samizdat311
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> I felt it go into my skin and watched it suck for a bit, but it didn't get particularly engorged on it. No mark the next day.
So it might follow that with one resistant (R) and one non-resistant person (NR) exposed to a few dozen mosquitoes, NR will end up with lots of visible bites while R will be relatively unscathed - even though the mosquitoes might have sampled them each equally.
I know too that some mammals (e.g. mice) will sample a small amount of food (e.g. rodent poison), and then return later to try more if the food hasn't had ill effects.
I'm not sure that mosquitoes have anything like a memory capacity for this, but maybe something similar mediated via pheromones could be happening. (And something like pheromones could also signal to other mosquitoes that there's good eatin' to be had).
The current dip in the UK is trending toward the former. But it's further complicated by the fact that levels of immunity in the population will continue to oscillate up and down. (Nevermind that once schools open in September, 20% of the population with relatively sparse vaccination will be mixing in large cohorts).
Another factor in herd immunity is vaccine efficacy - which is somewhere between 86% and 95% for the mRNA vaccines (and will continue to change). A herd immunity threshold of 90% presupposes a vaccine with 100% efficacy - when your vaccines are not that effective (not to mention, losing effectiveness over time) it bumps the threshold even higher.
Right now, much of the population has some level of "sterilising immunity" from the first round of vaccines and previous infection (i.e. having enough circulating antibodies to potentially block symptomatic infection and transmission). But everything we know about existing respiratory viruses (and indications so far this year) suggest antibodies will wane.
Of course, indications are most people will come away with robust cell-based immunity. (Those plucky T-cells and B-cells). But eradication for the UK looks *very* close to impossible given the near-total-abandonment of public health measures recently.
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.