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.
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.
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.
It also isn't obvious why AY.4.2 would be less virulent based on its genetic. Besides, contrary to what many may assume, more transmissible SARSCoV2 strains are not necessarily expected to be less virulent.
Viruses kill their host cells when they replicate. a strain replicating faster will be more infectious, and also cause more tissue damage to its host. Alpha and Delta are believed to be more virulent because they are more transmissible.
It is not impossible for a lineage to gain an advantage by being less symptomatic (less virulent), with carriers spreading it whilst unaware they're infected, but the advantage of faster replicating (more virulent) strains is not trivial to offset in a virus such as SARSCoV2.

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More from @BallouxFrancois

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.
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.
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.
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.
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.
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.
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.
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).
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.
Read 6 tweets
4 Nov
This looks like a potentially excellent piece of news ...
But, it could actually have been largely anticipated that loss of smell and other neurological manifestations of COVID19 were probably not caused by direct damage to the brain, as I hypothesised in this piece from June this year.
Amy got there first with this excellent thread.
Read 6 tweets
1 Nov
Today's covid drama ...

JCVI minutes fleetingly mention that infection during childhood likely increases immunisation in adults. Many misunderstood 'adults' as others in society rather than the children themselves as 'adults in the future'.
Massive outrage ensued and much bile was spilled against the 'JCVI anti-vaxers'. Many angry twitter threads got written and even the odd 'opinion piece' in semi-scientific journals was penned about a nefarious plot intent on sacrificing children to protect adults.
I appreciate everyone's on edge at this stage of the pandemic. Though, I respectfully recommend the next time something may be unclear to you, rather than erupting into paranoid, neurotic, conspiracy mode, please just enquire what was really meant.
Read 4 tweets

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