The COVID-19 Science and Medicine Question Thread
- Thread starter Roccus7
- Start date
I got back a negative china virus (as expected) from the blood drawn during my 6 month checkup on 28 April. I have to call back to get the exact cholesterol numbers if I want. I got the feeling that everyone is having their blood tested for china virus if blood is drawn for any reason.
TonySmjc
Well-Known Angler
I’d did it in reverse
I wanted a second COVID-19 Antibody test so I got my blood work at the same time
And since the dr offered two
COVID-19 Antibody test
I did both
I’ve been on a keto diet for quite a while so it good to get my blood work done anyway
I wanted a second COVID-19 Antibody test so I got my blood work at the same time
And since the dr offered two
COVID-19 Antibody test
I did both
I’ve been on a keto diet for quite a while so it good to get my blood work done anyway
Last edited by a moderator:
You won't get a number, as I already explained. Northwell and Quest use the same test, the Abbott Architect COVID-19 assay, which provides a Negative or Positive Result.
You must mean a COVID-19 Antibody Test or SARS-COV-2 Antibody Test, the same viral entity. There is no scientifically recognized virus that you refer to.
Since your blood was tested, it would be the Antibody Test which tests for the occurrence of a former infection, not a current infection. The tests for current infections are start with a pharyngeal swab and test for either viral nucleic acids or antigens.
TonySmjc
Well-Known Angler
Yes thank you I know and understand that I shouldn’t get a number value
I’m also trying to reconcile why my gp said
“ northwell is providing him a number value”
I’m not arguing if they should or if it’s proper I get that it’s not either
But I believe and trust the man when he says that they are Doing just that
Stand by I will eventually get to speak with him
Maybe Friday when the second quest results come back
But I fully expect them to be negative at this point
I'd be highly surprised that he will be able to give you a number. You had this discussion with him a day or two after the test was initiated by Northwell. My guess is that the early info the docs got was incorrect.
I assume that the test got run at a centralized lab. If that lab provides your doctor with a number, they are running the assay improperly and all involved are liable of malpractice charges.
Regardless, the value as I explained before, is worthless. It has no diagnostic value as I explained.
TonySmjc
Well-Known Angler
I’m up to 10 ppl
That have lived with ppl that have either had a positive swab for covid or a positive anti body test
Where they weren’t abel to distance or take many if any measures to mitigate the spread within their homes
And have tested negative for anti bodies
Even stranger it always seems to be only one within the household
Mostly one out of 4 I’m one case me one of two
And in one other one of three husband and daughter yes mother no
I’m the other 8 one child of two negative
That to me is staggering when you listen to how contagious this is supposed to be
That have lived with ppl that have either had a positive swab for covid or a positive anti body test
Where they weren’t abel to distance or take many if any measures to mitigate the spread within their homes
And have tested negative for anti bodies
Even stranger it always seems to be only one within the household
Mostly one out of 4 I’m one case me one of two
And in one other one of three husband and daughter yes mother no
I’m the other 8 one child of two negative
That to me is staggering when you listen to how contagious this is supposed to be
TonySmjc
Well-Known Angler
Pre-vetted
Covid-19 (COVID-19 = SARS-CoV-2, essentially)
There May Be a Unique Coronavirus Immune Response
By Derek Lowe 21 May, 2020
We’re starting to get a clearer picture of how the SARS-CoV-2 coronavirus works when it infects the body, and there are some surprises emerging. This new paper in Cell is an example (here’s a writeup on it at Stat).
We already know the RNA sequence of the virus very well, naturally, and that’s allowing us both to track mutations and to lay out exactly what proteins it forces a cell to make once it get ahold of the machinery. That post has some background on some of these, and this earlier one mentions a number of them as well, with an eye to existing drugs that might interact with them. There aren’t very many in total – viruses in general are rather stripped-down. Recall that they start off by forcing the expression of a long polypeptide that (with the help of hijacked cellular proteins) starts cleaving itself into many of these necessary viral pieces, an alarmingly compact and efficient “autoloader” mechanism. The limited number of viral proteins means that you can usually assign a clear and necessary function (or more than one) to every one of them – it’s a lot like working at a small startup! There are no associate VPs in charge of facilitation of planning modalities in a viral genome; they are lean and mean.
