Read on Twitter
1) THREAD: The evidence FOR & AGAINST the new UK SARS-CoV-2 variant being more transmissible than the original, making it a new strain.
2) In order for a variant to be classified as a 'new strain' it must satisfy ONE or BOTH of the following criteria:
A. Different features - transmission, illness severity
B. Unrecognisable to immune memory components of patients who had original strain = common reinfection.
A. Different features - transmission, illness severity
B. Unrecognisable to immune memory components of patients who had original strain = common reinfection.
3) So far, A has been suggested to be the case with this variant. 'It's 70% more transmissible' according to various media outlets.
Today we will interrogate this claim.
DISCLAIMER: We will use data to support potential hypotheses, rather than stating that either is fact.
Today we will interrogate this claim.
DISCLAIMER: We will use data to support potential hypotheses, rather than stating that either is fact.
FOR 1:
Growth. Seq data shows that the variant has grown by 70% in the last month, now dominating positive cases. This is where the '70% more transmissible' point comes from.
It's exponential growth could suggest some functional advantage, such as higher transmission.
Growth. Seq data shows that the variant has grown by 70% in the last month, now dominating positive cases. This is where the '70% more transmissible' point comes from.
It's exponential growth could suggest some functional advantage, such as higher transmission.
FOR 2:
Infection Simulation. Cells were infected in-vitro w/both variant (d69/70) and original (WT) strains. The number of viral particles produced were measured. Variant viral particles were twice as high as the original, suggesting a selective advantage.
Infection Simulation. Cells were infected in-vitro w/both variant (d69/70) and original (WT) strains. The number of viral particles produced were measured. Variant viral particles were twice as high as the original, suggesting a selective advantage.
AGAINST 1a:
Social behaviour. Suggesting a selective advantage is the reason for the growth of this variant, ignores changes in social behaviour, such as the Founders' Effect, explained in the tweet below. https://twitter.com/SimplyBiochem/status/1340745191754522624?s=20
Social behaviour. Suggesting a selective advantage is the reason for the growth of this variant, ignores changes in social behaviour, such as the Founders' Effect, explained in the tweet below. https://twitter.com/SimplyBiochem/status/1340745191754522624?s=20
AGAINST 1b:
The founders' effect is where a variant enters a new population with minimal competitors e.g. Lockdown; lack of social mixing. If the variant was prevalent in essential workers, it would have no competition.
Exponential growth kicked off in W43. Lockdown began W45.
The founders' effect is where a variant enters a new population with minimal competitors e.g. Lockdown; lack of social mixing. If the variant was prevalent in essential workers, it would have no competition.
Exponential growth kicked off in W43. Lockdown began W45.
AGAINST 2a:
The infection simulation was carried out in-vitro and not in-vivo. This means it was done in a flask, using a human cell-line, rather than in a living animal (or less likely) human model. This means that the data cannot be directly interpreted to human infection.
The infection simulation was carried out in-vitro and not in-vivo. This means it was done in a flask, using a human cell-line, rather than in a living animal (or less likely) human model. This means that the data cannot be directly interpreted to human infection.
AGAINST 2b:
Susceptibility between different viruses differs between cell lines. Due to inherent characteristics of this cell line (HEK-293), the variant might have been better able to replicate and infect other cells.
This data must be repeated in other cell lines & in vivo.
Susceptibility between different viruses differs between cell lines. Due to inherent characteristics of this cell line (HEK-293), the variant might have been better able to replicate and infect other cells.
This data must be repeated in other cell lines & in vivo.
AGAINST 3:
Colder weather increases susceptibility to C-19 & other respiratory viruses. Whilst you'd expect to see growth of all variants, if this variant had no competition in a specific location, the colder weather would have exacerbated its growth. https://twitter.com/SimplyBiochem/status/1339197850509586438?s=20
Colder weather increases susceptibility to C-19 & other respiratory viruses. Whilst you'd expect to see growth of all variants, if this variant had no competition in a specific location, the colder weather would have exacerbated its growth. https://twitter.com/SimplyBiochem/status/1339197850509586438?s=20
4) So there we have it.
The data supporting higher transmission of the variant does exist. However it needs more for confirmation.
Even if it is more transmissible, saying 'it's 70% more' so, is probs an overestimate at it ignores changes in social behaviour & colder weather.
The data supporting higher transmission of the variant does exist. However it needs more for confirmation.
Even if it is more transmissible, saying 'it's 70% more' so, is probs an overestimate at it ignores changes in social behaviour & colder weather.
5) Thoughts on the thread!
6) Huge credits to the @GuptaR_lab for their amazing work on variant infection in cell lines and to @alanmcn1 who shared the UoB Turnkey lab data, showing a 70% prevalence in the variant.
Please do feel free to correct us if any of our assumptions are off!
Please do feel free to correct us if any of our assumptions are off!
