And why are some respiratory viruses more likely to infect the lungs?
@JuliaLBach8 and I have a simple proposal called temperature dependent viral tropism (TDVT)
2⃣We suggest that (virtually all) respiratory viruses sense temperature in order to keep out of the lungs, so that they can keep us moving around doi.org/10.1002/rmv.22…
3⃣Remarkably, several recent studies show that CoV-2 is thermally-sensitive (more active at low temp) in cells & animals – just as we predicted!
But superimposed on the noise is a 365-day cycle⬇️
In many diverse climates, all respiratory viruses – which are often unrelated - have WINTER seasonality
Other viruses eg rabies, polio are more common summer/variable
5⃣ @JuliaLBach8 and I believe the explanation is simple and it’s what folk wisdom has always told us – we get colds when we’re chilled.
Our review: doi.org/10.1002/rmv.22…
6⃣That’s why standing still outside, and shivering outside, are correlated with an increased risk of dying of a respiratory illness. And why wearing a parker (anorak), and sweating outside, are correlated with reduced risk doi.org/10.1016/S0140-…
7⃣CoV-2 seems to be less thermally sensitive than eg rhinovirus, because it gets into our lungs more often. However, if you look at the right level (continents) you can see it has retained significant thermal sensitivity because it’s clearly seasonal:
8⃣It has been suggested that low humidity – or high humidity – are drivers of seasonality
However, when both flu virus & CoV2 are suspended in realistic solutions (ie not salt) humidity has little effect on virus survival in air doi.org/10.1093/infdis… doi.org/10.1093/infdis…
🔟There’s lots of biochemical evidence for this idea of viral biochemical heat-sensitivity. For example, the “switch” that controls the transition from transcription to replication in influenza is controlled by temperature doi.org/10.1186/1743-4…
11/ #TDVT has important practical implications. For example a small heater in the bedroom of Covid patients may be helpful
14/ It's very interesting to see that CoV-2 is indeed thermally-sensitive in the lab. We sent this letter to Virologica Sinica - let's see if they get it! ⬇️
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1/🧵No one seemed to want to do this, so I finally went ahead and looked at vaccines/deaths in OurWorldInData ⬇️
I've plotted excess deaths in the last 12 months against CoV-19 booster doses ⬇️
There is a clear correlation (correl coeff = 0.50)
2/ Strangely, there's a much stronger correlation between vaccine doses given and CoV-19 deaths: apparently, more vaccine doses corresponded to more deaths in the last 12 months, corr coeff = 0.72 ⬇️
3/ This is unexpected, but @StabellBenn &others point out that non-live vaccines can "damp down" the immune system
It seems mRNA vaccines are like non-live ones so this may be the explanation
The first vaccines might have been helpful but boosters may've been counter-productive
🧵1⃣ Why do we get more colds&flu - & Covid - in winter than summer?
This question has confused & perplexed scientists for ~60 yrs
Turns out the main explanation is quite simple: virtually all respiratory viruses - including CV2 - are thermally-sensitive doi.org/10.1016/j.imj.…
2⃣CoV-2 has been shown to be thermally-sensitive in the wet-lab and in animals (see table⬇️from our letter)
Many other respiratory viruses have been shown to be thermally-sensitive in the wet-lab⬇️, although they may rapidly lose this sensitivity if they are propagated at 37°C
3⃣My co-author @JuliaLBach8 & I showed that many/most respiratory viruses possess natural thermal sensitivity - they replicate faster below normal body temperature, confining them to the cooler upper airways. doi.org/10.1002/rmv.22…
I’m reposting this thread re the evolution of viral proofreading / the puzzling shape of epidemics, to get it all in one place
🧵I haven’t yet seen any scientists tackling the puzzling surges and rapid collapses of cases that we often see in Covid-19, eg South Africa and India⬇️(where lockdowns may not be very effective). Also seen in other countries such the UK, Austria and France⬇️
There must be a reason for these surges, and this is clearly important. I suggest a biological mechanism involving the emergence of low-fidelity strains that evolve faster than the ancestral ones
1/ Once again I’m struck by something that’s been staring us in the face, but which we all seem to have missed
🧵
2/ Almost certainly, the main pandemic threat from “novel” viruses doesn’t arise when they first appear in humans. Whether they’re from animals or labs, it’s probably letting them fester that’s dangerous. Here’s why -
3/ Novel human viruses tend to be either mild (flu-like symptoms) or horribly pathogenic. There are several well-known viral hemorrhagic fevers that regularly appear, including Lassa (400,000 cases per year), Marburg, Ebola
2⃣I’ve read Day et al. and it has a strange omission
The authors don’t mention the fact that CoV-2 is what I'd call a “standard” respiratory virus, that is, it's transmitted directly from the nose and throat of one person to the nose and throat of another.
3⃣The authors also don’t mention that most respiratory viruses are mild most of the time - even influenza – which Galanti et al found was asymptomatic in ~50% of cases