And that means that they are stark naked examples of evolution in action as well. Recall that the guiding principle of evolution is “Whatever works”. That’s literally it, and nowhere more so than in something as small and as quickly reproducing as a virus. You know that old line about how an oak tree is just an acorn’s way of making more acorns? Viruses live it – the only thing they do is make more virus. There are no added complications for something like feeding behavior, because they don’t eat. There are thus no variations in metabolism, because they don’t have any metabolism. There are no crazy features driven by sexual selection, because they don’t mate. They infect cells and make more virus, and that’s it. And they do it very quickly, over and over. Any change that even slightly assists in infecting cells and making more viral particles that can make more viral particles will be amplified, any change that slightly decreases that efficiency will disappear.
This new paper is concerned with a vital part of that viral business: dealing with the immune defenses of the organisms that they infect. Recall that the human immune system has, broadly speaking, two branches. You have the adaptive part, the one that raises specific neutralizing antibodies and targets T cells at an infection. That one takes a while to get going; there’s a lot to sort through and building up all those targeted weapons doesn’t happen overnight. And you have the innate immune system, which is the “always on” response that recognizes a number of general signs of infection and is ready to act immediately. If that by itself can clear an infection, it certainly will – otherwise it sort of holds the line until the adaptive immune system can range in the artillery and commence firing.
For viruses, the innate immune system is mostly recognizing weirdo RNA species as a sign of infection – these are things that shouldn’t be floating around, and when they show up it sets off the alarm. The receptors that pick these things up (such as the Toll-like receptors, TLRs) set off some serious transcription factor activity, namely NF-kappaB and various interferon regulator factors (IRFs). These head down to the DNA level and alter transcriptional activity, which has a lot of downstream sequels, too: for example, type I and type III interferon proteins (depending on the cell type) start being produced, which in turn set off a list of further interferon-stimulated genes. Over 300 of those are known, so you can see that listing all the effects is a task that gets out of hand really fast, which is a common problem in immunology. These interferons can be secreted to warn neighboring cells, and in addition, a whole list of chemokines are produced and excreted to recruit various types of circulating white blood cells. Viruses that affect organisms (like us) with such defenses have had plenty of brutal selection pressure, and the pathogens we notice now are the ones that have assembled ways of infecting us anyway.
The list of viral countermeasures is a long one – this battle has been going on for a while – and here’s an article that details ten of the most common ones. Many of these come down to hiding as much as possible from the cellular receptors as well as blocking them and their downstream partners with specific viral products. As the article says, this is a sort of arms race, and it has boundary conditions. An immune system varied and powerful enough to immediately wipe out every foreign pathogen could be hard to contain; we have enough problems with autoimmune disease as it stands. And a pathogen that ripped right through its host’s defenses and ran at full speed might well be quickly lethal, which could cut down on the opportunities for spreading. The successful pathogens (looking at the situation from their viewpoint) are the ones that spread in a way that leaves them constant opportunities for growth.
This new paper compares the transcriptional changes that kick in during infection with the current coronavirus to the past SARS and MERS cornaviruses as well as several other (non-corona) respiratory viruses. And it turns out that the SARS-CoV-2 is an unusual one: it manages to block the interfeon-I and III response quite thoroughly, while setting off a larger-than-normal cytokine secretion response. None of the other viruses studied have that profile. If you add IFN-I back to the infected cells in culture, they clear the virus very strongly – the machinery is working, but it’s just not being engaged. Likewise, the overall transcriptional profile of the virus in cells is unique. It’s not that it sets off more changes; in fact, it actually shows fewer transcriptional differences than the other viruses it’s being compared to. But the pattern of genes that are affected is a new one. There’s plenty of expression of a whole list of chemokines, that’s for sure: CCL20, CXCL1, IL-1B, IL-6, CXCL3, CXCL5, CXCL6, CXCL2, CXCL16, and TNF.
