Over pretty much the last year you could observe, in different countries all around the world, that the reproduction number was 'magically' floating around 1.
Only recently did I learn that this effect was puzzling for epidemiologists as well and was only solved around 2012 (?) in a model that assumes a network of information about the disease in parallel to the network of disease transmission. The resulting feedback loops lead to the meta-stability of R=1. Super interesting how society acts as this distributed information processor, similar to 'the market' in economics.
You can almost see the phenomenon in real time during this pandemic. Countries that have low trust in authorities will still freak out when the epidemic hits biblical proportions, and do various forms of impromptu distancing measures which will bring the R number down. Then when the signs of panic subside, they'll loosen them. And so on.
Societies with high trust in authorities will still pressure their authorities to loosen up when things feel safe, with predictible results, leading to further lockdowns.
Then all of this will come back in the future and kick you in the teeth. Either we're going to have to accept this as a way of life, which is more detrimental. Or we're pushing off the inevitable.
This was uncertain to most people last year, but now we’ve seen so many examples that it really shouldn’t be so controversial any longer. But if it wasn’t, we wouldn’t be discussing it.
The covid virus is evolved to fit exactly into the niche of societal behavior where it will be a big fucking problem but not so bad that it’s immediately obvious to enough people.
Influenza is pretty promiscuous. In normal conditions, very few people aren't exposed to it: either their existing immune resistance (vaccinated or otherwise) is up to the job, or it isn't.
Mutation is therefore the primary driver of flu, year upon year. This is why vaccines are continually reformulated for a best-guess at what strains are going to be dominant.
We had just concluded a northern-hemisphere flu season when travel restrictions started to kick in. This was followed by at least a 90% reduction in international travel, and for most of what remained, it was mandated that new arrivals isolate for long enough to eliminate any influenza they might have carried.
Lockdowns would mean less mutation to begin with, since it happens in human hosts. And such mutations as did present are going to have a tough time jumping oceans, and even when they do arrive, spreading through the populace is substantially inhibited.
Ironically, the universal mask mandates are likely to be more effective against flu than against COVID. Like it or not, masking has minimal effect on spreading aerosols, although using a "real" mask, and being pretty careful to wear it right, can mitigate inhaling those aerosols.
Influenza is believed to be spreadable through aerosols, but the primary vector is droplets, while the opposite appears to be true for SARS2. Bog-standard cloth masks are fairly good at keeping droplets off people and surfaces.
https://www.pennmedicine.org/updates/blogs/penn-physician-bl...
> The principal mode by which people are infected with SARS-CoV-2 (the virus that causes COVID-19) is through exposure to respiratory droplets carrying infectious virus.
https://www.cdc.gov/coronavirus/2019-ncov/science/science-br...
From what I can tell, you may have your flu/covid mixed up. Covid is spread through respiratory droplets, the spread of which is reduced by wearing a mask.
The claim that "lack of infection spread in hospital settings" rules out airborne transmission due to masking is also questionable. The opposite seems true. As I understand it, infections in hospital settings have been routinely documented throughout the pandemic despite masking, contact protocols, etc. - which implicates airborne rather than droplet/fomite transmission.
This is a really good article in the Lancet recently which solidified my opinion on this. It offers 10 items of evidence for airborne transmission being the primary driver of the pandemic.
https://www.thelancet.com/journals/lancet/article/PIIS0140-6...
For me, the key points are:
> Second, long-range transmission of SARS-CoV-2 between people in adjacent rooms but never in each other's presence has been documented in quarantine hotels.7
> Sixth, viable SARS-CoV-2 has been detected in the air. In laboratory experiments, SARS-CoV-2 stayed infectious in the air for up to 3 h with a half-life of 1·1 h.12 Viable SARS-CoV-2 was identified in air samples from rooms occupied by COVID-19 patients in the absence of aerosol-generating health-care procedures13 and in air samples from an infected person's car.14 Although other studies have failed to capture viable SARS-CoV-2 in air samples, this is to be expected. Sampling of airborne virus is technically challenging for several reasons, including limited effectiveness of some sampling methods for collecting fine particles, viral dehydration during collection, viral damage due to impact forces (leading to loss of viability), reaerosolisation of virus during collection, and viral retention in the sampling equipment.3 Measles and tuberculosis, two primarily airborne diseases, have never been cultivated from room air.15
> Seventh, SARS-CoV-2 has been identified in air filters and building ducts in hospitals with COVID-19 patients; such locations could be reached only by aerosols.16
> Eighth, studies involving infected caged animals that were connected to separately caged uninfected animals via an air duct have shown transmission of SARS-CoV-2 that can be adequately explained only by aerosols.17
> Tenth, there is limited evidence to support other dominant routes of transmission—ie, respiratory droplet or fomite.9, 24 Ease of infection between people in close proximity to each other has been cited as proof of respiratory droplet transmission of SARS-CoV-2. However, close-proximity transmission in most cases along with distant infection for a few when sharing air is more likely to be explained by dilution of exhaled aerosols with distance from an infected person.9 The flawed assumption that transmission through close proximity implies large respiratory droplets or fomites was historically used for decades to deny the airborne transmission of tuberculosis and measles.
At exactly one, it's indeterminate; you could see a subexponential growth or decay. With no exponential terms remaining, lower-order terms that are ordinarily hidden by exponential growth become the dominant observables. (Since epidemic spread is also random, you're much more likely to see the stochastic terms show up in the overall statistics in these cases. You really can be lucky or unlucky with Rt ~= 1, but there's no persistent luck with Rt >> 1.)
This is also important before community spreading sets in, and it is the mechanism by which contact tracing can work. Rather than change the general susceptibility of the population to the disease (changing the effective reproduction number), contact tracing tries to operate at the level of individual cases in ways that cannot be scaled to uncontrolled community spreading (even if Rt is close to 1).
> and the border closures kept mutations from traveling: and influenza is notoriously mutation-prone.
Perhaps, but are influenza mutations an important effect within a single flu season? I know the determination of to-be-dominant strains has a great effect on the composition of each season's flu vaccine, but as far as I am aware we don't see declining flu vaccine efficacy over a season.