[2006alum]

New research is debunking several popular fictions that have been roaming around the net for the past month or two:

The notion that "many people had it this past winter, and it was circulating widely on the West Coast long before January":
[tweet]https://twitter.com/SFGate/status/1263254435913822208?s=20[/tweet]

The notion that "we are close to herd immunity in the harder hit regions of the world":
[tweet]https://twitter.com/K_G_Andersen/status/1263246859054641152?s=20[/tweet]

That Sweden's herd immunity strategy is about to pay off:
[tweet]https://twitter.com/CT_Bergstrom/status/1263242035680559105?s=20[/tweet]

That the extent of the government-imposed lockdown in Western developed countries significantly alters the economic outcome:
[tweet]https://twitter.com/living_sweden/status/1263472607397064705?s=20[/tweet]

That's the bad news. The good news, and the main thing that gives me cause for hope is that it does appear that SARS-COV-2 does not transmit as easily on surfaces as initially speculated, and that super-spreader events of large people in closed spaces seems to the primary cause of transmission. This suggests that if most people wear masks and limit their exposure to crowded or confined spaces, we may be able to keep the R0 to <1 at least through the end of the summer. 

This is good news in part because I've completely given up hope on our governments' (plural) ability to effectively test, trace, track and isolate. America is just too much of a non-conformist, decentralized libertarian mess to get the necessary government services up and running and a population compliant enough to follow orders.

[2006alum]

New research is debunking several popular fictions that have been roaming around the net for the past month or two:

The notion that "many people had it this past winter, and it was circulating widely on the West Coast long before January":
[tweet]https://twitter.com/SFGate/status/1263254435913822208?s=20[/tweet]

The notion that "we are close to herd immunity in the harder hit regions of the world":
[tweet]https://twitter.com/K_G_Andersen/status/1263246859054641152?s=20[/tweet]

That Sweden's herd immunity strategy is about to pay off:
[tweet]https://twitter.com/CT_Bergstrom/status/1263242035680559105?s=20[/tweet]

That the extent of the government-imposed lockdown in Western developed countries significantly alters the economic outcome:
[tweet]https://twitter.com/living_sweden/status/1263472607397064705?s=20[/tweet]

That's the bad news. The good news, and the main thing that gives me cause for hope is that it does appear that SARS-COV-2 does not transmit as easily on surfaces as initially speculated, and that super-spreader events of large people in closed spaces seems to the primary cause of transmission. This suggests that if most people wear masks and limit their exposure to crowded or confined spaces, we may be able to keep the R0 to <1 at least through the end of the summer. 

This is good news in part because I've completely given up hope on our governments' (plural) ability to effectively test, trace, track and isolate. America is just too much of a non-conformist, decentralized libertarian mess to get the necessary government services up and running and a population compliant enough to follow orders.

[M T]

As for the "new Stanford study" of 1700 throat swabs is that they had other samples that didn't show any COVID until (IIRC) the second week of February, and then but a single case that week.

Yet, two (non-traveling) people died of COVID-19, on Feb. 6 and Feb 17.

It is tough to prove a negative.

[M T]

As for the "new Stanford study" of 1700 throat swabs is that they had other samples that didn't show any COVID until (IIRC) the second week of February, and then but a single case that week.

Yet, two (non-traveling) people died of COVID-19, on Feb. 6 and Feb 17.

It is tough to prove a negative.

[2006alum]

As for the "new Stanford study" of 1700 throat swabs is that they had other samples that didn't show any COVID until (IIRC) the second week of February, and then but a single case that week.

Yet, two (non-traveling) people died of COVID-19, on Feb. 6 and Feb 17.

It is tough to prove a negative.

True, but the fact that none of the 1,700 throat swabs of patients with flu-like symptoms in November and December came back positive for COVID-19 suggests that, at a minimum, it was not widely spreading prior to January, which would also be consistent with the first death coming on Feb. 6. 

As I said, all this debunks is the notion that it was widely circulating at the end of 2019, not that there no cases of it in January 2020.