These cell culture results carried over quite well to animal models of infection (ferrets, in this case). Looking at nasal epithelial cells from the infected animals over time, the same lack of interferon response and strong cytokine secretion was observed, with what the authors describe as “a unique gene signature enriched for cell death and leukocyte activation“. Compared to influenza A virus infection in the same ferret model, the coronavirus transcriptional response was much less dramatic, but very distinctive. The team was even able to check transcription in human lung tissue (2 post-mortem samples compared to 2 different healthy patients). That’s a very small sample, necessarily, but it showed a very similar profile: no interferon upregulation and plenty of cytokine transcription. They were able to check circulating levels of these in a larger number of patients (24 infected cases versus 24 uninfected controls), and these results were also consistent: they tested negative for interferon, but showed elevation of CXCL9 (which attracts T cells) and CXCL16 (which attracts NK cells), CCL8 and CCL2 (recruiting monocytes and/or macrophages), and CXCL8 (which attracts neutrophils). A sudden oversupply of these cell types might be behind the pathology of the disease, which could be characterized, if these hypotheses are correct, as a uniquely imbalanced response: far too little interferon and far too many cytokines, too early.
I expect we’ll see quite a few other papers in this area; we’ll see if this picture holds up. But it certainly seems consistent with what people have been seeing in the clinic, and it bodes well for the therapies that are aiming to dampen the cytokine response pathways. Does this mean that administration of IFN-I or IFN-III would also be beneficial?
Covid-19 (COVID-19 = SARS-CoV-2, essentially)
There May Be a Unique Coronavirus Immune Response
By Derek Lowe 21 May, 2020
We’re starting to get a clearer picture of how the SARS-CoV-2 coronavirus works when it infects the body, and there are some surprises emerging. This new paper in Cell is an example (here’s a writeup on it at Stat).
We already know the RNA sequence of the virus very well, naturally, and that’s allowing us both to track mutations and to lay out exactly what proteins it forces a cell to make once it get ahold of the machinery. That post has some background on some of these, and this earlier one mentions a number of them as well, with an eye to existing drugs that might interact with them. There aren’t very many in total – viruses in general are rather stripped-down. Recall that they start off by forcing the expression of a long polypeptide that (with the help of hijacked cellular proteins) starts cleaving itself into many of these necessary viral pieces, an alarmingly compact and efficient “autoloader” mechanism. The limited number of viral proteins means that you can usually assign a clear and necessary function (or more than one) to every one of them – it’s a lot like working at a small startup! There are no associate VPs in charge of facilitation of planning modalities in a viral genome; they are lean and mean.
And that means that they are stark naked examples of evolution in action as well. Recall that the guiding principle of evolution is “Whatever works”. That’s literally it, and nowhere more so than in something as small and as quickly reproducing as a virus. You know that old line about how an oak tree is just an acorn’s way of making more acorns? Viruses live it – the only thing they do is make more virus. There are no added complications for something like feeding behavior, because they don’t eat. There are thus no variations in metabolism, because they don’t have any metabolism. There are no crazy features driven by sexual selection, because they don’t mate. They infect cells and make more virus, and that’s it. And they do it very quickly, over and over. Any change that even slightly assists in infecting cells and making more viral particles that can make more viral particles will be amplified, any change that slightly decreases that efficiency will disappear.
This new paper is concerned with a vital part of that viral business: dealing with the immune defenses of the organisms that they infect. Recall that the human immune system has, broadly speaking, two branches. You have the adaptive part, the one that raises specific neutralizing antibodies and targets T cells at an infection. That one takes a while to get going; there’s a lot to sort through and building up all those targeted weapons doesn’t happen overnight. And you have the innate immune system, which is the “always on” response that recognizes a number of general signs of infection and is ready to act immediately. If that by itself can clear an infection, it certainly will – otherwise it sort of holds the line until the adaptive immune system can range in the artillery and commence firing.
