Much is being said about Covid variants spreading sequentially faster. A couple of days ago I posted a comment on this in response to @jburnmurdoch
As we approach endemicity new variants are expected to outcompete others faster. Reason being recovered subpopulation (less immune to novel variants as long as there is some immune escape) grows as we approach endemicity increasing the benefit of novelty.
Illustration from model:
When replacement is by immune escape the second variant (B) outcompetes previous faster than first variant (A) had done:
When replacement is by a mixture of immune escape and increased transmissibility this appears to happens to a lesser extent:
Finally when replacement is by increased transmissibility alone this does not seem to happen:
Just sharing this for now to illustrate what I meant.
More explanatory details are being written up.

One think I should perhaps add now is that B relates to A in the exact same way that A relates to Wildtype (otherwise the whole exercise would be meaningless).
* thing
x-tick labels in bottom panel are time since relative incidence crosses a specified threshold (2% but could be something else). x-tick labels in bottom panel are not the same as above panels.

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More from @mgmgomes1

24 Nov
Tweet que e cada vez menos novidade mas infelizmente ainda nao totalmente esclarecido principalmente em Portugal:
Levando em conta heterogeneidades realistas na susceptibilidade/exposição ao SARS-CoV-2 o limiar da imunidade de grupo para linhagens iniciais tera sido menos de 30%.
Se nao tivessem emergido variantes mais transmissíveis nem vacinas (como se equacionava ha mais de 1 ano) estes limiares teriam sido ultrapassados no inverno passado. Vale o que vale mas cada vez temos mais argumentos a suportar esta afirmação.
Desde então temos vivido num equilíbrio precário entre aumento de transmissibilidade do virus (devido as variantes) e diminuição de transmissibilidade (devido as vacinas) que mantem o R efectivo em torno de 1.
Read 8 tweets
6 Sep
1/7
Has the herd immunity threshold (HIT) been used sensibly in the Covid19 pandemic? No! Why does that matter?
2/7
An epidemic (with several waves) may last longer than expected because: (1) it had high potential to begin with and mitigation prevented it from growing vertically so it grew horizontally (single HIT number thinking); or...
3/7
(2) it didn't have as high potential as one might think but viral evolution, seasonality, waning immunity, population renewal, kept it going (dynamic HIT thinking).
Read 8 tweets
24 Aug
Don't know how common this feeling is among mathematical epidemiologists but as someone who has worked on population dynamics of infection & immunity for 20 years I felt hopeless to see herd immunity threshold (HIT) concept degenerating in front of my eyes during pandemic. Thread
1/n
HIT is an abstract concept essential to our work but it was hijacked early in the Covid-19 pandemic and disseminated with all sorts of distortions that prevented the impact of its application by those qualified.
2/n
A population invaded by an infectious agent (say a virus) achieves HIT when the sum of the immunities acquired by all its individuals is such that the virus cannot cause another epidemic wave.
Read 23 tweets
27 May
Our newest #COVID19 paper (with Marcelo Ferreira @ChikinaLab @WesPegden @rjaaguas) is on medRxiv. Individual variation models applied to England and Scotland.

Frailty variation models for susceptibility and exposure to SARS-CoV-2 medrxiv.org/content/10.110…
With 20% of their populations immunised by natural infection and their vulnerable vaccinated, many countries, like England and Scotland, appear to be in a comfortable position to redirect remaining vaccines to more susceptible regions.
More susceptible regions = closer to white on a combination of both these maps: ImageImage
Read 8 tweets
24 Dec 20
1/ I want to share a special moment with all who happen to be looking this way. This is the happiest I've been since April 27, when I posted on medRxiv a preprint with title "Individual variation in susceptibility or exposure to SARS-CoV-2 lowers the herd immunity threshold".
2/ In that preprint we study two mathematical models of the COVID-19 pandemic: one accounting for individual variation in susceptibility to infection; the other accounting for individual variation in exposure to infection (heterogeneous connectivity).
3/ We describe how both models tell us that herd immunity thresholds are expected to be lower when individual variation is higher. Many colleagues have posted very insightful comments on our work and here I want to highlight @joel_c_miller and @BallouxFrancois.
Read 6 tweets
9 Dec 20
TWIMC: I've been Mathematician and Mother for ~30 years (now also Grandmother) and this is what matters. I spent the last 10 years studying individual variation on characteristics that are under selection but that have no heritability repercussions in the time scale under study.
In these studies I have "used" (please make a note of this word) primarily host-pathogen systems but my curiosity for completely different systems was particularly vivid last year and I was happily moving away from infectious diseases when the pandemic started.
Early in the Covid pandemic I started being approached by reporters who wanted to understand what was happening and what to expect over times to come. To respond to them I started studying the data and interpreting it in light of my models.
Read 11 tweets

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