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Glenn Ledder
30:21
Are you assuming that all asymptomatic patients eventually become symptomatic?
Joshua Macdonald
37:18
yes, COVID-19 reporting methods make it very difficult - for all of case data, test data, and death data
Glenn Ledder
43:28
Are you assuming that all of the vaccinations are administered to susceptible individuals? In reality, we are also vaccinating people who are immune by virtue of having survived the disease.
Rebecca Tyson (she/her)
45:46
I think you said that you were aiming for 90% of the US population getting accinated. That seems wildly optimistic.
Joshua Macdonald
47:32
yes, particularly in the south, there is difficulty with reaching above 70% vaccination
Joshua Macdonald
47:41
very interesting talk
Rebecca Tyson (she/her)
49:04
Yes, very interesting!
Rebecca Tyson (she/her)
49:47
There was a recent article published by Caroline Colijn with modelling work showing that we have to aim for 90% coverage if we don't want a bad 4th wave due to variants.
Rebecca Tyson (she/her)
49:51
in Canada
Joshua Macdonald
52:43
estimates for R0 in US are around 2-3 (CI 2.21-2.36) so naively (not accounting for different vaccine efficacies, J&J is about 78% effective this would suggest needed immunization level of
Joshua Macdonald
53:16
[1/.95](1-1/3)
Glenn Ledder
01:03:44
R0 is much higher than 2-3 based on epidemiological measurements. The doubling time of hospitalizations in the early stages was about 3 days, which is consistent with R0 on the order of 5-6. Using a more sophisticated version of the same argument, a group at Los Alamos estimated 5.7 in a paper published last July. That was the original strain. The British strain is probably around 7 and the delta strain could be as high as 10. Hospitalization data is critical because it is far more reliable than data of reported cases.
Joshua Macdonald
01:04:53
thank you @Glenn
Glenn Ledder
01:05:05
On the plus side, most people who survive COVID-19 must have acquired immunity, so the fraction of vaccination acceptance and success does not need to be as high to reach herd immunity as would have been the case without acquired immunity.
Glenn Ledder
01:05:31
Early papers were based on statistical analysis of reported cases, so they missed the fact that some 40% of patients never have symptoms.
Joshua Macdonald
01:05:46
yes
Rebecca Tyson (she/her)
01:06:13
Glenn (Ledder), do you have a doi for that Los Alamos paper?
Joshua Macdonald
01:06:24
seconded ^
Glenn Ledder
01:07:29
Great research work, Cameron, and well presented!
Joshua Macdonald
01:07:29
very nice talk Dr. Browne
Rebecca Tyson (she/her)
01:08:18
I wish we had access to the fairphone in NA!
Glenn Ledder
01:10:59
wwwnc.cdc.gov/eid/article/26/7/20-0282_article, Sanche et al, High Contagiousness and Rapid Spread of Acute
Rebecca Tyson (she/her)
01:11:05
Thank you!
Joshua Macdonald
01:11:08
thanks
Glenn Ledder
01:11:14
Respiratory Syndrome Cornoavirus 2
Glenn Ledder
01:11:41
Sorry--accidentally touched the Enter key instead of the Shift key :-(
Stanca Ciupe
01:13:11
Great talk, Cameron. Have you looked at the differences between sequential CTL escapes versus concurrent CTL escape from multiple epitopes? There is data that shows that concurrent escape can happen early, first 100 days.
Cameron Browne
01:16:05
Thanks Stanca! Yes, the model assumes concurrent immune response. The sequential escape is represented by the nested network, which is just a subnetwork to the whole system and is stable iff the “relevant epistasis measures” in virus fitnesses are positive.
Cameron Browne
01:17:11
When looking at the patient data, sometimes there is sequential escape, other times it follows different pathways
Stanca Ciupe
01:18:25
Thanks!
Rebecca Tyson (she/her)
01:29:37
Nice talk!
Miranda Teboh Ewungkem
01:30:34
Nice talk. Pugliese do you have a preprint or paper?
Andrea Pugliese
01:31:55
I have a preprint only on the analysis of Zarnitsyna immune model and extensions. I can send it. The rest is still in preparation.
Cameron Browne
01:33:36
Great talk Andrea! For the within-host model, did you find that peak viral load was relatively constant through primary, secondary or third infection in the model without target cells?
Michael Cortez
01:52:10
I am going to try to restart
Hayriye Gulbudak
01:56:00
Thank you all!