Under the plausible assumption that essentially everyone will get infected by SARSCoV2 at some point, the area under the curve of infections / pop size will asymptotically tend towards 100% eventually, in every country (below confirmed cases until now as a proxy).
1/
In the future, it should be possible to work out, up to a point, what the best pandemic mitigation strategy may have been in terms of various metrics, such as excess mortality, educational achievements or social cohesion.
2/
"Hindsight is notably cleverer than foresight", and any such past (and current) prediction was (is) based on major - and generally unstated assumptions - such as the evolution of the virus or the efficacy of vaccines.
3/
Also, even with the benefit of hindsight, pre-existing factors such as poverty, deprivation, healthcare quality, population health, and whatnot may still explain a far larger fraction of the variance than various pandemic mitigation strategies enforced by different countries.
4/
We should be able to learn a lot about what may work (and what doesn't), and in what settings, in terms of mitigation strategies if and when the next pandemic comes along.
5/
That said, if we were serious about reducing future morbidity and mortality, we shouldn't just spend our energy devising clever plans for when the next pandemic hits, but start addressing current underlying structural inequities.
6/

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More from @BallouxFrancois

20 Nov
I don't know who patient zero was for SARS-CoV-2, and I doubt we'll ever know. We actually hardly ever identify 'patient zero' for disease outbreaks and epidemics, which is not necessarily a bad thing as it could lead to blame and ostracism of innocent people.
1/
A Mexican boy was identified as 'patient zero' for the 2009 H1N1 epidemic/pandemic. He actually wasn't 'patient zero' in all likelihood, as much as the media cherish such stories.
science.org/doi/full/10.11…
2/
An emerging disease is unlikely to be identified before the number of cases reach ~1/CFR (CFR: Case Fatality Rate). For a disease like COVID19 with fairly 'undiagnostic' symptoms relative to other respiratory virus infections, the threshold is likely much higher.
3/
Read 9 tweets
18 Nov
The frequency of the AY.4.2 SARSCoV2 lineage is still slowly increasing in the UK, now reaching ~15% of all cases. Results from a recent study (REACT-1) suggest it might cause a smaller proportion of symptomatic infections.
1/
gov.uk/government/col…
AY.4.2 causing a lower proportion of symptomatic infections might explain its increase in frequency, with asymptomatic carriers unwittingly transmitting it more often. This would be good news in principle - fewer symptoms -> less morbidity/mortality.
2/
That said, this result requires confirmation before being taken at face value. The statistical significance is very marginal (P = 0.04) and this may likely turn out to have been a 'false positive' finding.
3/
Read 6 tweets
12 Nov
Biology fieldwork (late 20th century). Image
There's actually a semi-serious message behind my sharing this pic. As a young biologist, I handled birds, bats, rodents, insectivores and whatnot without taking any precaution. No one did. I've been scratched and bitten by half the vertebrates in Europe.
Was this reckless, or does it imply that the baseline risk of pathogen pandemic-causing spillovers into humans is low. This raises a set of interesting questions. BTW, European wildlife is as riddled with pathogens as African or Asian ones, including myriad coronaviruses.
Read 4 tweets
10 Nov
A significant proportion of healthcare workers (HCWs) in the UK exposed to SARSCoV2 during the 1st wave of COVID19 never tested positive for PCR or antibodies. Instead, they controlled infection through expansion of pre-existing X-reactive T-cells.
1/
nature.com/articles/s4158…
The ability to control infections through pre-existing T-cell immunity likely stemmed from constant pre-pandemic low-level exposure of HCWs to endemic coronaviruses. Such X-reactive T-cell immunity may not be sufficient to control infections by the more aggressive α/δ strains.
2/
More positively, the results reinforce the importance of long-lasting T-cell immunity (i.e. decades) and could inform the design of the next generation of SARSCoV2 vaccines.
3/
Read 6 tweets
9 Nov
Challenge accepted! let's try to start studying up on covid together. I suggest we first go through some of the arguments for or against SARCoV2 being a neurotropic virus.
1/
The first question we may wish to ask is whether SARSCoV2 is found in the brain. Evidence remains limited to date but this recent study in Cell suggests SARSCoV2 isn't present in the brain in COVID19 patients, in line with most recent, solid evidence.
2/
cell.com/cell/fulltext/…
So, we may wish to ask what protects the brain against SARSCoV2 infection. A possible answer may be that the cell receptor gene called ACE2 that the virus needs to infect cells in our body is actually not highly expressed at all in our brain.
3/
proteinatlas.org/ENSG0000013023…
Read 9 tweets
8 Nov
The ideal control for long-covid studies would be a group of people who believe they may have been infected, but weren't (i.e. placebo covid-19). A new study on a large cohort essentially achieved that experimental design.
1/
jamanetwork.com/journals/jamai…
The study found that persistent physical long-term symptoms were associated more with the belief of having experienced COVID-19 infection than with having laboratory-confirmed SARS-CoV-2 infection, with the notable exception of loss of smell (anosmia).
2/
The should not be interpreted as evidence that long-covid isn't real. Though, it stresses the difficulty of teasing apart the actual long-term physiological effects of SARSCoV2 infection with the nocebo effect of believing to have had covid.
3/
Read 6 tweets

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