[2006alum]

As for the "new Stanford study" of 1700 throat swabs is that they had other samples that didn't show any COVID until (IIRC) the second week of February, and then but a single case that week.

Yet, two (non-traveling) people died of COVID-19, on Feb. 6 and Feb 17.

It is tough to prove a negative.

True, but the fact that none of the 1,700 throat swabs of patients with flu-like symptoms in November and December came back positive for COVID-19 suggests that, at a minimum, it was not widely spreading prior to January, which would also be consistent with the first death coming on Feb. 6. 

As I said, all this debunks is the notion that it was widely circulating at the end of 2019, not that there no cases of it in January 2020.

[M T]

....and that super-spreader events of large people in closed spaces seems to the primary cause of transmission.

Do you know of any study or other evidence that indicates super-spreader events seem to be "the primary cause of transmission"?

To me, it feels like gun violence.  The mass shootings get all the press but "Regardless of the definition being used, fatalities in mass shooting incidents in the U.S. account for a small fraction of all gun murders that occur nationwide each year." (source)

I'm a little leery of chaining multiple infections from any particular event.  If Joe infects 30 people by a super-spreading event, should we account a subsequent 50 household infections to him, or to the person who infected Joe, or to household infections?

Since I have a different sense of this, I'd appreciate finding numbers behind what apparently is your sense.  Maybe I've missed this research and you've seen it.

[M T]

....and that super-spreader events of large people in closed spaces seems to the primary cause of transmission.

Do you know of any study or other evidence that indicates super-spreader events seem to be "the primary cause of transmission"?

To me, it feels like gun violence.  The mass shootings get all the press but "Regardless of the definition being used, fatalities in mass shooting incidents in the U.S. account for a small fraction of all gun murders that occur nationwide each year." (source)

I'm a little leery of chaining multiple infections from any particular event.  If Joe infects 30 people by a super-spreading event, should we account a subsequent 50 household infections to him, or to the person who infected Joe, or to household infections?

Since I have a different sense of this, I'd appreciate finding numbers behind what apparently is your sense.  Maybe I've missed this research and you've seen it.

[2006alum]

This is probably the best recent read I've seen on this:

[tweet]https://twitter.com/kakape/status/1262863846387134470?s=20[/tweet]

That’s why in addition to R, scientists use a value called the dispersion factor (k), which describes how much a disease clusters. The lower k is, the more transmission comes from a small number of people. In a seminal 2005 Nature paper, Lloyd-Smith and co-authors estimated that SARS—in which superspreading played a major role—had a k of 0.16. The estimated k for MERS, which emerged in 2012, is about 0.25. In the flu pandemic of 1918, in contrast, the value was about one, indicating that clusters played less of a role.

Estimates of k for SARS-CoV-2 vary. In January, Julien Riou and Christian Althaus at the University of Bern simulated the epidemic in China for different combinations of R and k and compared the outcomes with what had actually taken place. They concluded that k for COVID-19 is somewhat higher than for SARS and MERS. That seems about right, says Gabriel Leung, a modeler at the University of Hong Kong. “I don’t think this is quite like SARS or MERS, where we observed very large superspreading clusters,” Leung says. “But we are certainly seeing a lot of concentrated clusters where a small proportion of people are responsible for a large proportion of infections.” But in a recent preprint, Adam Kucharski of LSHTM estimated that k for COVID-19 is as low as 0.1. “Probably about 10% of cases lead to 80% of the spread,” Kucharski says.

That could explain some puzzling aspects of this pandemic, including why the virus did not take off around the world sooner after it emerged in China, and why some very early cases elsewhere—such as one in France in late December 2019, reported on 3 May—apparently failed to ignite a wider outbreak. If k is really 0.1, then most chains of infection die out by themselves and SARS-CoV-2 needs to be introduced undetected into a new country at least four times to have an even chance of establishing itself, Kucharski says. If the Chinese epidemic was a big fire that sent sparks flying around the world, most of the sparks simply fizzled out.

