I've noticed that explanations for resp-vir seasonality involving humidity are becoming more popular

Eg doi.org/10.1101/2020.0… by @EdsardRavelli
1/
The problem is that we essentially have ONE observation - that hundreds of often unrelated viruses in all regions (outside the Tropics) with very diverse climates, have winter seasonality
2/
If we say the winter surge of colds in one place is due to eg school buses, business travel and humidity, but somewhere else it's sports events, snow and sunshine, we are cheating. We’re “overfitting” - we are using too many variables to model a 1-d phenomenon
3/
So we’re looking for one main factor that drives seasonality – maybe two.

Seasonality COULD be driven by temperature and humidity, 50: 50. That is possible, although it would be a coincidence.
4/
Can we seriously propose that dry air is the main driver all over the world? It doesn’t work well. For example, it’s much drier in Mediterranean countries in summer, but of course they have colds in winter
5/
Another problem for humidity is that respiratory infections tend to surge in the AUTUMN - before humidity has really changed. See examples below.

But temperature has dipped
6/
I'm not saying that humidifying your house isn't a great idea, or that it has no effect on viruses. Just it's not the main driver of seasonality.

It's a problem that temperature and humidity are so closely correlated - which is why we need experiments (see our paper)
7/
Bear in mind that winter seasonality isn't a new phenomenon. Eg here is flu 1964-75, when many people had poor heating and no air conditioning
8/
My point is, if you stand still outside for more than 2 mins in winter and get chilled, you are in some danger of dying from a respiratory infection.

But if you dress up warmly and go skiing and breath this cold dry air which we are told is so dangerous . . . you feel fine!
All explained in our paper, written with @JuliaLBach8

doi.org/10.1002/rmv.22…
I forgot to say, the theory that says that dry conditions produce finer aerosols containing virions, which are more stable, doesn't work in the Tropics

Influenza and colds both arrive in the RAINY season in Fortaleza and Singapore. This is also true in eg India Indonesia
This hospital in Bangkok believes that the problem is chilling

bangkokpattayahospital.com/en/healthcare-…

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More from @PatrickSSte

6 Aug
One reason I’m convinced that viruses moderate their pathogenicity much more than is often appreciated comes from observations of hemorrhagic fevers, which give fascinating insights
/1


en.wikipedia.org/wiki/Viral_hem…
People occasionally pick up viruses from animals especially rodents & bats. Usually they cause mild flu-like symptoms but here's the extraordinary thing: if they get a hold they often cause internal & external bleeding & are fatal – in spite of NOT being well-adapted to humans
/2
Ebola is one example. There are many others eg Rift Valley, Lujo, Bolivian and Brazilian hem. fevers. Ebola, Marburg, Crimean-Congo and Lassa hem. fevers can spread from person to person.
/3


facebook.com/watch/?v=27782…
Read 7 tweets
26 Jul
THREAD (quite long - sorry!)

IMO you can’t understand CoV-2 or any other virus without understanding the "virulence-transmission trade-off hypothesis"
This hypothesis was introduced in the 1950s to explain observations of myxomatosis. Basically, very mild strains became moderate, while very virulent ones also became moderate

cambridge.org/core/journals/…
The hypothesis says a virus must balance the amount of shedding against the time during which the shedding takes place – the time will be reduced if viral virulence is too great
Read 24 tweets
25 Jul
1/ The Nobel laureate André Lwoff suggested part of the hypothesis in 1959, when he noted that the degree of virulence of viruses is often related to their level of thermal sensitivity

journals.asm.org/doi/pdf/10.112…
2/ In 1979, Richman and Murphy developed this further, discussing many examples of thermal sensitivity in natural and lab‐made viral strains, and noting that the near‐universal attenuation of ts strains made them good candidates for vaccines.
doi.org/10.1093/clinid…
3/ The full hypothesis was proposed by Shaw Stewart and discussed at length in 2016, focusing on seasonality and the natural selection of strains with varying degrees of thermal sensitivity and pathogenicity

doi.org/10.1016/j.mehy…
Read 7 tweets
16 Jul
1/5

The UK 10-day self-isolation period is highly disruptive to industry.

But it may also be counter-productive in combating Covid-19.
2/ 5

We know that Covid-19 incubation periods vary hugely, with some illnesses appearing 2 or 3 days after exposure, but others taking 14 days or more.

Some of this variation is likely to be related to the properties of the particular “isolate” (ie strain) involved.
3/ 5

It is also likely that strains with short incubation periods are more pathogenic. This is the basis of the “virulence-transmission trade-off hypothesis” and has been proposed for several viruses including influenza and myxomatosis.
Read 6 tweets
25 Oct 20
Is the SPIKE protein wrong target for vaxs?

• Unbiased screen found 29 "shared epitopes" that were main targets for T-cells

• Notably, only 3 of 29 epitopes were located in spike protein

• Most epitopes were located in ORF1ab / nucleocapsid protein

cell.com/immunity/fullt…
Anyway

"Frequent BACTERIAL infections of respiratory tract are often a harbinger of ANTIBODY disorders"

"Respiratory VIRAL infections are more significant in patients with T-CELL immune deficiencies"

So why do virtually all vaxs target SPIKE PROTEIN?

ncbi.nlm.nih.gov/pmc/articles/P…
Also may be very serious

ncbi.nlm.nih.gov/pmc/articles/P…
Read 4 tweets

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