RugbyRebels

morepork wrote:Agreed, but keeping people out of the ICU? Dunno.

Not as intended; another knee jerk reaction and the dangers therein.
https://www.bbc.co.uk/news/52012242

Son of Mathonwy wrote:

morepork wrote:

Son of Mathonwy wrote: I can't read the ft, but I think the article is here:
https://www.econjobrumors.com/topic/cor ... st_5465580

If true* new infections should slow down soon rather than grow exponentially. But with the sudden shutdown, hopefully new infections will slow down anyway, so how can we tell? Someone needs to do some random testing of the population soon!

* Seems too good to be...

As they say, "neutralisation assays which provide reliable readout of protective immunity", would provide that data, but these are not trivial assays. I've done lots of them for viral gene therapy vectors. You would need to collect serum from an appropriately sampled population, expose cultured cells to the serum then expose those cells to live, virulent coronovirus (you could use a pseudotyped attenuated viral capsid but given the virus is new to science, this would take as long as a vaccine), then assay for the viral genome inside the cells some days later. The idea being pre-existing antibodies to the virus in serum will block entry of the capsid into cells. There are so many technical variables here I don't know where to start. What cell type most closely models the cells infected by the virus in humans (vital for the structure-function relationship between a viral antigen, the host cell surface entity that antigen binds to, and an antibody), and on and on and on. All of this technical variance combined with the unknown natural variance in host immune response in an infected population that has arisen mere months ago would make it outrageously difficult to determine the sample size (number of patients needed to be sampled to give a true representation of the actual population mean) required to give the data appropriate statistical power (i.e. minimise the chances of a false negative result). More pointedly, all of this relies on an assumption that seropositivity confers resistance to infection. That is a fucking big gamble in the middle of an exponential rise in deaths and, frankly, not something that resources should be allocated to.

So we're some way from knowing what antibodies to Covid-19 look like? We can't just test for the presence of them, we need to use more indirect methods?

I'm sure they could do it in Star Trek. C'mon guys, raise your game.

At the moment we don't know if antibodies raised in response to infection are inactivating, that is, do they prevent the virus from entering the host cell. It's not what they look like, it's what they do to viral function. Answering that question will dictate a timeline applicable also to the development of a vaccine....a long time. A seropositive individual will have multiple species of antibody, and if one or some of those species inhibit the interaction of the viral capsid with the host cell membrane, they will block entry of that capsid, so collecting serum from infected individuals will answer that question. However, the absence of a valid inactivating antibody test renders the hypothesis presented in the article refractory to testing. My original point was that the functional inactivating antibody assays proposed by the article are currently unavailable because we know very little about why the host cell is conducive to infection because the host cell itself an incompletely defined entity, and relying on the currently afflicted human population to validate the assay is unethical, if not downright arse about face. Refining a valid inactivating antibody assay would require, ideally, most of the population being infected and then drawing serum from an appropriate sample size of that population to account for the inevetible sampling and technical variance that produces statistical noise. We are currently in no position to accommodate this academic exercise. If the hypothesis is wrong, many die unnecessarily. The hypothesis has merit, but as there is no practical path to testing it currently, it should not be a factor in public health decisions that need to be made right now.


This waffle probably lacks clarity, but so does justification for testing the hypothesis at this point in time.

A sobering read about the risks faced by front line medics, anaesthetists and surgeons in particular...

https://www.bloomberg.com/opinion/artic ... t-risk-too

Sent from my CPH1951 using Tapatalk

My wife and I have several of the minor symptoms today. We’ve got plenty of everything except milk, so someone will need to go get milk tomorrow or Thursday... have to take precautions not to infect anyone else.

morepork wrote:

Son of Mathonwy wrote:

morepork wrote:

