Thread by @PatrickSSte

1/ I feel there are still some important points to make about this question of whether and how quickly Covid will become like a common cold

2/ The first point is CoV-2 is a respiratory virus. It spreads straight from your nose and throat to mine. This is a very distinct group of viruses with something surprising (and, really, unexplained) in common – the illnesses they cause are much more common in cold weather.

3/ They’re also mild in the vast majority of cases – so CoV-2 will be very unusual if it remains as pathogenic as this for long. (Though of course rhinovirus, adenovirus, parainfluenza etc regularly hospitalize children and others 👇)

4/ I think everyone agrees that we need to think about the “trade-off” model of the evolution of parasites: short-sighted selection says that the virus would become super-virulent. However long-sighted selection says it won’t be transmitted well if it’s *too* virulent.

5/ (As an example of trade-off in action, why are colds so such much more common than Ebola, Marburg & Lassa viral hemmorhagic fevers, which can all spread from person to person? Something either stops VHFs or makes them mild over time.)

6/ (Just as well, or complex life-forms might well be impossible.)

So clearly selection is reducing pathogenicity, at least in the extreme cases.

7/ Scientists talking about trade-off often say “if a virus is too virulent, it may kill its host too quickly”

True, but trade-off isn’t only or mainly about death. For viruses such as CoV-2 that AREN'T spread by insects etc, a crucial question is whether *mobility* is reduced.

8/ (Ewald, 1985, pointed out that viruses that are spread by vectors tend to be more virulent, p < 0.0005. He suggests that for them it doesn’t matter much whether the host moves around because the vectors can come to the host. doi.org/10.1146/annure…)

9/ So respiratory viruses need to both reduce their virulence, & have long incubation periods, so that their hosts remain infectious for longer

Since most resp viruses are mild, seems that (fortunately for us) a long incubation period IS correlated with mild symptoms in respvirs

10/ People often point out that other endemic viruses such as measles and smallpox remain virulent and have not become as mild as colds.

11/ However measles and smallpox occupy a different niche: they go through the lymphatic system, before getting into the blood. This probably slows them up and makes their hosts infectious for longer.

12/ Timing: so when will CoV-2 become like a common cold?

We don’t know but there are clues: the first is the autumn surge of colds, which is very common, shown below 👇

The highest number of colds all year can appear in early autumn – which is certainly not the coldest season

13/ The only reasonable explanation of this autumn surge that I know of – which is falsifiable – is that these viruses have adapted to the high summer temperatures, and they get “caught out” by a drop of a few degrees in autumn.

14/ So it seems viral pathogenicity can significantly adapt over a few months. Similarly, viral strains that come from the Tropics seem to become mild in a few months. See our paper for details
doi.org/10.1002/rmv.22…

15/ So why isn’t CoV-2 already noticeably milder?

Here I want to have my argumentative cake & eat it by saying our interventions may possibly have slowed up up attenuation. Eg we may have enforced the wrong kind of track & trace:

16/ our relatively slow track & trace could have stopped the slow-burning, asymptomatic or mild strains, but allowed the more aggressive, fast-acting ones to proliferate. Could we have accidentally made things much worse?

17/ After all, 70% of respiratory viruses detected by Galanti and colleagues by multiplex PCR in New York City were asymptomatic (including influenza at ~50%) 👇doi.org/10.1017/S09502…

18/ Letting mild and asymptomatic infections spread could be very important in moderating this disease. In fact yuou could argue that only symptomatic people should take tests

19/ All fascinating !

Of course much of this is speculative, but most of it is falsifiable

So, what we need, urgently, are experiments

#TradeOffModel #tdvt

The point about fast and slow strains came up with reference to Omicron in South Africa

https://twitter.com/PatrickSSte/status/1469990017254711300