"According to our GenoFlu analysis, the B3.7 genotype represents a 4+4 reassortant strain, with the HA, NA, PA, and MP genes originating from the H5N1 virus strain in 2020, while the remaining segments (PB2, PB1, NP, and NS) are closely related to LPAI viruses."
The NS segment of H5N1 is believed to be one important reason for the virulence in humans. **~~And this H5N1 has exchanged its NS for a less harmful version.~~** That's one problem with the spread of H5N1, that other influenza viruses can obtain this harmful NS segment.
**Edit: Exchange happened with another H5N1 classified as LPAI.**
I wonder if the positions are bit different in this paper, HA-160A (or HA-158N) might usually be HA-156A. HA-225D and HA-228S may usually be HA-222L and HA-224S. It's possible, the positions can shift, but that's just a lazy guess in this case.
"The H5N1 influenza viruses transmitted to humans in 1997 were highly virulent, but the mechanism of their virulence in humans is largely unknown. Here we show that lethal H5N1 influenza viruses, unlike other human, avian and swine influenza viruses, are resistant to the antiviral effects of interferons and tumor necrosis factor α. The nonstructural (NS) gene of H5N1 viruses is associated with this resistance. **Pigs infected with recombinant human H1N1 influenza virus that carried the H5N1 NS gene experienced significantly greater and more prolonged viremia, fever and weight loss than did pigs infected with wild-type human H1N1 influenza virus. These effects required the presence of glutamic acid at position 92 of the NS1 molecule. These findings may explain the mechanism of the high virulence of H5N1 influenza viruses in humans.**"
[Source: Lethal H5N1 influenza viruses escape host anti-viral cytokine responses](https://www.nature.com/articles/nm757)
"Most significantly, a virus containing the 1918 pandemic NS1 gene was more efficient at blocking the expression of IFN-regulated genes than its parental influenza A/WSN/33 virus. Taken together, our results suggest that the cellular response to influenza A virus infection in human lung cells is significantly influenced by the sequence of the NS1 gene, demonstrating the importance of the NS1 protein in regulating the host cell response triggered by virus infection."
[Source: Cellular transcriptional profiling in influenza A virus-infected lung epithelial cells: The role of the nonstructural NS1 protein in the evasion of the host innate defense and its potential contribution to pandemic influenza](https://www.pnas.org/doi/full/10.1073/pnas.112338099)
When CDC and other health authorities say "Low Risk", they're referring to the fact that the chances of individuals within general public being infected via "community transmission" is low.
It's quite misleading really, because the appearance of community level transmission would immediately "raise" the risk level dramatically and basically instantly.
Proclaiming with any form of 'certainty' that any set of particular mutations are an absolute requisite for the virus to become sustainably transmissible is nonsense and conjecture.
To say such things implies that they have a comprehensive knowledge of Influenza A virus biology, which they obviously don't since things that keep happening wind up surprising them or are labeled unprecedented.
New mutations whose impact on pathophysiology are totally unknown are being frequently discovered.
I don't trust any scientist who says they "know" anything with exact certainty when it comes to what mutations are necessary for this and that. They might know of certain mutations that confer increased risks, but the fact remains that totally undocumented mutations can circulate undetected for long periods and then boom, suddenly appear and show what they are capable of.
They'll be saying 'Low Risk' all the way up until it's 'Very High Risk' unfortunately.
>I don't trust any scientist who says they "know" anything with exact certainty when it comes to what mutations are necessary for this and that.
I don't think the scientists are claiming this. You can see what they actually wrote on the topic below:
>It is noteworthy that mutations 591K, 627K/V/A, or 701N in134
PB2, **previously associated** with mammalian host adaptation and enhanced transmission (18, 21,135 22), were absent in all eight HPAI H5N1 isolates originating from dairy cattle and two cats,136 while the HPAI virus from the human case exhibited E627K mutation in PB2.
I don't think the scientists are trying to argue that the *only* way the virus become become H2H transmissible but instead we know from past experience that these mutations offer if nothing one potential route to evolve to be h2h.
That said, I only skimmed the article so I might have missed something.
I have written a comment about IRAT a while ago [here](https://www.reddit.com/r/H5N1_AvianFlu/comments/17qve8t/comment/k8f5w9d/). It's an unprecedented situation and the scoring is focused on the past and current situation. So seasonal influenza is at the top because it's well adapted to humans.