As they say, "neutralisation assays which provide reliable readout of protective immunity", would provide that data, but these are not trivial assays. I've done lots of them for viral gene therapy vectors. You would need to collect serum from an appropriately sampled population, expose cultured cells to the serum then expose those cells to live, virulent coronovirus (you could use a pseudotyped attenuated viral capsid but given the virus is new to science, this would take as long as a vaccine), then assay for the viral genome inside the cells some days later. The idea being pre-existing antibodies to the virus in serum will block entry of the capsid into cells. There are so many technical variables here I don't know where to start. What cell type most closely models the cells infected by the virus in humans (vital for the structure-function relationship between a viral antigen, the host cell surface entity that antigen binds to, and an antibody), and on and on and on. All of this technical variance combined with the unknown natural variance in host immune response in an infected population that has arisen mere months ago would make it outrageously difficult to determine the sample size (number of patients needed to be sampled to give a true representation of the actual population mean) required to give the data appropriate statistical power (i.e. minimise the chances of a false negative result). More pointedly, all of this relies on an assumption that seropositivity confers resistance to infection. That is a fucking big gamble in the middle of an exponential rise in deaths and, frankly, not something that resources should be allocated to.

So we're some way from knowing what antibodies to Covid-19 look like? We can't just test for the presence of them, we need to use more indirect methods?

I'm sure they could do it in Star Trek. C'mon guys, raise your game.

At the moment we don't know if antibodies raised in response to infection are inactivating, that is, do they prevent the virus from entering the host cell. It's not what they look like, it's what they do to viral function. Answering that question will dictate a timeline applicable also to the development of a vaccine....a long time. A seropositive individual will have multiple species of antibody, and if one or some of those species inhibit the interaction of the viral capsid with the host cell membrane, they will block entry of that capsid, so collecting serum from infected individuals will answer that question. However, the absence of a valid inactivating antibody test renders the hypothesis presented in the article refractory to testing. My original point was that the functional inactivating antibody assays proposed by the article are currently unavailable because we know very little about why the host cell is conducive to infection because the host cell itself an incompletely defined entity, and relying on the currently afflicted human population to validate the assay is unethical, if not downright arse about face. Refining a valid inactivating antibody assay would require, ideally, most of the population being infected and then drawing serum from an appropriate sample size of that population to account for the inevetible sampling and technical variance that produces statistical noise. We are currently in no position to accommodate this academic exercise. If the hypothesis is wrong, many die unnecessarily. The hypothesis has merit, but as there is no practical path to testing it currently, it should not be a factor in public health decisions that need to be made right now.


This waffle probably lacks clarity, but so does justification for testing the hypothesis at this point in time.

I’m not remotely an expert so shoot me down if this makes no sense but:

If it becomes possible to test for antibodies on mass (something like a pregnancy test has been mentioned) and if a larger than expected number of the general public appear to have antibodies, and if having these antibodies they are not dead, does this prove the model?

My main area of concern about that study would be the assumptions. They have chosen a % of people to be the risk group and some numbers for transmitability (is that a word?). Do these hold water?

canta_brian wrote:

morepork wrote:

Son of Mathonwy wrote: So we're some way from knowing what antibodies to Covid-19 look like? We can't just test for the presence of them, we need to use more indirect methods?

I'm sure they could do it in Star Trek. C'mon guys, raise your game.

At the moment we don't know if antibodies raised in response to infection are inactivating, that is, do they prevent the virus from entering the host cell. It's not what they look like, it's what they do to viral function. Answering that question will dictate a timeline applicable also to the development of a vaccine....a long time. A seropositive individual will have multiple species of antibody, and if one or some of those species inhibit the interaction of the viral capsid with the host cell membrane, they will block entry of that capsid, so collecting serum from infected individuals will answer that question. However, the absence of a valid inactivating antibody test renders the hypothesis presented in the article refractory to testing. My original point was that the functional inactivating antibody assays proposed by the article are currently unavailable because we know very little about why the host cell is conducive to infection because the host cell itself an incompletely defined entity, and relying on the currently afflicted human population to validate the assay is unethical, if not downright arse about face. Refining a valid inactivating antibody assay would require, ideally, most of the population being infected and then drawing serum from an appropriate sample size of that population to account for the inevetible sampling and technical variance that produces statistical noise. We are currently in no position to accommodate this academic exercise. If the hypothesis is wrong, many die unnecessarily. The hypothesis has merit, but as there is no practical path to testing it currently, it should not be a factor in public health decisions that need to be made right now.


