Chicken/egg problem: Did we lose credibility and then started telling 'em what they want to hear to get them back to the fold, or did we tell them what they wanted to hear and lose credibility?
CDC lost a lot of senior scientific leadership in 2017, and Redfield did little to stop the exodus. Administration attempts to silence people like Messonnier, sideline Birx and Fauci, and promote untenable/questionable therapies and concepts also undermined both the CDC and science in general.
A LOT of this comes back to inadequate communication. My folks (scientists) overall failed to communicate convincingly with the public and were overwhelmed by opposing narratives that minimized science in favor of ideology. I was and remain guilty. This pandemic shifted me back into science mode, rather than clinical mode. In a clinical setting, I've always done pretty well at explaining and answering questions, but this time I've found myself answering questions in a manner that's somewhat put-offish, because I'm citing research a lot of folks can't or don't want to read, and I'm viewed as elitist because I do read the material. Were I to slow down and explain more completely, perhaps I'd have made a difference. In my organization, my explanations have to go through a copy editor before it goes to the humans.
Early on, we knew little about how immunity conferred by infection would stand to this virus. It was a new and novel virus, and a beta coronavirus, as well. Based solely on history, we could expect a short-lived immunity that might neutralize, or might moderate symptoms and severity. We actually saw much higher response in terms of neutralization for the mRNA vaccines, at a level that left many of us looking for answers as to "why is it so good?!"
Caution requires not racing to conclusions based on "prior knowledge". One of our sayings in this business is, when you've seen one pandemic, you've seen one pandemic. In other words, because naturally-conferred immunity might work for one virus, and might have long duration, it doesn't mean it'll work for another,
Another issue: Immunity conferred by infection by ancestral strains, eg, WU-1, Alpha, Beta, even Delta, provides almost no immunity to infection, severe disease or death if that's your sole source of immune response, when Omicron is concerned. One of Omicron's claims to fame is is evasion of prior rendered immunity. It's much more capable of evading ancestral-derived infection-conferred immunity than earlier variants were.
Finally, the duration of the primary immune response (neutralizing antibodies) has been seen as highly variable in the overall population. And, early, there was little discerned by lab studies that were reproducible, about cellular immunity imprinting and training. These data are starting to become more clear, and it appears B cell response to the variants, at least from vaccination, is pretty robust. Similarly, CD-4+ T-cell response appears better and less subject to the dreaded "Antigenic Original Sin", a misnomer, which really represents the immune system working properly.
CDC did recognize the potential for infection-conferred immune response fairly early. That said, I'm reasonably certain I was infected in JAN 2020, but a qualitative antibody assay 6 weeks post-event failed to show any positive response. And, if I was, indeed, infected in January, it failed to prevent a documented infection in June/July.
Overall, CDC, and others have recognized a hybrid response, infection-conferred immune response as well as vaccine-conferred immunity, as the best solution.
The early studies out of Israel showed the benefits of a hybrid response. It also makes sense when you consider that infection theoretically results in a response to the entire virus, or at least to those sites that are exposed, while the response to the vaccine is focused on the spike protein. Wouldn’t you think that a multi-valent mRNA vaccine that incorporated elements of the nucleocapsid protein, along with spike, wouid be advantageous?
Going for the spike was the easy target with the highest probability of success, which was achieved. If you can find it, I've commented before that we'll eventually have to address other sites than spike and RBD for eventual success. There are new vaccines based on other technologies than mRNA which look for the capsid protein.
One other thought: Early studies out of Israel had results that were often seen as too solid to be true, and we were already gun-shy following the hydroxychloroquin scandal in France. Further, Israel had only one vaccine (Pfizer) while we were looking at a broader choice. Finally, we've seen differences in different countries with regard to effectiveness against different VOCs.
IgM is the initial response while IgG is initiated when first exposure occurs. Later, B cells will reinitiate IgG secretion specific for the agent (SARS-CoV-2 in this case) at issue. IgG can be detected for some period but will decrease if no stimulus remains. It's possible, in the lab, to initiate B-cell response to a stimulus which would release IgG for assay.
The 2019 flu season was hallmarked by both poor guesses for the strains involved and a predominant type-A strain that was poorly covered by the A vaccine. Doing this from memory. I'm off for 2 weeks of remote work tomorrow morning.
The variables involved actually favor WU-1 over influenza. I'm disinclined to go into the details but understand that I was in a hotel in Boston, although not the same hotel where some 500 participants acquired an atypical viral pneumonia of unknown etiology. I was still venturing out into the community unmasked at that point (as were we all) but I'm convinced we already had community circulation of COVID on a much broader scale than appreciated. And I was effectively vaccinated for influenza, and had recently received a booster of the quadravalent flu vaccine after discussion with my primary care doc.
IgG assays were non-specific, although they were trying to assign some significance in early March 2020. Since my symptoms were very mild, the IgG level could have remained low. I'll note that, despite the finding of no elevation of antibodies (and they would have identified only IgG in the test performed by Labcorp at the time) there was no mechanism to determine if they were specific for COVID at the time.
Following my infection in late June, I was enticed to become a high-titre plasma donor. My quantitative titers remained markedly elevated for over 4 months. This is consistent with reactivation of the cellular immune system. And, on reflection months later, my PCP was of the opinion I had, indeed, been an early case.
It is impossible to rule out influenza, or another CoV. However too many things were going on to rule out COVID, either.
No disagreement with anything you are saying - it's pretty much herding cats in terms of getting the nation on the same page w/respect to Covid.
I did chuckle out loud reading this: "I think our leadership is bowing to pressure from the public."
The antithesis of leadership? Who is leading who? :-)
This notion of telling the public what they want to hear has led to a loss of institutional credibility when we need it most.