For viruses, the innate immune system is mostly recognizing weirdo RNA species as a sign of infection – these are things that shouldn’t be floating around, and when they show up it sets off the alarm. The receptors that pick these things up (such as the Toll-like receptors, TLRs) set off some serious transcription factor activity, namely NF-kappaB and various interferon regulator factors (IRFs). These head down to the DNA level and alter transcriptional activity, which has a lot of downstream sequels, too: for example, type I and type III interferon proteins (depending on the cell type) start being produced, which in turn set off a list of further interferon-stimulated genes. Over 300 of those are known, so you can see that listing all the effects is a task that gets out of hand really fast, which is a common problem in immunology. These interferons can be secreted to warn neighboring cells, and in addition, a whole list of chemokines are produced and excreted to recruit various types of circulating white blood cells. Viruses that affect organisms (like us) with such defenses have had plenty of brutal selection pressure, and the pathogens we notice now are the ones that have assembled ways of infecting us anyway.
The list of viral countermeasures is a long one – this battle has been going on for a while – and here’s an article that details ten of the most common ones. Many of these come down to hiding as much as possible from the cellular receptors as well as blocking them and their downstream partners with specific viral products. As the article says, this is a sort of arms race, and it has boundary conditions. An immune system varied and powerful enough to immediately wipe out every foreign pathogen could be hard to contain; we have enough problems with autoimmune disease as it stands. And a pathogen that ripped right through its host’s defenses and ran at full speed might well be quickly lethal, which could cut down on the opportunities for spreading. The successful pathogens (looking at the situation from their viewpoint) are the ones that spread in a way that leaves them constant opportunities for growth.
This new paper compares the transcriptional changes that kick in during infection with the current coronavirus to the past SARS and MERS cornaviruses as well as several other (non-corona) respiratory viruses. And it turns out that the SARS-CoV-2 is an unusual one: it manages to block the interfeon-I and III response quite thoroughly, while setting off a larger-than-normal cytokine secretion response. None of the other viruses studied have that profile. If you add IFN-I back to the infected cells in culture, they clear the virus very strongly – the machinery is working, but it’s just not being engaged. Likewise, the overall transcriptional profile of the virus in cells is unique. It’s not that it sets off more changes; in fact, it actually shows fewer transcriptional differences than the other viruses it’s being compared to. But the pattern of genes that are affected is a new one. There’s plenty of expression of a whole list of chemokines, that’s for sure: CCL20, CXCL1, IL-1B, IL-6, CXCL3, CXCL5, CXCL6, CXCL2, CXCL16, and TNF.
These cell culture results carried over quite well to animal models of infection (ferrets, in this case). Looking at nasal epithelial cells from the infected animals over time, the same lack of interferon response and strong cytokine secretion was observed, with what the authors describe as “a unique gene signature enriched for cell death and leukocyte activation“. Compared to influenza A virus infection in the same ferret model, the coronavirus transcriptional response was much less dramatic, but very distinctive. The team was even able to check transcription in human lung tissue (2 post-mortem samples compared to 2 different healthy patients). That’s a very small sample, necessarily, but it showed a very similar profile: no interferon upregulation and plenty of cytokine transcription. They were able to check circulating levels of these in a larger number of patients (24 infected cases versus 24 uninfected controls), and these results were also consistent: they tested negative for interferon, but showed elevation of CXCL9 (which attracts T cells) and CXCL16 (which attracts NK cells), CCL8 and CCL2 (recruiting monocytes and/or macrophages), and CXCL8 (which attracts neutrophils). A sudden oversupply of these cell types might be behind the pathology of the disease, which could be characterized, if these hypotheses are correct, as a uniquely imbalanced response: far too little interferon and far too many cytokines, too early.
