The B117 variant is now the dominant strain of SARS-CoV-2 in the UK, Ireland, Israel, Denmark. Likely also Portugal, Belgium, France, Italy, Norway.
Yet for the most part, these are not the countries where COVID-10 cases are rising (see below). What gives?
One explanation is that B117's transmission is being offset by restrictions, population immunity, etc. And that those countries w high B117 (UK, Ireland, Portugal) have locked down most. There is likely some truth to this - but not too much correlation w stringency index (below).
But it's also worth considering B117 and non-B117 COVID as separate epidemics. For example, look at Danish data below - it's tempting to think of B117 (red) as "replacing" non-B117 (grey). But that's not what's actually happening...
What's happening is 2 simultaneous epidemics, one of B117 and one of non-B117. (In reality, each new strain is its own epidemic, so it's more than just 2.) So it's arguably better to look at this as two separate epidemic curves. Viewed this way, B117 looks less scary.
If we estimate transmission of a variant that is gaining steam with one that is in decline, the new variant will look much more transmissible.
This is partially because the virus mutates to become more transmissible, but also because new variants take hold in new networks.
It's therefore difficult to compare transmissibility of a variant spreading in a new network to one that has been transmitting for a longer time.
It would be better to compare each variant at the same point in its epidemic curve - but those are at different points in time.
But a key take-home message is that - at least right now - new variants do not seem to be fueling out-of-control epidemics in countries where they have taken hold.
This is good news.
In summary:
- The B117 variant is likely dominant in a large number of locations.
- These places aren't experiencing major surges of COVID-19 cases.
- We need to keep monitoring.
- But there is reason for optimism that we can manage the pandemic, even as new variants take hold.
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In the past week, COVID cases have fallen in the majority of countries across the globe (see below for weekly change). But not all countries are locked down.
A thread on what might be - and what probably isn't - happening.
1. Lockdowns/restrictions have almost certainly had a major effect in countries that instituted them. Look at the peaked curves in the UK and South Africa - natural processes are generally smoother. But it's notable that current declines are even sharper than w the 1st lockdowns.
2. If this were just due to seasonality, one might expect similar behavior as with flu. But historically, flu rates in the US generally do not start to fall until March (see non-red lines below). Seasons likely contributed to the Oct rise, but likely not the Jan decline.
Many are interpreting data from Denmark as strong evidence of increased transmissibility of B117.
With the caveat that I believe this prevailing hypothesis to be credible, if not likely...
A thread on how Danish data can be explained w/o invoking increase in transmissibility.
First, Denmark should be applauded for their rigorous genomic surveillance. Other countries should follow their example!
The data, in brief, show an increase in the percentage of sequenced cases that are B117, from 0.2% in early December to (prelim) 12% in mid-Jan.
This was, however, occurring in the context of a dramatic fall in cases throughout the country, likely reflecting the effects of a country-wide lockdown.
A counterpoint to the alarm bells that are sounding over novel SARS-CoV-2 variants.
Is it possible that we are misinterpreting differences in human behavior as differences in the biological fitness of viral variants?
A thread to explain this hypothesis...
1. Infectious disease transmission is heterogeneous (overdispersed), largely due to human behavior.
Large "superspreading events", differences in behavior, and/or people who have many contacts generate an outsized number of transmission events.
2. This makes it easy for viral variants - even those with no inherent transmission advantage - to take over a population.
Imagine an infected person attending a large indoor gathering with hundreds of people. That viral strain will expand - because of behavior, not biology.
After some conversations with a trainee, I've recognized at least 7 "academic phenotypes" based on underlying core professional goals.
A thread, aimed primarily at junior researchers learning to navigate the academic world.
Take-home: know your phenotype, know your superiors'.
Phenotype -> core goal:
Politician -> power
Performer -> fame/pubs
Pragmatist -> things that work
Inquirer -> knowledge/insight
Idealist -> a better world
Epicurean -> pleasure/time off
Humanist -> relationship
We are all each of these to some extent. But more some than others.
Step 1: Recognize your (actual & ideal) phenotype by asking yourself which goals you would sacrifice for others.
Ex.: would you delay promotion to achieve an ideal?
Be honest w yourself about which phenotypes you (a) are, (b) want to be.
This may be controversial, but here's a thread on 5 problems I see with the #JohnSnowMemorandum.
I agree with the concept, but am worried about the message it sends.
I sympathize w/ those who have signed, submit this in the spirit of scientific debate.
First, I am no fan of surrender (aka "herd immunity") strategy articulated in #GreatBarringtonDeclaration. "Those...not vulnerable should immediately be allowed to resume life as normal" suggests vulnerable & non-vulnerable can be (a) identified & (b) kept apart. Both fallacies.
Second, full disclosure, I have a personal stake - an immediate family member has been in the hospital for months, with no visitation due to COVID restrictions. My pandemic life is not OK.