This waffle probably lacks clarity, but so does justification for testing the hypothesis at this point in time.

I’m not remotely an expert so shoot me down if this makes no sense but:

If it becomes possible to test for antibodies on mass (something like a pregnancy test has been mentioned) and if a larger than expected number of the general public appear to have antibodies, and if having these antibodies they are not dead, does this prove the model?

My main area of concern about that study would be the assumptions. They have chosen a % of people to be the risk group and some numbers for transmitability (is that a word?). Do these hold water?

A pregnancy kit. Not so much. To test for antibodies you need an antigen for them to bind to. Coronovirus has four major structural proteins in various tertiary conformations. Which protein in which conformation is the one that will accurately test seropositivity? Also, If the antibodies are not inactivating, then who cares? Inactivating antibody assays takes days (at least) and require a laboratory to conduct. Current test kits assay for viral nucleic acid sequence and are many, many times more sensitive and specific than an antibody assay. The biggest/riskiest assumption is that the specific antibody/antigen that this hypothetical study will actually be inactivating. There are people working on the antibody thing for vaccine development. I'm sure they sing out when they have some data, and until they do, I'd rather policy weren't predicated on quite so massive an assumption.

morepork wrote:The biggest/riskiest assumption is that the specific antibody/antigen that this hypothetical study will actually be inactivating.

Can we assume that for a person to recover, at least one type of antibody they produced is inactivating?

Alternatively, if none of them are inactivating, does this mean:
1) they would not be immune to a second infection,
or
2) it's impossible - they would not recover in this case?

Another point - what can be gained from a comparison between the serum of a recovered person and an uninfected person? Can the antibodies be detected, or are they simply too small, or the situation too complex for them to be identified?

morepork wrote:

canta_brian wrote:

morepork wrote:
At the moment we don't know if antibodies raised in response to infection are inactivating, that is, do they prevent the virus from entering the host cell. It's not what they look like, it's what they do to viral function. Answering that question will dictate a timeline applicable also to the development of a vaccine....a long time. A seropositive individual will have multiple species of antibody, and if one or some of those species inhibit the interaction of the viral capsid with the host cell membrane, they will block entry of that capsid, so collecting serum from infected individuals will answer that question. However, the absence of a valid inactivating antibody test renders the hypothesis presented in the article refractory to testing. My original point was that the functional inactivating antibody assays proposed by the article are currently unavailable because we know very little about why the host cell is conducive to infection because the host cell itself an incompletely defined entity, and relying on the currently afflicted human population to validate the assay is unethical, if not downright arse about face. Refining a valid inactivating antibody assay would require, ideally, most of the population being infected and then drawing serum from an appropriate sample size of that population to account for the inevetible sampling and technical variance that produces statistical noise. We are currently in no position to accommodate this academic exercise. If the hypothesis is wrong, many die unnecessarily. The hypothesis has merit, but as there is no practical path to testing it currently, it should not be a factor in public health decisions that need to be made right now.


This waffle probably lacks clarity, but so does justification for testing the hypothesis at this point in time.

I’m not remotely an expert so shoot me down if this makes no sense but:

If it becomes possible to test for antibodies on mass (something like a pregnancy test has been mentioned) and if a larger than expected number of the general public appear to have antibodies, and if having these antibodies they are not dead, does this prove the model?

My main area of concern about that study would be the assumptions. They have chosen a % of people to be the risk group and some numbers for transmitability (is that a word?). Do these hold water?

A pregnancy kit. Not so much. To test for antibodies you need an antigen for them to bind to. Coronovirus has four major structural proteins in various tertiary conformations. Which protein in which conformation is the one that will accurately test seropositivity? Also, If the antibodies are not inactivating, then who cares? Inactivating antibody assays takes days (at least) and require a laboratory to conduct. Current test kits assay for viral nucleic acid sequence and are many, many times more sensitive and specific than an antibody assay. The biggest/riskiest assumption is that the specific antibody/antigen that this hypothetical study will actually be inactivating. There are people working on the antibody thing for vaccine development. I'm sure they sing out when they have some data, and until they do, I'd rather policy weren't predicated on quite so massive an assumption.