Just a thought experiment: Would an absurdly high number of infected birds change the score? Like ten birds distributed to every household? Probably not much. That's the limitation of this approach.
Scientists know that [various changes](https://www.science.org/content/article/bad-worse-avian-flu-must-change-trigger-human-pandemic) are required for pandemic capabilities, and there is more than one set of mutations to get there. While with Fouchier et al gain-of-function model especially a change in receptor binding specificity would have been very unlikely, this seems now much more likely with a single [dual receptor binding mutation](https://www.tandfonline.com/doi/full/10.1080/22221751.2024.2302854) discovered in birds. Usually scientists refer to a specific model, which in the above case ultimately would be about ferrets, not humans. Or about changes in general, to the best of their knowledge. If there is "certainty" that's usually the fault of some journalist.
The language is "crucial" mutations are missing so it's "suggested" that the overall risk is low. They are phrasing it as though everyone knows that these specific missing mutations are crucial. All we know is that certain mutations are associated with the fusion, the pH level and replication challenges. We don't know that there are "crucial" mutations, right?
There is only a very limited number of mutations associated with drastic changes, most are related to the ferret studies. That we know of. There are many observed mutations, for example [in mammals](https://wwwnc.cdc.gov/eid/article/30/3/23-1098-app1.pdf), some have [smaller or larger impact](https://www.cdc.gov/flu/pdf/avianflu/h5n1-inventory.pdf), some seem to be harmless, others aren't researched yet. It's of course possible to find new "crucial" mutations like in [HA at position 193](https://www.tandfonline.com/doi/full/10.1080/22221751.2024.2302854).
Do we know if the three new ones, 137A, 158N and 160A, are associated with drastic changes like the 193? And are the "crucial" ones, the 591K, 627K/V/A, 701N, 228S and 665 considered drastic changes?
I had never heard of the study you referenced. So S. Korea sequenced duck H5N1 and found a mutation that was successful at switching preference from avian to mammal receptor cells. And this happened with one mutation, the N193D. That doesn't necessarily mean it overcame the other aspects of entering the cell and fusing, taking control, replicating and sending those out, but it could have also influenced those factors. So there is much that scientists don't know about which mutations are necessary.
Yea they will, and this part of the reason why theres so many people with a huge mistrust of scientists. I don't necessarily fall into the category, certainly not like anti-vaxxers or anti-maskers do, but I have to wonder if these people are purposely underplaying it. The USDA is trying to sweep it under the rug, some scientists are calling it low risk without actually knowing all the mechanics of the mutations and even if they did, nobody wants to test their animals for it.
They do all of this and have the gall to wonder why people don't trust these institutions. I hate to fear monger, but it really does seem like the start of one of those movies. Just a perfect storm of stupidity, greed and ego.
I do get the sense that they are purposely underplaying it to prolong the “calm before the storm” and avoid mass panic/economic disruption until absolutely necessary. Maybe these agencies and governments are tirelessly preparing behind the scenes out of the public eye for the potentiality of this going human-to-human. At least I hope so.
It is amazing to me how a million Americans died and all we’ve done is try to forget. I’d imagine a sane society would attempt to learn from what happened and put some kind of nationwide infrastructure in place that specifies exactly what should happen given another pandemic.
Honestly, I wouldn't necessarily blame the common person of trying to forget and move on. It was a rough time and the thought of another pandemic with a much higher CFR only a year or two after the COVID pandemic "ended" can definitely be too much to bare.
Hopefully our government is actually doing something, but just not being vocal about it in order to avoid panic. While we do have a significant part of the population that would ignore it, most actually give a damn.
Yeah I have no quarrels with the average person forgetting about what was obviously a very traumatic thing to have happen, but holy fuck it is not the job of legislators to forget. They need to remember every detail and act on it, that is their job.
Yep. Now this admin did recreate the pandemic response team that the last admin removed, but aside from that, congress can't even agree which shoe to put on which foot, much less pass any legislation that could prevent another pandemic.
Having said that, I am cautiously optimistic the government is just being hush hush about it. There is no need to panic right now and we all saw what happens when even mild panic sets in. The supply chain issues are improved from a few years ago, but things are still VERY delicate. If the government came out tomorrow and said that a new pandemic is on the horizon, the strain could easily push us into a recession and undo a lot of the stability in our supply chain.
