I’m looking at the article I posted a couple of days ago: Public health interventions and epidemic intensity during the 1918 influenza pandemic.
I don’t have the bandwidth to read Hatchett et al closely at the moment … but wanted to clarify that their study does not offer a great deal of hope that we could develop herd immunity via more people infected with milder illness, thus fewer deaths. (It’s the study of immunity in Gangelt Municipality that supports herd-immunity-via-lower-viral-dose/lower-death.)
The authors assume the opposite, in fact:
We hypothesized that early implementation of multiple NPIs [nonpharmaceutical interventions, or social distancing] in an immunologically naïve population would slow the progression of the epidemic, resulting in a flatter epidemic curve, but that over time aggregate outcomes would approach those observed in cities not implementing such measures, until roughly comparable levels of herd immunity were achieved.
They conclude that:
Cities in which multiple interventions were implemented at an early phase of the epidemic also showed a trend toward lower cumulative excess mortality, but the difference was smaller (≈20%) and less statistically significant than that for peak death rates. This finding was not unexpected, given that few cities maintained NPIs longer than 6 weeks in 1918. Early implementation of certain interventions, including closure of schools, churches, and theaters, was associated with lower peak death rates, but no single intervention showed an association with improved aggregate outcomes for the 1918 phase of the pandemic. These findings support the hypothesis that rapid implementation of multiple NPIs can significantly reduce influenza transmission, but that viral spread will be renewed upon relaxation of such measures.
On the other hand:
Philadelphia ultimately experienced a peak weekly excess pneumonia and influenza (P&I) death rate of 257/100,000 and a cumulative excess P&I death rate (CEPID) during the period September 8–December 28, 1918 (the study period) of St. Louis, on the other hand, experienced a peak P&I death rate, while NPIs were in place, of 31/100,000 and had a CEPID during the study period of 347/100,000.
719 excess deaths per 100,000 in Philadelphia versus 347 excess deaths per 100,000 in St. Louis
Those figures include deaths from September 8 through December 28, 1918, when the 2nd wave ended. (Most US deaths occurred during that 2nd wave.)
CHART: Excess P&I [pneumonia and influenza] mortality over 1913–1917 baseline in Philadelphia and St. Louis, September 8–December 28, 1918.
One thing to notice: St. Louis’s reward for early lockdown was a second wave of illness, which Philadelphia seems to have missed.
There was a statistically significant inverse correlation of the height of the first and second peaks (Spearman ρ = −0.53, P = 0.03), so that cities that had low peaks during the first wave were at greater risk of a large second wave. Cities that had lower peak mortality rates during the first wave also tended to experience their second waves after a shorter interval of time, ≈6–8 weeks after the first peak vs. 10–14 weeks for cities with higher peak mortality rates (Spearman ρ = −0.84, P < 0.0001). These patterns were also observed in cities that implemented NPIs sooner…. Finally, and this is perhaps the most important observation, no city in our analysis experienced a second wave while its main battery of NPIs was in place. Second waves occurred only after the relaxation of interventions.
Policy makers here in the US don’t seem to be talking about the second-wave issue publicly. Not that I’ve seen, anyway.
Know your enemy
Can lockdown produce herd immunity with fewer deaths?
Social distancing and immunity
gasstationwithoutpumps on viral load and COVID-19 models
Social distancing and the 2nd wave
Viral dose, viral load