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.
Any suffering and ill health is equally real, irrespective of its cause, be it tissue damage or stress. Also, there is no clear boundary between psychological and physical illness. For example, stress is a common cause of herpes (HSV) reactivation.
Long-covid is a major challenge for the individuals affected, but also for society more generally. The causes of long covid are diverse and likely range from the trauma experienced during the pandemic to direct physiological injury caused by SARSCoV2 infection.
I appreciate this may sound insensitive and heartless, but I believe that for many long covid sufferers, healing will come primarily through regaining a sense of hope, confidence and joy once the pandemic will be over rather than from any medical intervention.

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More from @BallouxFrancois

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
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
31 Oct
Not everyone seems to grasp the remit of a vaccine regulatory agency such as the JCVI. In short, it is to advise whether the benefits of vaccinating a specific demographic group (e.g. healthy 12-15 years olds) *significantly* exceed the risks for this group alone.
When the JCVI concluded on the basis of the evidence available at the time that the risk / benefit balance of vaccinating healthy 12-15 year olds was marginal, it made sense them not advising for it. A health intervention should only be undertaken when clearly beneficial.
The 'significant benefit' bit is particularly important in the context of vaccines. Non-negligible rates of adverse vaccine effects in children would likely fuel far more vaccine hesitancy (covid19 and otherwise) than the most ideological antivaxer could ever hope to spread.
Read 4 tweets
29 Oct
Early 2020 what worried me most is how long immunity following COVID-19 infection / vaccination may last for. We now have good data on that, despite people apparently disagreeing whether this is 'nothing' or 'a lot', even when agreeing on the numbers.
Many of those discussions feel remarkably sterile to me. While vaccines reduce morbidity / mortality, in particular if the most at risk in society have been vaccinated, they won't suppress transmission of SARS-CoV-2 on their own (Measles vaccines like).
Whatever a society chooses to do, and irrespective of how many people get vaccinated and re-vaccinated, it is unlikely to change the fact that eventually essentially everyone, everywhere will get exposed to the virus multiple times in their life time.
Read 6 tweets

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