Today at @bakercornell we received sad news that Prof LeLand 'Skip' Carmichael passed away last night in Ithaca.
Skip was cherished family of Baker Institute and @cornellvet.
Instrumental in identification of epizootic Canine Parvovirus, development of the vaccine. #virology
In ~1976 a severe haemorrhagic enteritis broke out in dogs and quickly spread worldwide. Skip and his team were key in identifying the parvovirus, and recognizing its likely homology to feline panleukopenia virus.
That homology was the basis for a rapidly developed vaccine based on FPV... which was improved to an attenuated formula developed at Baker by 1981. That has been the basis for all CPV vaccine formulations since.
Real nice summary from @Alexander_Tin on the @NEJM report from NIH/UCLA on pasteurization of #H5N1. Catches all the nuances.
Short: If you *experimentally* spike raw milk w/ high titer virus and run 72C/short ( US standard) it leaves a small amount of virus. 68C/long was better.
In the real world, one can assume that milk bulk at processing and pasteurization is not going to be that high in #H5N1 titer unless 100% of milk is coming from infected cows at peak virus shed.
So we have several independent /rigorous validations of FDA guidance and assurance.
I want to note that these lab experiments were done with a US #H5N1 2.3.4.4b isolate (A/mountainlion/MT/1/2024), but not a cattle-origin genotype B3.13 isolate.
Also, I repeat: experiments are experiments. Don't push too far ahead on single observation.
Lots of fair questions in this article. I do not envy the heavy task of the USDA and supporting labs and researchers, but there has to be more information sharing to the best of their ability. #influenza #H5N1
This thread from @DuckSwabber (via Richard Wrbby, St Jude) has some great historical items on #influenza in the mammary glands of ruminants (ie human flu in cow, PR8 lab strain in goats). #H5N1
Note that the mammary gland produces a localized antibody response. Checking milk pool of suspect herds for H5-reactive antibodies may work in addition to presence of virus.
That SARS-CoV-2 came to be extremely efficient at human-to-human transmission after emergence (more so than 2003 SARS-CoV-1 or MERS) is not evidence of pre-adaptation. That's post hoc reasoning.
Evolution does not care how you think 'this should work.'
Studying mechanisms of spillover and emergence, I've been stuck on the concept of correlated fitness evolution (re: host shifts).
Viral populations do not exist in evolutionary stasis in their 'natural' host environment.
Evolution of virus populations in hosts (even under neutral drift) may produce genotypes that expand fitness function outside of selective pressures. These fitness gains may never be explored! Because the spillover never occurs, or dead-ends. When it does - can it feel like fate?
Please do not make #Deltacron a thing. It's not a thing. Some of you should know better.
Summary: Cyprus uploaded 24 genomes to GISAID on Jan 7 that appear to be Delta-Omicron recombinants. This is likely contamination from single sequencing run.
Some tweet sources below:
Tom was right on top of this at the start. There seems to be a biased PCR amplicon from the ARTIC primer set that put a particular fragment of Omicron in with Delta fragments. #Deltacron
As @PeacockFlu mentioned, below details how the Delta sequences are NOT MONOPHYLETIC. Same Omicron fragment in multiple different Delta backbones. So you have to believe this #Deltacron recomb happened dozens of times just Cypus, just last few days. Nope.
Did this 5 years ago on FB. Updating. The best 365 films I've ever seen (no order). Based on my ratings (4.5 or 5 stars) on @letterboxd. I post one a day in a thread with an image.
To be clear, because I've collapsed into exasperation tweets:
This headline is not just incorrect, but false and misleading. #SARSCoV2 D614G has been a present lineage in Europe and NAmerica since the beginning of the pandemic. G has become more dominant than D. /1
We are not certain why G overtook D. Serendipity founder effects. Marginal increase in infectiousness. Some combination. With so many susceptible hosts, it seems unlikely there was any sufficient selection for G to 'outcompete' D. /2