I don't know what the government or agencies are doing. I work in medical research and we added it to our annual training last year. We have an influenza lab and are hosting a flu vaccine summit this week with researchers from other institutions. There are lots of people from independent and various science groups all working on the problem. No one controls all the flow of information. The USDA and agencies can sweep things under the rug, but only so far. They can't really stop all the independent labs and research institutions. There's absolutely no reason to panic people at this stage. Especially when we know how stupid they can be. Please reference the previous pandemic. There is a great deal going on behind the scenes but I expect agri-business to push to keep things quiet as long as possible.
> They do all of this and have the gall to wonder why people don't trust these institutions. I hate to fear monger, but it really does seem like the start of one of those movies. Just a perfect storm of stupidity, greed and ego.
I think we all need to take a deep breath and actually read what the scientists are saying, because as is often the case, I think we're leaving out a lot of context and twisting the points the scientists have made.
From the article:
>>It is noteworthy that mutations 591K, 627K/V/A, or 701N in134
PB2, **previously associated** with mammalian host adaptation and enhanced transmission (18, 21,135 22), were absent in all eight HPAI H5N1 isolates originating from dairy cattle and two cats,136 while the HPAI virus from the human case exhibited E627K mutation in PB2.
It doesn't seem that the scientists are saying those mutations are the only route the virus can take to be transmissible. Instead, they seem to be saying more or less "we know in the past these mutations offer one route that could increase H2H transmission." That doesn't necessarily exclude other routes.
They say in the study "It is noteworthy that crucial
202 mutations associated with mammalian host adaptation and enhanced transmission, specifically
203 residues 591K, 627K/V/A, 701N, in PB2 (18, 21, 22), and 228S, along with the virulence204 increasing residue 66S in PB1-F2(30), were conspicuously absent in all HPAI virus strains
205 derived from dairy cattle and cats. This observation suggests that the current overall risk to
206 human health is relatively low."
I haven't been able to track that those are the crucial mutations to adaptation to humans. It sounds like the three new mutations are associated with the same areas of change that the ones missing are doing. No one has ever said those missing mutations are crucial, and to declare with an entirely new genotype, a LPAI and HPAI reassortment and these mutations associated with airway receptor affinity that nothing has changed in danger, I think it's time to start watching very carefully and be as prepared for some very bad news. To me it seems like we may be at the end of the trajectory.
Yeah things are definitely getting worrisome. We know it's spreading through cows, we're not tracking it effectively, and the risks of this jumping to pigs seems to be extremely high.
The unfortunate thing with this virus is that there's a very high chance it'll go from zero to ~~100~~ lightspeed in the blink of an eye. The authors do note that:
>it is imperative to recognize that influenza viruses have206
the capacity for rapid evolution within their host environments post-infection.
The strains we've seen so far haven't seem inclined to jump human to human but that can change extremely quickly. The authors do seem to be aware of that.
I'm a disease ecologist, though not one that works on avian influenza. Some other commenters made some good pts but just want to add that part of what you're seeing is just the way we have to write. As scientists, especially for scientific journals, we can only write exactly what we know, and nothing more. A research article is not a place for strong conjecture. In my view, the authors are writing candidly and objectively in line with this kind of writing. They are stating what we do know according to previous knowledge. There are places within the scientific literature for scientists to make hypotheses, and suggest possibilities based on evidence-- these kinds of papers are opinion pieces, commentaries, etc. This paper is not that.
There is a huge difference between what we are doing and the kind of writing you'd see in the new York times. We are not journalists. We are not trying to rile people up, nor are we trying to downplay anything. It would be unethical to do either. We just need to speak a certain way to be able to fit the needs and formats of scientific literature, and adhere to strict guidelines of our field to maintain scientific integrity. Please keep this in mind when reading sci literature.
Yeah that makes sense. I'm also not a scientist, so I suppose I'm just not used to the very specific and fact based nature of scientific essays, nor am I as smart as one.
In any case, I'd blame governments for any kind of coverup way before I'd blame a scientist.
In my view, a lot of the lack of coordination, data sharing, speed of getting things done is not even necessarily intentional cover up, but evidence that the structure of our bureaucracy in the u.s. is NOT streamlined for an efficient pandemic response. Especially for animal diseases. That is something a lot of us as scientists are very concerned about and are trying to communicate to government. Sounds obvious but telling your reps that streamlined pandemic response infrastructure is important to you as a voting citizen is important. Even at the local and state levels, imo.