The tests he's talking about only look like pregnancy tests. They test for antibodies IGM and IGG...

UK coronavirus mass home testing to be made available 'within days'

https://www.theguardian.com/world/2020/ ... _clipboard

Sent from my CPH1951 using Tapatalk

Son of Mathonwy wrote:

morepork wrote:The biggest/riskiest assumption is that the specific antibody/antigen that this hypothetical study will actually be inactivating.

Can we assume that for a person to recover, at least one type of antibody they produced is inactivating?

Alternatively, if none of them are inactivating, does this mean:
1) they would not be immune to a second infection,
or
2) it's impossible - they would not recover in this case?

Another point - what can be gained from a comparison between the serum of a recovered person and an uninfected person? Can the antibodies be detected, or are they simply too small, or the situation too complex for them to be identified?

Any foreign body will raise antibodies as part of the normal immune response. If that response is inefficient, then some virus will get through a second time. The antibody response is designed to stop foreign objects from getting on or in a cell, so the response will inactivate at some level (prevent the viral capsid from binding). It's a complex biological response that has correspondingly complex sampling issues. As an example, there is a naturally occurring non-pathogenic virus in humans, AAV, that piggybacks on the life cycle of another virus that causes the common cold. AAV is used in gene therapy applications in humans and so the inactivating antibody question has been comprehensively studied for AAV. About 90% of the human population are seropositive for AAV antibodies, but less than half of these individuals have inactivating antibodies. The ability to distinguish inactivating antibodies from non in seropositive individuals is the result of decades of studying the bijebus out of AAV, which is a naturally replication-deficient entity. Can't replicate, so not much mutation going on. Contrast this with the influenza virus, which is able to replicate, and does so at a rate of 10s of thousands of copies per day. Every little error during replication of the viral genome introduces an ocassional change in sequence coding for capsid proteins that your seropositive individuals have antibodies to. This is antigenic drift. The higher the rate of replication, the greater the chance of of drift in the capsid protein antigen. This is why flu shots change from year to year. Influenza has an infectious period of 4-7 days and usually burns itself out. Corona virus has an infectious period of at least 14 days (probably longer), which give twice the time to replicate and shift antigens, and is why it's such a virulent little mother. Add to this rosy picture the fact that the current coronavirus has jumped from animals to humans, so there is a dramatically different antigen profile confronting the human immune system (antigenic shift) that it is utterly powerless against. This is why flu vaccines will not work on coronavirus. Given the longer infectivity time, the corresponding increase in replication rate (1 into 2, 2 into 4, 4 into 8, and so on over time) and the radical antigenic shift presented by coronavirus, how will the immune system keep up with a). the initial overwhelming infection, and b). the inevitable antigenic drift that will be going on. It's an evolution by mutation beast. Even if you by some chance found an inactivating species of antibody in a recovered person, there are almost half a million people world wide that are infected, and counting. That inactivating serum could be rendered redundant within a matter of weeks, and so recovered patient becomes susceptible patient once more once they come into contact with cousin fuckface on the overnight flight from wherever. The more we allow this to spread, the greater the replicating, mutating population of virus becomes, and the harder it will be to apply any treatment or vaccine breakthrough.

Viruses don't do much but inject nucleic acid into cells and make more viruses, but by fuck they are good at countering any attempt by the body to stop that process from marching on. The day health authorities recognised zoonotic animal to human transmission, a big red PANDEMIC communication should have gone out to every country on the globe.

Donny osmond wrote:

morepork wrote:

canta_brian wrote:
I’m not remotely an expert so shoot me down if this makes no sense but:

If it becomes possible to test for antibodies on mass (something like a pregnancy test has been mentioned) and if a larger than expected number of the general public appear to have antibodies, and if having these antibodies they are not dead, does this prove the model?

My main area of concern about that study would be the assumptions. They have chosen a % of people to be the risk group and some numbers for transmitability (is that a word?). Do these hold water?