Chicken/egg problem: Did we lose credibility and then started telling 'em what they want to hear to get them back to the fold, or did we tell them what they wanted to hear and lose credibility?
CDC lost a lot of senior scientific leadership in 2017, and Redfield did little to stop the exodus. Administration attempts to silence people like Messonnier, sideline Birx and Fauci, and promote untenable/questionable therapies and concepts also undermined both the CDC and science in general.
Good questions.
Regardless what the motivations and rationale were at the time, the result was lost institutional credibility when the truth was uncovered.
Whether that truth fit one's narrative about the pandemic is another discussion.
A LOT of this comes back to inadequate communication. My folks (scientists) overall failed to communicate convincingly with the public and were overwhelmed by opposing narratives that minimized science in favor of ideology. I was and remain guilty. This pandemic shifted me back into science mode, rather than clinical mode. In a clinical setting, I've always done pretty well at explaining and answering questions, but this time I've found myself answering questions in a manner that's somewhat put-offish, because I'm citing research a lot of folks can't or don't want to read, and I'm viewed as elitist because I do read the material. Were I to slow down and explain more completely, perhaps I'd have made a difference. In my organization, my explanations have to go through a copy editor before it goes to the humans.
As did the refusal of the CDC to acknowledge immunity developed from infection - they totally ignored it
Early on, we knew little about how immunity conferred by infection would stand to this virus. It was a new and novel virus, and a beta coronavirus, as well. Based solely on history, we could expect a short-lived immunity that might neutralize, or might moderate symptoms and severity. We actually saw much higher response in terms of neutralization for the mRNA vaccines, at a level that left many of us looking for answers as to "why is it so good?!"
Caution requires not racing to conclusions based on "prior knowledge". One of our sayings in this business is, when you've seen one pandemic, you've seen one pandemic. In other words, because naturally-conferred immunity might work for one virus, and might have long duration, it doesn't mean it'll work for another,
Another issue: Immunity conferred by infection by ancestral strains, eg, WU-1, Alpha, Beta, even Delta, provides almost no immunity to infection, severe disease or death if that's your sole source of immune response, when Omicron is concerned. One of Omicron's claims to fame is is evasion of prior rendered immunity. It's much more capable of evading ancestral-derived infection-conferred immunity than earlier variants were.
Finally, the duration of the primary immune response (neutralizing antibodies) has been seen as highly variable in the overall population. And, early, there was little discerned by lab studies that were reproducible, about cellular immunity imprinting and training. These data are starting to become more clear, and it appears B cell response to the variants, at least from vaccination, is pretty robust. Similarly, CD-4+ T-cell response appears better and less subject to the dreaded "Antigenic Original Sin", a misnomer, which really represents the immune system working properly.
CDC did recognize the potential for infection-conferred immune response fairly early. That said, I'm reasonably certain I was infected in JAN 2020, but a qualitative antibody assay 6 weeks post-event failed to show any positive response. And, if I was, indeed, infected in January, it failed to prevent a documented infection in June/July.
Overall, CDC, and others have recognized a hybrid response, infection-conferred immune response as well as vaccine-conferred immunity, as the best solution.
The early studies out of Israel showed the benefits of a hybrid response. It also makes sense when you consider that infection theoretically results in a response to the entire virus, or at least to those sites that are exposed, while the response to the vaccine is focused on the spike protein. Wouldn’t you think that a multi-valent mRNA vaccine that incorporated elements of the nucleocapsid protein, along with spike, wouid be advantageous?
Going for the spike was the easy target with the highest probability of success, which was achieved. If you can find it, I've commented before that we'll eventually have to address other sites than spike and RBD for eventual success. There are new vaccines based on other technologies than mRNA which look for the capsid protein.
One other thought: Early studies out of Israel had results that were often seen as too solid to be true, and we were already gun-shy following the hydroxychloroquin scandal in France. Further, Israel had only one vaccine (Pfizer) while we were looking at a broader choice. Finally, we've seen differences in different countries with regard to effectiveness against different VOCs.
IgM is the initial response while IgG is initiated when first exposure occurs. Later, B cells will reinitiate IgG secretion specific for the agent (SARS-CoV-2 in this case) at issue. IgG can be detected for some period but will decrease if no stimulus remains. It's possible, in the lab, to initiate B-cell response to a stimulus which would release IgG for assay.
The 2019 flu season was hallmarked by both poor guesses for the strains involved and a predominant type-A strain that was poorly covered by the A vaccine. Doing this from memory. I'm off for 2 weeks of remote work tomorrow morning.
The variables involved actually favor WU-1 over influenza. I'm disinclined to go into the details but understand that I was in a hotel in Boston, although not the same hotel where some 500 participants acquired an atypical viral pneumonia of unknown etiology. I was still venturing out into the community unmasked at that point (as were we all) but I'm convinced we already had community circulation of COVID on a much broader scale than appreciated. And I was effectively vaccinated for influenza, and had recently received a booster of the quadravalent flu vaccine after discussion with my primary care doc.
IgG assays were non-specific, although they were trying to assign some significance in early March 2020. Since my symptoms were very mild, the IgG level could have remained low. I'll note that, despite the finding of no elevation of antibodies (and they would have identified only IgG in the test performed by Labcorp at the time) there was no mechanism to determine if they were specific for COVID at the time.
Following my infection in late June, I was enticed to become a high-titre plasma donor. My quantitative titers remained markedly elevated for over 4 months. This is consistent with reactivation of the cellular immune system. And, on reflection months later, my PCP was of the opinion I had, indeed, been an early case.
It is impossible to rule out influenza, or another CoV. However too many things were going on to rule out COVID, either.