Hail to thee Immuninati! 😉
I was just listening to one of Simon Whistler’s many interesting/amusing YT posts (You have competition in productivity and channel empire building there, Vincent! 😉 ), when I couldn’t help noticing that all the examples of Pasteur’s vaccination feats, seem to be of him actually using his vaccines to cure–not just immunise–animals, and, eventually, people, who were already sick.
I believe that you have mentioned that some species, like anthrax, are slow growing enough for a vaccine to work if the site of infection is far enough away from vital organs, for there to be time to train the immune system to attack it before it becomes lethal, but, from this account, it almost seems as if Pasteur was applying a kind of homoeopathic principle: that a small amount of a poisonous substance can provoke the body into fighting off much bigger, lethal, amounts.
What did Pasteur actually think he was doing? Did he theorise about an immune system? Did he really cure rather than immunise his patients?
Perhaps you could go into this in more detail in one of your podcasts, when we run out of CoViD-19 discoveries! 😉
Amazed at all your wonderful output.
Where it’s now a chilly 20C after a week of very sticky 30C sleepless nights. (Air conditioning is rare in homes here, but it is catching on in cars, where a lucky few can escape to on their way to work!)
Perhaps it is just because I don’t understand fully, but the study below where they infected 16 volunteers with 229E seems pretty much to fit the profile for SARS-CoV-2. Or maybe I miss the mark and risk some Racanyelling.
The volunteers were administered a nasal wash with 229E. They say 10 became “infected” as indicated by “viral shedding” measured by nasal wash, freezing at -70 and then cell culture. The “uninfected” group had elevated 229E specific IgA by nasal wash as compared to the “infected” group. Hmm.
Of the 10 “infected”, 8 got colds of varying severities and all had IgG and IgA come up more in serum as opposed to the “uninfected” group.
They then rechallenged everyone a year later with 229E. The original “uninfected” 5 (it seems someone did not care to return) became “infected” as measured by the same “viral shedding” assay and/or a rise in serum IgG. This and/or clause seems to be missing from the original stratification criteria I believe. One of these got a cold. 6 of the 9 that returned from the original “infected” group became “infected” again by the “viral shedding” and/or serum IgG criteria but no one got a cold. Everyone in the rechallenge that “shed” virus, did it substantially shorter than the first go round. All told, of the 14 that returned after a year one got a cold.
Though a small sample size, doesn’t this seem to fit the current understanding of infections in the pandemic? Of 15, 5 were “uninfected” but had an immune response and no symptoms (or is it signs?). Of the 10 “infected”, 8 got colds. So 5+2 or 7/15 were “asymptomatic” but generally mounted an immune response and virus could be cultured from some of this group. The people that got a cold had varying severities and all “shed virus” and none became symptomatic on rechallenge after a year.
Would love to hear the experts chime in.
Hello Immune Team,
Thanks so much for your informative podcast and for pivoting to devote so much recent effort to COVID-related topics. Much of what I know about immunology I’ve learned from your podcast and from TWiV. I’m sure that many listeners are like me in benefiting from your clear explanations of complicated topics. Below are a couple of recent papers about immune responses to SARS-CoV-2 that you might consider for future episodes.
C. Atyeo et al., “Distinct early serological signatures track with SARS-CoV-2 survival,” Immunity, doi:10.1016/j.immuni.2020.07.020, 2020.
Y. Zuo et al., “Neutrophil extracellular traps in COVID-19,” JCI Insight, doi:10.1172/jci.insight.138999, 2020.
B.J. Barnes et al., “Targeting potential drivers of COVID-19: Neutrophil extracellular traps,” J Exp Med, doi:10.1084/jem.20200652, 2020.
Thanks for your continued efforts!
Rick in Maryland
High Immune folks,
Or perhaps you are no more immune than the rest of us, only more aware of it. I’ve been listening to Immune and Twiv since April (or March. I started with TWIV 598). Having studied the physical sciences and worked as an engineer I am naive about things biological, but I hope I am learning a lot listening to you.
There is a question that nags at me. On the one hand I hear (from you) that SARS CoV-2 is not found in the blood since it infects the mucosa. On the other hand tests for antibodies look in the blood. This feels like a disconnect. How can antibodies in the blood protect against a virus that is not found in the blood?
I expect that I will continue listening to both Immune and Twiv long after SARS CoV-2 is no longer the central topic. Thank you for the wonderful work.
Jim — a mere Mathematician
Hello Wonderful Immune Hosts!
You all are just terrific, and since I’m never exactly sure when Immune will drop, I inevitably squeal a little with happiness when it shows up. Always a lovely surprise! Then it’s time to get pen and paper and commence listening and note-taking.
I have a quick question—what does “T cell exhaustion” mean? Does it mean that you’ve run low on that sort of T cell ( I’m guessing no)? Or does it mean that individual T cells are, well, tired? What would actually be going on (or maybe, NOT going on) in an exhausted T cell? How does cellular immunity recover from exhaustion?
Thank you all for all your work putting this show together, it’s a labor of love that I so appreciate. Brianne’s addition to the podcasts since the pandemic started is fantastic as well. I love hearing smart women scientists talk science! Thank you Vincent, for your amazing work to host all these podcasts and bringing these superstar people together. It’s why I donate to your Patreon—your podcasts are so valuable to me.
Cold mornings, mild warm afternoons these days 🙂
Dear Immune hosts,
I’m listening to ep. 34 from August 25. One small terminological nitpick that really bothers me: there’s no such thing as 67% homology. Homology is binary: either two peptides are homologous (share a common evolutionary origin), or they are not. What you’re talking about is *sequence similarity*, not homology. See e.g. https://www.cell.com/cell/pdf/0092-8674(87)90322-9.pdf
I also checked the original paper, and I didn’t find a single mention of “homology”. Instead they talk about “sequence identity” (misspelled as “identify”), which is also a correct term.
Also, you were wondering where 67% comes from. A possible answer is that 67% is 2/3 = 66.66… rounded to a whole percentage number.
Dear esteemed Immune hosts,
Can I thoroughly recommend TWIV 684 (Persistence of SARS-Cov-2 immune memory released 22nd November) to Immune listeners, especially the Shane Crotty conversation. One point Shane made got me thinking; around 75 minutes into the podcast Shane referred to work Stan Perlman had done on SARS which found that CD4+ T cells alone rather than specific B cells or cytotoxic T cells were able to control the SARS virus in animals.
This was the first time I have come across the suggestion that a CD4 T cell is able to control the response to a pathogen without involving B cells or cytotoxic T cells. Assuming I have this right, have the Immune Experts any thoughts on how this could occur? I immediately thought of gamma IFN activation of macrophages, but presumably it could also be via priming of epithelial cells (?increased MHC expression) or some NK cell activation?
Keep up the great podcasting…
Ps I thought this was more of a question for Immune than TWIV.
It is currently 89F and 57% humidity in Bangkok (18:00h). We had 3 additional COVID-19 case reported today, with a total YTD 3878 reported cases and 60 deaths.
In case you have not seen this already, this report is a good summary with numerous links to additional information and databases regarding diagnostics related to SARS-CoV-2/COVID-19.