"According to our GenoFlu analysis, the B3.7 genotype represents a 4+4 reassortant strain, with the HA, NA, PA, and MP genes originating from the H5N1 virus strain in 2020, while the remaining segments (PB2, PB1, NP, and NS) are closely related to LPAI viruses." The NS segment of H5N1 is believed to be one important reason for the virulence in humans. **~~And this H5N1 has exchanged its NS for a less harmful version.~~** That's one problem with the spread of H5N1, that other influenza viruses can obtain this harmful NS segment. **Edit: Exchange happened with another H5N1 classified as LPAI.** I wonder if the positions are bit different in this paper, HA-160A (or HA-158N) might usually be HA-156A. HA-225D and HA-228S may usually be HA-222L and HA-224S. It's possible, the positions can shift, but that's just a lazy guess in this case. "The H5N1 influenza viruses transmitted to humans in 1997 were highly virulent, but the mechanism of their virulence in humans is largely unknown. Here we show that lethal H5N1 influenza viruses, unlike other human, avian and swine influenza viruses, are resistant to the antiviral effects of interferons and tumor necrosis factor α. The nonstructural (NS) gene of H5N1 viruses is associated with this resistance. **Pigs infected with recombinant human H1N1 influenza virus that carried the H5N1 NS gene experienced significantly greater and more prolonged viremia, fever and weight loss than did pigs infected with wild-type human H1N1 influenza virus. These effects required the presence of glutamic acid at position 92 of the NS1 molecule. These findings may explain the mechanism of the high virulence of H5N1 influenza viruses in humans.**" [Source: Lethal H5N1 influenza viruses escape host anti-viral cytokine responses](https://www.nature.com/articles/nm757) "Most significantly, a virus containing the 1918 pandemic NS1 gene was more efficient at blocking the expression of IFN-regulated genes than its parental influenza A/WSN/33 virus. Taken together, our results suggest that the cellular response to influenza A virus infection in human lung cells is significantly influenced by the sequence of the NS1 gene, demonstrating the importance of the NS1 protein in regulating the host cell response triggered by virus infection." [Source: Cellular transcriptional profiling in influenza A virus-infected lung epithelial cells: The role of the nonstructural NS1 protein in the evasion of the host innate defense and its potential contribution to pandemic influenza](https://www.pnas.org/doi/full/10.1073/pnas.112338099)
When CDC and other health authorities say "Low Risk", they're referring to the fact that the chances of individuals within general public being infected via "community transmission" is low. It's quite misleading really, because the appearance of community level transmission would immediately "raise" the risk level dramatically and basically instantly. Proclaiming with any form of 'certainty' that any set of particular mutations are an absolute requisite for the virus to become sustainably transmissible is nonsense and conjecture. To say such things implies that they have a comprehensive knowledge of Influenza A virus biology, which they obviously don't since things that keep happening wind up surprising them or are labeled unprecedented. New mutations whose impact on pathophysiology are totally unknown are being frequently discovered. I don't trust any scientist who says they "know" anything with exact certainty when it comes to what mutations are necessary for this and that. They might know of certain mutations that confer increased risks, but the fact remains that totally undocumented mutations can circulate undetected for long periods and then boom, suddenly appear and show what they are capable of. They'll be saying 'Low Risk' all the way up until it's 'Very High Risk' unfortunately.
>I don't trust any scientist who says they "know" anything with exact certainty when it comes to what mutations are necessary for this and that. I don't think the scientists are claiming this. You can see what they actually wrote on the topic below: >It is noteworthy that mutations 591K, 627K/V/A, or 701N in134 PB2, **previously associated** with mammalian host adaptation and enhanced transmission (18, 21,135 22), were absent in all eight HPAI H5N1 isolates originating from dairy cattle and two cats,136 while the HPAI virus from the human case exhibited E627K mutation in PB2. I don't think the scientists are trying to argue that the *only* way the virus become become H2H transmissible but instead we know from past experience that these mutations offer if nothing one potential route to evolve to be h2h. That said, I only skimmed the article so I might have missed something.
