Well BOTH Quest and Northwell use the test from Abbott and they're both negative at 0.99 or 1.00 S/CO. Northwell is misusing the test in that the only thing that's supposed to be reported is POSITIVE or NEGATIVE per the package insert. I could provide you a copy if you would care to read it. In case you're interested the cutoff for a positive is NOT 1.0, but 1.4 or greater for this COVID antibody test. Many qualitative tests including some Abbott ones use a cutoff value of 1.00. If Northwell has decided to deviate from that, it's another example of them misusing the test. Since the test is not an-FDA approved In Vitro Diagnostic, Northwell can monkey with things without being "illegal", but they're dancing with the devil there.
This is a qualitative test and not a measure of antibody, so a signal of 2 doesn't even suggest that that patient has 1/2 the antibody of a patient with a signal of 4.0.
Shall I go to heaven or a-fishing? - H. D. Thoreau Veni. Vidi. Cepi. - with apologies to Gaius Julius Caesar
Sorry I wasn’t specific I didn’t mean the cut off was actually 1 I was using it as and example I should have said greater than x all the numbers were just examples
What Is accurate is that they arnt simply using positive and negative but an actually value I don’t know at what point they just say negative , if they ever do
I believe you on the package insert
so if 1.4 is a positive And 1.39 is a negative While I understand it’s not a percentage of anti bodies Would not 1.2 to 1.39 indicate the presence of some antibodies and isn’t that a better measure than just a straight cutoff number ?
and more out of curiosity ,dancing with the devil as in Giving ppl a false sense of security that they have some form of anti body immunity when I’m fact they dont? And if that’s correct is 1.30 really that much worse than 1.4 How low can it go before it’s just garbage information or is 1.4 the drop dead number Speculation on their purpose for doing it this way as opposed to a straight plus/minus
Test was designed to report a NEGATIVE or POSITIVE result; the numeric value is irrelevant. That's why I'm extremely concerned that Northwell has chosen to provide a value; it is assay malpractice plain and simple.
The cutoff is determined by testing hundreds of negative patients to develop a "Normal Distribution". Then you start running known positives, as many as you can get your hands on. IF the Assay Gods are smiling favorably upon you, the signals of the 2 populations will be separated by at least 5 Std Deviations of the Normal Population's. If the Gods really love you, it will be 9 Std Devs or higher, this is Assay Nirvana. At that level, the odds of a false result are minimized.
If the number of Std Deviations is less than 5, you start working with the formulation to get better signal separation between the Normal and Sick populations. After you think you've got the cutoff correct you validate that by testing sensitivity and specificity by running samples that you know could be difficult to detect to test your sensitivity and samples that could give you a false positive to test your specificity. Finally you get a hold of timed samples from a patient that were taken over a few weeks that also have corresponding PCR (diagnostic tests) so you can see if and when the person developed antibodies. Hit any snags during this testing, then it's reformulation time.
NEVER in this process do you correlate the amount of antibody to the signal. There are 100s of reasons why not, but suffice it to say that a QUANTITATIVE Antibody Assay is a major, complex challenge since you may have hundreds of COVID-19 antibodies, each with a vastly different activity. For example if you have 10 mg of low reactivity AbX and 1 ug of high reactivity AbY, you might think your reaction is due to AbX, when it's really AbY driving the reactivity.
A quantitative Ab assay has no diagnostic value when trying to determine if someone is positive or negative. However it is crucial for determining which patients have high-reactivity antibodies for a possible treatment for others. Then you begin testing for reactivity for specific epitopes by linear dilutions, a very labor-intensive testing protocol, but essential to determine donors that can fulfill the need for plasma donations with adequate titers for treating other patients.
There should be no confusion regarding the amount of antibody and the protection you have. The assay only determines IF the person has a level of COVID-19 indicative of a former infection. It says nothing about the efficacy of these antibodies, especially since nobody at this time knows what antibodies and what titer are needed to prevent COVID-19. As the vaccine candidates go through clinical trials, these data will be generated, along with the studies transfusing plasma from cured COVID-19 patients into sick patients.
Shall I go to heaven or a-fishing? - H. D. Thoreau Veni. Vidi. Cepi. - with apologies to Gaius Julius Caesar
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.
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
Northwell results came back negative The nurse wasn’t abel to give me any more than that as far as a numerical rating And the doctor wasn’t available
The 2nd quest test isn’t back yet Maybe by Friday
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.
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.
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.
Shall I go to heaven or a-fishing? - H. D. Thoreau Veni. Vidi. Cepi. - with apologies to Gaius Julius Caesar
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. 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.
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
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.
Shall I go to heaven or a-fishing? - H. D. Thoreau Veni. Vidi. Cepi. - with apologies to Gaius Julius Caesar
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
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.
We already know the RNA sequence of the virus very well, naturally, and that’s allowing us both to [track mutations]('https://blogs.sciencemag.org/pipeline/archives/2020/04/21/watching-for-mutations-in-the-coronavirus') 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]('https://blogs.sciencemag.org/pipeline/archives/2020/03/26/what-the-coronavirus-proteins-are-targeting') 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]('https://blogs.sciencemag.org/pipeline/archives/2020/04/10/more-on-screening-for-coronavirus-therapies') 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.
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]('https://en.wikipedia.org/wiki/Toll-like_receptor'), 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]('http://Viruses that affect organisms (like us) with such defenses have had plenty of time and no end of brutal selection pressure, and the pathogens we notice now are the ones that have assembled ways of infecting us anyway.') 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?
***
A lawyer with his briefcase can steal more than a hundred men with guns- Mario Puzo
We already know the RNA sequence of the virus very well, naturally, and that’s allowing us both to [track mutations]('https://blogs.sciencemag.org/pipeline/archives/2020/04/21/watching-for-mutations-in-the-coronavirus') 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]('https://blogs.sciencemag.org/pipeline/archives/2020/03/26/what-the-coronavirus-proteins-are-targeting') 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]('https://blogs.sciencemag.org/pipeline/archives/2020/04/10/more-on-screening-for-coronavirus-therapies') 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.
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]('https://en.wikipedia.org/wiki/Toll-like_receptor'), 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]('http://Viruses that affect organisms (like us) with such defenses have had plenty of time and no end of brutal selection pressure, and the pathogens we notice now are the ones that have assembled ways of infecting us anyway.') 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?
***
Possible explanation for the Cytokine Storm seen in some patients most intriguing...
Shall I go to heaven or a-fishing? - H. D. Thoreau Veni. Vidi. Cepi. - with apologies to Gaius Julius Caesar
In the “other” thread on this subject there is some recent chatter about UV effects on killing or Chasing the bug Do you see any facts or legitimate scientific positive results in that or is it no different than the drinking bleach theory??
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...
Shall I go to heaven or a-fishing? - H. D. Thoreau Veni. Vidi. Cepi. - with apologies to Gaius Julius Caesar
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.
