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.
Some may dislike this 'immuno-geneticky' stuff. Thus let's go basic. If SARSCoV2 often infected our brain, encephalitis should be a common complication. It isn't. A review explicitly biased towards studies reporting encephalitis, found it at ~0.5%.
Though, if SARSCoV2 were not neurotropic, why do we see so many neurological symptoms and sequelae upon COVID-19 infection? That's a good question, in particular as concerns the characteristic loss of smell (anosmia).
I wrote a piece a while ago arguing that loss of smell was actually most unlikely to be due to damage to our brain. It's the sustentacular (''sniffing cells') that likely suffer.
My wonderful friend and colleague Amy wrote this amazing thread pointing to loss of smell (anosmia) being most likely caused by infection of sensory cells, rather than brain cells.
To summarise.
- SARSCoV2 is not a neurotropic virus
- Encephalitis is an exceptionally uncommon complication of COVID19
- Anosmia heals in ~99% cases
- Anosmia does not seem to be linked to brain damage
Some replies suggest a misunderstanding of my point. I'm stating that based on all the available evidence, SARSCoV2 doesn't seem to infect the central nervous system (CNS). This doesn't mean it can't be detected in brains of patients who died from severe systemic infection.

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More from @BallouxFrancois

Jan 15
The account below got suspended overnight. They stated they were badly struggling with their mental health, and admitted to having sent emails to public health professionals that having to wear a mask made them feel suicidal (which may be unwelcome but is not an offence).
1/ Image
I cursorily checked their account before replying and didn't find anything obnoxious or reprehensible in their timeline. I felt sorry and worried about them. I appreciate they may have posted something unacceptable since as they seem in a really bad state.
Though, if they had been mass-reported and suspended from twitter for their reply to me, I suggest to anyone involved to seriously reflect on their values and compassion levels.
Read 7 tweets
Jan 5
The next SARSCoV2 variant, and any after it, could be intrinsically less, as, or more virulent than Omicron. Though, the associated morbidity and mortality will further decrease over time, with more people having acquired immunity through vaccination and prior exposure.
No variant can become "totally impervious to vaccines and boosters" and protection from prior infection. A variant can largely escape 'neutralising antibodies' as Omicron does, and thus be more prone to (re-)infect immunised hosts.
Though, no variant will ever be able to bypass our cellular immunity (T-cell) response that controls the disease upon infection, and hence protects against the most severe symptoms. This stems from the myriad targets of T-cells (epitopes) in the viral genome.
Read 6 tweets
Jan 2
This interview by Mark Woolhouse should in principle not come as a surprise. He has been consistent in his views during the pandemic, even if he only occasionally expressed them in public.
For a previous example of one of his rare public pronouncements that may have been largely overlooked, see e.g. below.
Read 7 tweets
Jan 2
North South Wales (Australia) provides an interesting case study for Omicron's virulence in a population with negligible immunisation due to prior infection but very high vaccination coverage.
The dramatically lower case hospitalisation rate may be due to an (unknown) mix of:
- Omicron's intrinsic lower virulence
- High protection of vaccines against severe symptoms
- Lower 'infectious dose' for summer infections (fewer viral particles involved in the infection)
Whatever the causes - and mix thereof - behind Omicron's lower virulence in NSW, this is an excellent piece of news.
Read 4 tweets
Dec 31, 2021
I worry that Public Health (PH) has a serious image problem on its hands, and I say that as someone who believes we need more - but better - PH, rather than less to deal with many post-pandemic problems, such as obesity or mental health.
One problem is the politicisation of the field, both perceived and real. In the early stages of the pandemic being, I got involved in a discussion with senior PH practitioners. My views that PH should try to remain apolitical were deemed to be ignorant if not sinister.
Now more than ever, I feel PH should try to stay out of politics. This doesn't mean that the rights and wellbeing of any section of society shouldn't be fought for specifically, but that it should be in a non-partisan way, and not seen as a fight against others in society.
Read 7 tweets
Dec 27, 2021
This is not an easy message to convey, even to those who have have already accepted that zero-covid was toast. Essentially everyone will eventually get infected by SARS-CoV-2 in the near future, and likely more than once in their lifetime.
One can don an FFP2, FFP3, N95 mask, or a hazmat suit, or whatnot, but at this stage, all this may achieve is to delay the time until some of us will get infected, and thereby marginally prolong the pandemic.
Vaccine protection against infection is meh, though protection against severe symptoms, hospitalisation and death remains stellar (~20x), including against Omicron. There's also no moral failing in catching a respiratory virus. It's OK; it's life, which sucks at times.
Read 10 tweets

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