I expect we’ll see quite a few other papers in this area; we’ll see if this picture holds up. But it certainly seems consistent with what people have been seeing in the clinic, and it bodes well for the therapies that are aiming to dampen the cytokine response pathways. Does this mean that administration of IFN-I or IFN-III would also be beneficial?
Last edited:
Certain wavelengths of UV are effective killers of viruses and bacteria, as is sunlight which has lots of UV in it. That being said, the amount and strength of UV necessary to be effective against the viruses and bacteria would be lethal to us. UV works by destroying nucleic acids (DNA, RNA), no matter what organism is being irradiated.
So it's just like bleach, yeah you could drink an extremely dilute solution of Chlorox or sit under a very weak UV lamp without any ill effects, but these "human-safe" doses are also "virus safe" and therefore ineffective methods to prevent the onset of disease once infected.
AND NO!!! I'm not suggesting anyone should try these inane remedies...
So it's just like bleach, yeah you could drink an extremely dilute solution of Chlorox or sit under a very weak UV lamp without any ill effects, but these "human-safe" doses are also "virus safe" and therefore ineffective methods to prevent the onset of disease once infected.
AND NO!!! I'm not suggesting anyone should try these inane remedies...
Wife had her second eye laser surgery for cataract yesterday. Ophthalmologist went over how her DIY cotton mask was probably more effective than the "vaunted" N95s due to the vent. My GP said the same thing last week and I noticed none of any of the doctors' staffs wore N95s.
If folks don't put an N95 on properly with a good seal, something few folks actually do correctly, then yes a cloth mask is more effective.
Well when folks gown up with a known COVID-19 positive patient, they have N95s on or better, not the plain cloth or paper ones.
Interesting article on "Doing It Like A Boss" in the "Great White North" from the NYT. Reminiscent of the current situation in Maine where head of state CDC and governor working together to keep things pretty much in check, much to the dismay of many who care to ignore science. Complete article attached.
The Top Doctor Who Aced the Coronavirus Test
Dr. Bonnie Henry kept the disease in check in British Columbia without harsh enforcement methods. Now, she is leading the way out of lockdown.
By Catherine Porter
That Tuesday in March was the day Bonnie Henry had been preparing for her whole life.
Overnight, 83 people had tested positive for the novel coronavirus and three more had died. The pandemic had officially broken out in British Columbia.
Standing inside the provincial legislature’s press gallery, the preternaturally calm top doctor of Canada’s westernmost province declared a public health emergency. Under her orders and recommendations, schools closed, bars shuttered and social distancing measures were put in place.
“It seemed so surreal,” she said. “I felt like someone was standing on my chest.”
That day, March 17, Dr. Henry ended her presentation with a line that would become her trademark, and a mantra for many Canadians struggling to cope under a lockdown. It has since been hung in windows, painted on streets, printed on T-shirts, stitched on shoes, folded into songs and stamped on bracelets.
“This is our time to be kind,” she said in her slow and low-pitched voice that many call comforting, “to be calm and to be safe.”
In the next few months, Dr. Henry would prove to be one of the most effective public health officials in the world, with lessons for nations struggling to emerge from lockdowns.
While Ontario and Quebec, the two most populous provinces, are still grappling with hundreds of new cases every day, British Columbia has now reopened schools, restaurants and hair salons. This week, the province of five million reported fewer than 80 new cases.
“By all rights, British Columbia should have been clobbered,” said Colin Furness, an outspoken infection control epidemiologist in Toronto. The province is on the coast, above Washington State, he noted, with a large population that travels back and forth to China, where the outbreak began.
“They took decisive action, did it early without hesitation and communicated effectively,” Mr. Furness added. “People listened to her.”
The Top Doctor Who Aced the Coronavirus Test
Dr. Bonnie Henry kept the disease in check in British Columbia without harsh enforcement methods. Now, she is leading the way out of lockdown.
By Catherine Porter
That Tuesday in March was the day Bonnie Henry had been preparing for her whole life.