There's still a lot we don't know about COVID-19, obviously, but my guess is that the reason why we aren't seeing a brobdingnagian increase in COVID-19 cases as lockdowns are lifted is that the likely superspreader activities - crowded classrooms, open floor plan offices, choir practices, church services, movie theaters, sit-down restaurants, and dense mass transit - haven't resumed anywhere near to normal yet.

This is an entirely educated guess, but I am coming to the view that if we wear masks, avoid staying in crowded or confined spaces for more than a moment or two, and try to socialize outdoors as much as possible (easier to do in the summer, obviously), then we can keep the virus transmission low while being able to do ~70% of our normal activities. I'll be avoiding all of the above for the foreseeable future, but I increasingly think that picnics, outdoor exercise, counter take-away food service, and short-term visits to stores are all fairly low risk provided people keep a safe distance and don't linger near one another.

Of course, that's not going to save the restaurant industry, the commercial real estate industry, theme parks, movie theaters, or public transit systems. But it does give me hope that we can find a balance between "reopen everything" and "lockdown for 18 months."

[2006alum]

This is probably the best recent read I've seen on this:

[tweet]https://twitter.com/kakape/status/1262863846387134470?s=20[/tweet]

That’s why in addition to R, scientists use a value called the dispersion factor (k), which describes how much a disease clusters. The lower k is, the more transmission comes from a small number of people. In a seminal 2005 Nature paper, Lloyd-Smith and co-authors estimated that SARS—in which superspreading played a major role—had a k of 0.16. The estimated k for MERS, which emerged in 2012, is about 0.25. In the flu pandemic of 1918, in contrast, the value was about one, indicating that clusters played less of a role.

Estimates of k for SARS-CoV-2 vary. In January, Julien Riou and Christian Althaus at the University of Bern simulated the epidemic in China for different combinations of R and k and compared the outcomes with what had actually taken place. They concluded that k for COVID-19 is somewhat higher than for SARS and MERS. That seems about right, says Gabriel Leung, a modeler at the University of Hong Kong. “I don’t think this is quite like SARS or MERS, where we observed very large superspreading clusters,” Leung says. “But we are certainly seeing a lot of concentrated clusters where a small proportion of people are responsible for a large proportion of infections.” But in a recent preprint, Adam Kucharski of LSHTM estimated that k for COVID-19 is as low as 0.1. “Probably about 10% of cases lead to 80% of the spread,” Kucharski says.

That could explain some puzzling aspects of this pandemic, including why the virus did not take off around the world sooner after it emerged in China, and why some very early cases elsewhere—such as one in France in late December 2019, reported on 3 May—apparently failed to ignite a wider outbreak. If k is really 0.1, then most chains of infection die out by themselves and SARS-CoV-2 needs to be introduced undetected into a new country at least four times to have an even chance of establishing itself, Kucharski says. If the Chinese epidemic was a big fire that sent sparks flying around the world, most of the sparks simply fizzled out.

There's still a lot we don't know about COVID-19, obviously, but my guess is that the reason why we aren't seeing a brobdingnagian increase in COVID-19 cases as lockdowns are lifted is that the likely superspreader activities - crowded classrooms, open floor plan offices, choir practices, church services, movie theaters, sit-down restaurants, and dense mass transit - haven't resumed anywhere near to normal yet.

This is an entirely educated guess, but I am coming to the view that if we wear masks, avoid staying in crowded or confined spaces for more than a moment or two, and try to socialize outdoors as much as possible (easier to do in the summer, obviously), then we can keep the virus transmission low while being able to do ~70% of our normal activities. I'll be avoiding all of the above for the foreseeable future, but I increasingly think that picnics, outdoor exercise, counter take-away food service, and short-term visits to stores are all fairly low risk provided people keep a safe distance and don't linger near one another.

Of course, that's not going to save the restaurant industry, the commercial real estate industry, theme parks, movie theaters, or public transit systems. But it does give me hope that we can find a balance between "reopen everything" and "lockdown for 18 months."