of Hepatitis C and B surface proteins c100, NS5, HCCN-1, HBcore, c200 and several others. Such approaches have been rarely effective. There are currently 11 different strains of CoronaVirus and CoVid-19 is one strain. There have been studies to show slight mutations in all 3 of the SARS-Cov1, MERS-Cov and SARS-Cov-19 however there seems to be no indication of any greater virulence due to these slight mutations. Working in the Biopharma industry for 30+ yrs it is my opinion that viruses will not be shut down by vaccines or biologics but rather thru novel small molecule nucleotide and viral polymerase inhibitors such as Sofosbuvir/Ledaspivir which inhibit viral replication. The use of antivirals like remdesivir to treat Covid-19 post infections is still a long way off to determine efficacy since these were developed by my former client Gilead Sciences for the treatment of Ebola and Hanta virus and use of such antivirals that are virus specific are deemed for "Compassionate Use Only" meaning in order to administer them you have to be out of options. The amazing thing about viruses to me and what led my interest to pursue a career in Microbiology, is their ability to utilize different mechanisms for infection and replication and their ability to mutate in order to achieve this activity not to mention being around for 1000s if not millions of years!

What is needed right now is to provide the global public with FACTUAL Information and by providing FULL transparency into the EXISTING # of CoVid-19 reported cases to determine: TOTAL # of Cases Confirmed vs SUSPECTED (symptoms);  The TOTAL # of cases requiring hospitalization; The TOTAL # of Recoveries post infection or onset of symptoms (in other words, after reporting infection, after 3 weeks, those who are recovered should be added to the list of Recoveries), # of deaths DUE to single infection of CoVid-19 vs. co-infections, Deaths by age groups and Deaths Due to pre-existing conditions. While some of this information may be available it is NOT reported in the mASS media,  To Die FROM a virus is different than to Die WITH a virus and such transparency is needed. Once we have complete transparency with regard to data sets, we can then TRULY determine the seriousness of CoVid-19 as compared to similar infections (i.e.seasonal flu numbers) to determine if this is something MORE OR LESS serious of a RISK to people than the damage done to people from a global economic shut down. Infectious Disease experts, Virologists and Epidemiologists across the world should convene to make an assessment on the criticality of this epidemic in relation to other infections and POLITICS should not be involved with this assessment. From that point We Move On from there. Stay smokey my BOTLs!

[SigmundChurchill]

3 hours ago, Konablacksand said:

SigmundChurchill makes some very nice points and I applaud him and others like him who are treating the most critical and severe cases of SARS-CoV2 infections while putting themselves in a precarious position. While I agree with some of the high level opinions, there are some technical aspects that are a bit misconstrued specifically with the physiology of how Coronaviruses invade healthy host cells. Coronavirus do attach to the ACE2 receptor sites of human host cells through the mechanism of the S protein "spikes" which attach to ACE2 receptors, at that point, the virus produces an enzyme which deactivates the host cell immune response (MDA5 receptor) essentially "blocking" the alarm system which triggers an immune response, thus  allowing the virus' fusion peptides to attach itself to the host cell encode its RNA into the host cell in order to replicate itself. The use of ACE2 inhibitors to treat Covid-19 infections is dicey since ACE2 inhibitors trigger the production of more cellular ACE2 recpetors which then can cause more viruses to attach to more host cells and increasing replication. The hope for a vaccine is a long shot since most vaccines use live attenuated viruses but as Sigmund pointed out, we create Flu vaxes each year and none of them are even 90% effective (I used to mfg FluVirin at Novartis from 2000-2005 and I NEVER received a flu shot nor will I) Fatalities every flu season are not directly proportional to those not receiving flu vaccine but rather due to age, pre-existing medical conditions and susceptibilty to co-infections such as pneumonia. Creation of vaccines using surface protein antigens are rarely effective (harvesting a virus' surface proteins without the virus itself attached and using this to create an antigenic response in the immune system). I had worked with gp120 and gp41 surface proteins of HIV for a company that tried to create a HIV vaccine back in 2000. In addition I have worked in the manufacture of Hepatitis C and B surface proteins c100, NS5, HCCN-1, HBcore, c200 and several others. Such approaches have been rarely effective. There are currently 11 different strains of CoronaVirus and CoVid-19 is one strain. There have been studies to show slight mutations in all 3 of the SARS-Cov1, MERS-Cov and SARS-Cov-19 however there seems to be no indication of any greater virulence due to these slight mutations. Working in the Biopharma industry for 30+ yrs it is my opinion that viruses will not be shut down by vaccines or biologics but rather thru novel small molecule nucleotide and viral polymerase inhibitors such as Sofosbuvir/Ledaspivir which inhibit viral replication. The use of antivirals like remdesivir to treat Covid-19 post infections is still a long way off to determine efficacy since these were developed by my former client Gilead Sciences for the treatment of Ebola and Hanta virus and use of such antivirals that are virus specific are deemed for "Compassionate Use Only" meaning in order to administer them you have to be out of options. The amazing thing about viruses to me and what led my interest to pursue a career in Microbiology, is their ability to utilize different mechanisms for infection and replication and their ability to mutate in order to achieve this activity not to mention being around for 1000s if not millions of years!