A pregnancy kit. Not so much. To test for antibodies you need an antigen for them to bind to. Coronovirus has four major structural proteins in various tertiary conformations. Which protein in which conformation is the one that will accurately test seropositivity? Also, If the antibodies are not inactivating, then who cares? Inactivating antibody assays takes days (at least) and require a laboratory to conduct. Current test kits assay for viral nucleic acid sequence and are many, many times more sensitive and specific than an antibody assay. The biggest/riskiest assumption is that the specific antibody/antigen that this hypothetical study will actually be inactivating. There are people working on the antibody thing for vaccine development. I'm sure they sing out when they have some data, and until they do, I'd rather policy weren't predicated on quite so massive an assumption.

The tests he's talking about only look like pregnancy tests. They test for antibodies IGM and IGG...

UK coronavirus mass home testing to be made available 'within days'

https://www.theguardian.com/world/2020/ ... _clipboard

Sent from my CPH1951 using Tapatalk

That's good news. It will be quite variable depending on the stage of infection of an individual, but will provide useful data. It's not a gold standard test though, so any positives need to be followed up with a PCR-based diagnostic.

I don't necessarily agree with this statement in the Guardian article:

NHS workers or anyone else will be able to know if they have had the virus and are therefore immune, which means they could resume their normal lives, no longer having to work from home or keep their distance from other people. It is widely thought that having Covid-19 makes people immune to the disease or that if they get it a second time, they do not transmit it.

That's something that needs a very strict timeline. What stage of the virus life cycle are people in when they see a positive result? How long does the active virus persist?


Berlin-based Pharmact has already started shipping a 20-minute immunoassay containing three SARS-CoV-2 antigens: the N protein and the S1 and S2 domains of the S protein. It is designed to detect any patient antibody that recognizes these protein structures. It aims to scale production to one million tests during the month of April. As is typical for such a test, it detects both immunoglobulin (Ig) M and IgG antibodies, which are released during the initial and later stages of an infection, respectively. It has conducted validation studies that compared its test with PCR, using samples from 114 infected patients and 126 uninfected controls. The test scored highly in terms of specificity. “We had a true negative rate of 100% — zero false positives,” says Gunther Burgard, medical director at Pharmact. Its sensitivity was lower, however, as the IgM response does not offer a strong initial signal. During the early stage of the infection (days 4–10), the IgM component of the test provides a sensitivity of just 70%. This rises rapidly to 92.3% between days 11 and 24, and the IgG component of the test offers a sensitivity of 98.6% during this phase of the infection. Overall, the test has a false negative rate of 13%, Burgard says.

Stom wrote:My wife and I have several of the minor symptoms today. We’ve got plenty of everything except milk, so someone will need to go get milk tomorrow or Thursday... have to take precautions not to infect anyone else.

Take care of yourselves. Hope it passes quickly.

morepork wrote:The test scored highly in terms of specificity. “We had a true negative rate of 100% — zero false positives,” says Gunther Burgard, medical director at Pharmact. Its sensitivity was lower, however, as the IgM response does not offer a strong initial signal. During the early stage of the infection (days 4–10), the IgM component of the test provides a sensitivity of just 70%. This rises rapidly to 92.3% between days 11 and 24, and the IgG component of the test offers a sensitivity of 98.6% during this phase of the infection. Overall, the test has a false negative rate of 13%, Burgard says.[/i]

Is it just me, or is that the opposite way to how you want it to be. I'd prefer 0% false negatives and 13% false positives - I'd rather people be mistakenly told to isolate than mistakenly told to resume their lives.