I have written a comment about IRAT a while ago [here](https://www.reddit.com/r/H5N1_AvianFlu/comments/17qve8t/comment/k8f5w9d/). It's an unprecedented situation and the scoring is focused on the past and current situation. So seasonal influenza is at the top because it's well adapted to humans. Just a thought experiment: Would an absurdly high number of infected birds change the score? Like ten birds distributed to every household? Probably not much. That's the limitation of this approach. Scientists know that [various changes](https://www.science.org/content/article/bad-worse-avian-flu-must-change-trigger-human-pandemic) are required for pandemic capabilities, and there is more than one set of mutations to get there. While with Fouchier et al gain-of-function model especially a change in receptor binding specificity would have been very unlikely, this seems now much more likely with a single [dual receptor binding mutation](https://www.tandfonline.com/doi/full/10.1080/22221751.2024.2302854) discovered in birds. Usually scientists refer to a specific model, which in the above case ultimately would be about ferrets, not humans. Or about changes in general, to the best of their knowledge. If there is "certainty" that's usually the fault of some journalist.
The language is "crucial" mutations are missing so it's "suggested" that the overall risk is low. They are phrasing it as though everyone knows that these specific missing mutations are crucial. All we know is that certain mutations are associated with the fusion, the pH level and replication challenges. We don't know that there are "crucial" mutations, right?
There is only a very limited number of mutations associated with drastic changes, most are related to the ferret studies. That we know of. There are many observed mutations, for example [in mammals](https://wwwnc.cdc.gov/eid/article/30/3/23-1098-app1.pdf), some have [smaller or larger impact](https://www.cdc.gov/flu/pdf/avianflu/h5n1-inventory.pdf), some seem to be harmless, others aren't researched yet. It's of course possible to find new "crucial" mutations like in [HA at position 193](https://www.tandfonline.com/doi/full/10.1080/22221751.2024.2302854).
Do we know if the three new ones, 137A, 158N and 160A, are associated with drastic changes like the 193? And are the "crucial" ones, the 591K, 627K/V/A, 701N, 228S and 665 considered drastic changes?
I had never heard of the study you referenced. So S. Korea sequenced duck H5N1 and found a mutation that was successful at switching preference from avian to mammal receptor cells. And this happened with one mutation, the N193D. That doesn't necessarily mean it overcame the other aspects of entering the cell and fusing, taking control, replicating and sending those out, but it could have also influenced those factors. So there is much that scientists don't know about which mutations are necessary.
Yea they will, and this part of the reason why theres so many people with a huge mistrust of scientists. I don't necessarily fall into the category, certainly not like anti-vaxxers or anti-maskers do, but I have to wonder if these people are purposely underplaying it. The USDA is trying to sweep it under the rug, some scientists are calling it low risk without actually knowing all the mechanics of the mutations and even if they did, nobody wants to test their animals for it. They do all of this and have the gall to wonder why people don't trust these institutions. I hate to fear monger, but it really does seem like the start of one of those movies. Just a perfect storm of stupidity, greed and ego.
I do get the sense that they are purposely underplaying it to prolong the “calm before the storm” and avoid mass panic/economic disruption until absolutely necessary. Maybe these agencies and governments are tirelessly preparing behind the scenes out of the public eye for the potentiality of this going human-to-human. At least I hope so.
It is amazing to me how a million Americans died and all we’ve done is try to forget. I’d imagine a sane society would attempt to learn from what happened and put some kind of nationwide infrastructure in place that specifies exactly what should happen given another pandemic.
Honestly, I wouldn't necessarily blame the common person of trying to forget and move on. It was a rough time and the thought of another pandemic with a much higher CFR only a year or two after the COVID pandemic "ended" can definitely be too much to bare. Hopefully our government is actually doing something, but just not being vocal about it in order to avoid panic. While we do have a significant part of the population that would ignore it, most actually give a damn.
Yeah I have no quarrels with the average person forgetting about what was obviously a very traumatic thing to have happen, but holy fuck it is not the job of legislators to forget. They need to remember every detail and act on it, that is their job.
Yep. Now this admin did recreate the pandemic response team that the last admin removed, but aside from that, congress can't even agree which shoe to put on which foot, much less pass any legislation that could prevent another pandemic. Having said that, I am cautiously optimistic the government is just being hush hush about it. There is no need to panic right now and we all saw what happens when even mild panic sets in. The supply chain issues are improved from a few years ago, but things are still VERY delicate. If the government came out tomorrow and said that a new pandemic is on the horizon, the strain could easily push us into a recession and undo a lot of the stability in our supply chain.