What is needed right now is to provide the global public with FACTUAL Information and by providing FULL transparency into the EXISTING # of CoVid-19 reported cases to determine: TOTAL # of Cases Confirmed vs SUSPECTED (symptoms);  The TOTAL # of cases requiring hospitalization; The TOTAL # of Recoveries post infection or onset of symptoms (in other words, after reporting infection, after 3 weeks, those who are recovered should be added to the list of Recoveries), # of deaths DUE to single infection of CoVid-19 vs. co-infections, Deaths by age groups and Deaths Due to pre-existing conditions. While some of this information may be available it is NOT reported in the mASS media,  To Die FROM a virus is different than to Die WITH a virus and such transparency is needed. Once we have complete transparency with regard to data sets, we can then TRULY determine the seriousness of CoVid-19 as compared to similar infections (i.e.seasonal flu numbers) to determine if this is something MORE OR LESS serious of a RISK to people than the damage done to people from a global economic shut down. Infectious Disease experts, Virologists and Epidemiologists across the world should convene to make an assessment on the criticality of this epidemic in relation to other infections and POLITICS should not be involved with this assessment. From that point We Move On from there. Stay smokey my BOTLs!

Thank you.  

I think the only thing I disagree with here is the bolded part.  This goes against everything the CDC tells us, and I have read numbers and the studies that they use to back up that flu-related illness, hospitalizations and deaths are disproportionately found in patients that have NOT received the vaccine, especially in children. Yes, age, pre-existing conditions, etc are the major factors, and these people would especially benefit from the vaccine.

 

[havanaclub]

Thank you Elliot for all the first hand experience, information and explanations. Stay safe and thank you!!


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[Sir Diggamus]

Thank you for taking the time your experiences and thoughts.


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[tigger]

Thanks for your thoughts, and for what you're doing on the "front lines," Elliot. I can't imagine how awful it must be.

A quick question...have you heard anything about the effects or increase/decrease of mortality on people taking TNF-α inhibitors? I ask because my wife uses Embrel to treat RA, and we've been a little concerned, because she's considered immunocompromised. If overreaction if the immune system is a significant factor in many people dying, I'm wondering now if drugs like these might actually convey an advantage of sorts. 

[SigmundChurchill]

2 hours ago, tigger said:

Thanks for your thoughts, and for what you're doing on the "front lines," Elliot. I can't imagine how awful it must be.

A quick question...have you heard anything about the effects or increase/decrease of mortality on people taking TNF-α inhibitors? I ask because my wife uses Embrel to treat RA, and we've been a little concerned, because she's considered immunocompromised. If overreaction if the immune system is a significant factor in many people dying, I'm wondering now if drugs like these might actually convey an advantage of sorts. 

I’m out the door on my way to my shift, but I wanted to quickly answer this before I leave.  I don't know of any studies being done, but my initial thought would be that it might make her slightly more susceptible to catching the virus, while at the same time making it less likely for her to die from it.  There is an article in The Lancet that calls for trials to be done on these drugs to see if they are preventative in causing the deadly ARDS that the virus leads to.  

I have to go, but In the meantime, I will post the Lancet article.  Trials of anti-tumour necrosis factor therapy for COVID-19 are urgently needed

[TBird55]

God bless you Elliot.

[Euripidespants]

Sigmund. I’m curious if and how your institution is using ECMO to treat your patients. This past weekend I’ve seen our main hospital use it on several patients. Several of these have advanced disease on imaging, and several were not intubated (I am a radiologist). I didn’t get a chance to speak with one of the pulmonary/critical care docs directly this past weekend, but my understanding is they are seeing some success with the very sick patients. 

Thanks

[tigger]

1 hour ago, SigmundChurchill said:

I’m out the door on my way to my shift, but I wanted to quickly answer this before I leave.  I don't know of any studies being done, but my initial thought would be that it might make her slightly more susceptible to catching the virus, while at the same time making it less likely for her to die from it.  There is an article in The Lancet that calls for trials to be done on these drugs to see if they are preventative in causing the deadly ARDS that the virus leads to.  

I have to go, but In the meantime, I will post the Lancet article.  Trials of anti-tumour necrosis factor therapy for COVID-19 are urgently needed

Thank you. Interesting read!