Puja

It's a pretty good start. Just not gold standard. Follow it up with the PCR test and be sure. At least it will help apportion resources somewhat more efficiently. They could encourage participation by offering a packet of fags and a bottle of vodka for every positive result followed up.

morepork wrote:

canta_brian wrote:

morepork wrote:
At the moment we don't know if antibodies raised in response to infection are inactivating, that is, do they prevent the virus from entering the host cell. It's not what they look like, it's what they do to viral function. Answering that question will dictate a timeline applicable also to the development of a vaccine....a long time. A seropositive individual will have multiple species of antibody, and if one or some of those species inhibit the interaction of the viral capsid with the host cell membrane, they will block entry of that capsid, so collecting serum from infected individuals will answer that question. However, the absence of a valid inactivating antibody test renders the hypothesis presented in the article refractory to testing. My original point was that the functional inactivating antibody assays proposed by the article are currently unavailable because we know very little about why the host cell is conducive to infection because the host cell itself an incompletely defined entity, and relying on the currently afflicted human population to validate the assay is unethical, if not downright arse about face. Refining a valid inactivating antibody assay would require, ideally, most of the population being infected and then drawing serum from an appropriate sample size of that population to account for the inevetible sampling and technical variance that produces statistical noise. We are currently in no position to accommodate this academic exercise. If the hypothesis is wrong, many die unnecessarily. The hypothesis has merit, but as there is no practical path to testing it currently, it should not be a factor in public health decisions that need to be made right now.


This waffle probably lacks clarity, but so does justification for testing the hypothesis at this point in time.

I’m not remotely an expert so shoot me down if this makes no sense but:

If it becomes possible to test for antibodies on mass (something like a pregnancy test has been mentioned) and if a larger than expected number of the general public appear to have antibodies, and if having these antibodies they are not dead, does this prove the model?

My main area of concern about that study would be the assumptions. They have chosen a % of people to be the risk group and some numbers for transmitability (is that a word?). Do these hold water?

A pregnancy kit. Not so much. To test for antibodies you need an antigen for them to bind to. Coronovirus has four major structural proteins in various tertiary conformations. Which protein in which conformation is the one that will accurately test seropositivity? Also, If the antibodies are not inactivating, then who cares? Inactivating antibody assays takes days (at least) and require a laboratory to conduct. Current test kits assay for viral nucleic acid sequence and are many, many times more sensitive and specific than an antibody assay. The biggest/riskiest assumption is that the specific antibody/antigen that this hypothetical study will actually be inactivating. There are people working on the antibody thing for vaccine development. I'm sure they sing out when they have some data, and until they do, I'd rather policy weren't predicated on quite so massive an assumption.

I don’t think anybody but that psycho Cummings would produce policy in the basis of what was only a model.

Some good news. The curve is flattening:

Mellsblue wrote:Some good news. The curve is flattening:

That US line is looking nasty

canta_brian wrote:

Mellsblue wrote:Some good news. The curve is flattening:

That US line is looking nasty

NYC is about to go off.

morepork wrote:

canta_brian wrote:

Mellsblue wrote:Some good news. The curve is flattening:

That US line is looking nasty

NYC is about to go off.

Yep. My bro and sil are hunkered down at home and have been for weeks. They’re away from the epicentre as they live in Westchester but they ain’t looking forward to what the next few weeks hold.

morepork wrote:

canta_brian wrote:

Mellsblue wrote:Some good news. The curve is flattening:

That US line is looking nasty

NYC is about to go off.

Let me guess, democrats live in high density urban areas. Republicans in shit squishing isolation in the sticks.

How long before urban death tolls are down to GOD punishing them for tolerating gays, voting for Clinton and not owning enough guns.

My wife is making her own PPE.... We just need some decent marketing and could make a mint!

Hope everyone's family is fine...[emoji16]

Sent from my CPH1951 using Tapatalk

morepork wrote:

Son of Mathonwy wrote:

morepork wrote:The biggest/riskiest assumption is that the specific antibody/antigen that this hypothetical study will actually be inactivating.

Can we assume that for a person to recover, at least one type of antibody they produced is inactivating?

Alternatively, if none of them are inactivating, does this mean:
1) they would not be immune to a second infection,
or
2) it's impossible - they would not recover in this case?

Another point - what can be gained from a comparison between the serum of a recovered person and an uninfected person? Can the antibodies be detected, or are they simply too small, or the situation too complex for them to be identified?