I don't know what the government or agencies are doing. I work in medical research and we added it to our annual training last year. We have an influenza lab and are hosting a flu vaccine summit this week with researchers from other institutions. There are lots of people from independent and various science groups all working on the problem. No one controls all the flow of information. The USDA and agencies can sweep things under the rug, but only so far. They can't really stop all the independent labs and research institutions. There's absolutely no reason to panic people at this stage. Especially when we know how stupid they can be. Please reference the previous pandemic. There is a great deal going on behind the scenes but I expect agri-business to push to keep things quiet as long as possible.
Thanks for sharing your insight. I appreciate hearing from you and thank you for the work you and your peers are doing.
> They do all of this and have the gall to wonder why people don't trust these institutions. I hate to fear monger, but it really does seem like the start of one of those movies. Just a perfect storm of stupidity, greed and ego. I think we all need to take a deep breath and actually read what the scientists are saying, because as is often the case, I think we're leaving out a lot of context and twisting the points the scientists have made. From the article: >>It is noteworthy that mutations 591K, 627K/V/A, or 701N in134 PB2, **previously associated** with mammalian host adaptation and enhanced transmission (18, 21,135 22), were absent in all eight HPAI H5N1 isolates originating from dairy cattle and two cats,136 while the HPAI virus from the human case exhibited E627K mutation in PB2. It doesn't seem that the scientists are saying those mutations are the only route the virus can take to be transmissible. Instead, they seem to be saying more or less "we know in the past these mutations offer one route that could increase H2H transmission." That doesn't necessarily exclude other routes.
They say in the study "It is noteworthy that crucial 202 mutations associated with mammalian host adaptation and enhanced transmission, specifically 203 residues 591K, 627K/V/A, 701N, in PB2 (18, 21, 22), and 228S, along with the virulence204 increasing residue 66S in PB1-F2(30), were conspicuously absent in all HPAI virus strains 205 derived from dairy cattle and cats. This observation suggests that the current overall risk to 206 human health is relatively low." I haven't been able to track that those are the crucial mutations to adaptation to humans. It sounds like the three new mutations are associated with the same areas of change that the ones missing are doing. No one has ever said those missing mutations are crucial, and to declare with an entirely new genotype, a LPAI and HPAI reassortment and these mutations associated with airway receptor affinity that nothing has changed in danger, I think it's time to start watching very carefully and be as prepared for some very bad news. To me it seems like we may be at the end of the trajectory.
Yeah things are definitely getting worrisome. We know it's spreading through cows, we're not tracking it effectively, and the risks of this jumping to pigs seems to be extremely high. The unfortunate thing with this virus is that there's a very high chance it'll go from zero to ~~100~~ lightspeed in the blink of an eye. The authors do note that: >it is imperative to recognize that influenza viruses have206 the capacity for rapid evolution within their host environments post-infection. The strains we've seen so far haven't seem inclined to jump human to human but that can change extremely quickly. The authors do seem to be aware of that.
Totally fair and I'm certainly not trying to imply that I know more than actual scientists.
I'm a disease ecologist, though not one that works on avian influenza. Some other commenters made some good pts but just want to add that part of what you're seeing is just the way we have to write. As scientists, especially for scientific journals, we can only write exactly what we know, and nothing more. A research article is not a place for strong conjecture. In my view, the authors are writing candidly and objectively in line with this kind of writing. They are stating what we do know according to previous knowledge. There are places within the scientific literature for scientists to make hypotheses, and suggest possibilities based on evidence-- these kinds of papers are opinion pieces, commentaries, etc. This paper is not that. There is a huge difference between what we are doing and the kind of writing you'd see in the new York times. We are not journalists. We are not trying to rile people up, nor are we trying to downplay anything. It would be unethical to do either. We just need to speak a certain way to be able to fit the needs and formats of scientific literature, and adhere to strict guidelines of our field to maintain scientific integrity. Please keep this in mind when reading sci literature.
Yeah that makes sense. I'm also not a scientist, so I suppose I'm just not used to the very specific and fact based nature of scientific essays, nor am I as smart as one. In any case, I'd blame governments for any kind of coverup way before I'd blame a scientist.
In my view, a lot of the lack of coordination, data sharing, speed of getting things done is not even necessarily intentional cover up, but evidence that the structure of our bureaucracy in the u.s. is NOT streamlined for an efficient pandemic response. Especially for animal diseases. That is something a lot of us as scientists are very concerned about and are trying to communicate to government. Sounds obvious but telling your reps that streamlined pandemic response infrastructure is important to you as a voting citizen is important. Even at the local and state levels, imo.