Overnight, 83 people had tested positive for the novel coronavirus and three more had died. The pandemic had officially broken out in British Columbia.
Standing inside the provincial legislature’s press gallery, the preternaturally calm top doctor of Canada’s westernmost province declared a public health emergency. Under her orders and recommendations, schools closed, bars shuttered and social distancing measures were put in place.
“It seemed so surreal,” she said. “I felt like someone was standing on my chest.”
That day, March 17, Dr. Henry ended her presentation with a line that would become her trademark, and a mantra for many Canadians struggling to cope under a lockdown. It has since been hung in windows, painted on streets, printed on T-shirts, stitched on shoes, folded into songs and stamped on bracelets.
“This is our time to be kind,” she said in her slow and low-pitched voice that many call comforting, “to be calm and to be safe.”
In the next few months, Dr. Henry would prove to be one of the most effective public health officials in the world, with lessons for nations struggling to emerge from lockdowns.
While Ontario and Quebec, the two most populous provinces, are still grappling with hundreds of new cases every day, British Columbia has now reopened schools, restaurants and hair salons. This week, the province of five million reported fewer than 80 new cases.
“By all rights, British Columbia should have been clobbered,” said Colin Furness, an outspoken infection control epidemiologist in Toronto. The province is on the coast, above Washington State, he noted, with a large population that travels back and forth to China, where the outbreak began.
“They took decisive action, did it early without hesitation and communicated effectively,” Mr. Furness added. “People listened to her.”
Interesting snippets regarding impact of Blood Type on COVID infections. Just remember that a 50% increase in the LIKELIHOOD of something doesn't mean 50% will get that, just means that if your normal odds are 1:1000, your odds would be 1:750...
Preliminary results from more than 750,000 participants suggests type O blood is especially protective against SARS-CoV-2, the virus that causes COVID-19, the company said on Monday. The findings echo other research that has indicated a link between variations in the ABO gene and COVID-19.
Many other groups, including 23andMe competitor Ancestry Inc., are combing the genome to help make sense of the virus. It is known that factors such as age and underlying health conditions can determine how people fare once they’ve contracted COVID-19. But those factors alone don’t explain the wide diversity of symptoms, or why some people contract the disease and others don’t. Studying the genetics of the people who are more susceptible to SARS-CoV-2 could help identify and protect those more at risk, as well as help speed treatment and drug development.
Several other studies looking at both severity of illness and susceptibility to disease have also suggested blood type plays a role.
Research published last week prior to peer review suggested blood type may play a role in the severity of patients’ reactions to SARS-CoV-2. That study looked at the genes of more than 1,600 patients in Italy and Spain who experienced respiratory failure and found that having type A blood was linked to a 50 percent increase in the likelihood a patient would require a ventilator. An earlier Chinese study turned up similar results regarding a person’s susceptibility to COVID-19.
Preliminary results from more than 750,000 participants suggests type O blood is especially protective against SARS-CoV-2, the virus that causes COVID-19, the company said on Monday. The findings echo other research that has indicated a link between variations in the ABO gene and COVID-19.
Many other groups, including 23andMe competitor Ancestry Inc., are combing the genome to help make sense of the virus. It is known that factors such as age and underlying health conditions can determine how people fare once they’ve contracted COVID-19. But those factors alone don’t explain the wide diversity of symptoms, or why some people contract the disease and others don’t. Studying the genetics of the people who are more susceptible to SARS-CoV-2 could help identify and protect those more at risk, as well as help speed treatment and drug development.
Several other studies looking at both severity of illness and susceptibility to disease have also suggested blood type plays a role.
Research published last week prior to peer review suggested blood type may play a role in the severity of patients’ reactions to SARS-CoV-2. That study looked at the genes of more than 1,600 patients in Italy and Spain who experienced respiratory failure and found that having type A blood was linked to a 50 percent increase in the likelihood a patient would require a ventilator. An earlier Chinese study turned up similar results regarding a person’s susceptibility to COVID-19.
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