Any foreign body will raise antibodies as part of the normal immune response. If that response is inefficient, then some virus will get through a second time. The antibody response is designed to stop foreign objects from getting on or in a cell, so the response will inactivate at some level (prevent the viral capsid from binding). It's a complex biological response that has correspondingly complex sampling issues. As an example, there is a naturally occurring non-pathogenic virus in humans, AAV, that piggybacks on the life cycle of another virus that causes the common cold. AAV is used in gene therapy applications in humans and so the inactivating antibody question has been comprehensively studied for AAV. About 90% of the human population are seropositive for AAV antibodies, but less than half of these individuals have inactivating antibodies. The ability to distinguish inactivating antibodies from non in seropositive individuals is the result of decades of studying the bijebus out of AAV, which is a naturally replication-deficient entity. Can't replicate, so not much mutation going on. Contrast this with the influenza virus, which is able to replicate, and does so at a rate of 10s of thousands of copies per day. Every little error during replication of the viral genome introduces an ocassional change in sequence coding for capsid proteins that your seropositive individuals have antibodies to. This is antigenic drift. The higher the rate of replication, the greater the chance of of drift in the capsid protein antigen. This is why flu shots change from year to year. Influenza has an infectious period of 4-7 days and usually burns itself out. Corona virus has an infectious period of at least 14 days (probably longer), which give twice the time to replicate and shift antigens, and is why it's such a virulent little mother. Add to this rosy picture the fact that the current coronavirus has jumped from animals to humans, so there is a dramatically different antigen profile confronting the human immune system (antigenic shift) that it is utterly powerless against. This is why flu vaccines will not work on coronavirus. Given the longer infectivity time, the corresponding increase in replication rate (1 into 2, 2 into 4, 4 into 8, and so on over time) and the radical antigenic shift presented by coronavirus, how will the immune system keep up with a). the initial overwhelming infection, and b). the inevitable antigenic drift that will be going on. It's an evolution by mutation beast. Even if you by some chance found an inactivating species of antibody in a recovered person, there are almost half a million people world wide that are infected, and counting. That inactivating serum could be rendered redundant within a matter of weeks, and so recovered patient becomes susceptible patient once more once they come into contact with cousin fuckface on the overnight flight from wherever. The more we allow this to spread, the greater the replicating, mutating population of virus becomes, and the harder it will be to apply any treatment or vaccine breakthrough.

Viruses don't do much but inject nucleic acid into cells and make more viruses, but by fuck they are good at countering any attempt by the body to stop that process from marching on. The day health authorities recognised zoonotic animal to human transmission, a big red PANDEMIC communication should have gone out to every country on the globe.

I like the way you talk fancy boy, wanna cyber sex?

Mellsblue wrote:Some good news. The curve is flattening:

I think there's some dubiety about those figures, maybe the UK have changed the way they record figures or something like that? Don't know the details.

I realise just how useful this post is.

Sent from my CPH1951 using Tapatalk

Donny osmond wrote:

Mellsblue wrote:Some good news. The curve is flattening:

I think there's some dubiety about those figures, maybe the UK have changed the way they record figures or something like that? Don't know the details.

I realise just how useful this post is.

Sent from my CPH1951 using Tapatalk

Yep. That’s certainly cleared up that issue we didn’t realise we had.
Im thinking you’ve only written that post so as to use the word dubiety.

Mellsblue wrote:

Donny osmond wrote:

Mellsblue wrote:Some good news. The curve is flattening:

I think there's some dubiety about those figures, maybe the UK have changed the way they record figures or something like that? Don't know the details.

I realise just how useful this post is.

Sent from my CPH1951 using Tapatalk

Yep. That’s certainly cleared up that issue we didn’t realise we had.
Im thinking you’ve only written that post so as to use the word dubiety.

To be fair, I've just learned a new word, so it wasn't a completely pointless post.

Puja

https://www.sciencemag.org/news/2020/03 ... oronavirus

"Trump’s initial public remarks on the drug candidates at a 19 March briefing appeared to be based on anecdotal reports from China and the tiny French study, which Vanity Fair reports he learned of after Elon Musk tweeted about it and Fox News amplified the information."