T. Ryan Gregory Profile picture
Apr 5 4 tweets 2 min read Twitter logo Read on Twitter
The Provost at @uofg has never taught a course here at any level of any size.

I have taught >10,000 students, at every level from 1st year through 4th year and post-graduate. Huge lectures and small seminars, classroon/lab/field, in person and remote, solo and team taught.

1/
I think about this fact when I hear of possible decisions from the top like "cancel all courses with enrollments less than 15 students". I think about how I have taught courses with 400, 600, even 1,000 students, and other courses with 10 or 12.

2/
Some of the most impactful courses I have done -- for the students and for me as an educator and scholar -- have been in-depth, small discussion format courses and field courses. Those can be life-changing for students, lead to grad student recruitment, and inspire research.

3/
Only administrators with no real world experience at an insitution and no imagination would ever even consider a policy like that. Only arrogant micromanagers who have no trust in their people would refuse to let instructors and departments decide on such issues.

#SaveUofG

4/

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More from @TRyanGregory

Apr 6
Just to keep things clear(ish) if you're trying to follow variants:
🧵

XBB.1.5 ("Kraken") is the dominant variant in the world right now. We haven't seen this level of dominance by a single variant since pre-Omicron-soup.

public.tableau.com/app/profile/ra…

1/
Fortunately, and as some of us said from the outset, XBB.1.5 (Kraken) has not caused major waves of infections/hospitalizations/deaths. However, it has contributed to the pattern of ups and downs around an unsustainably high baseline in many places.



2/
With some very notable exceptions (e.g., China, where it's largely BF.7.14 and BA.5.2.48 derivatives), there are very few BA.5* lineage variants still present in significant percentages, after BA.5s (incl. BQ.1/BQ.1.1) caused waves in some places.

public.tableau.com/app/profile/ra…

/3
Read 8 tweets
Apr 5
In terms of COVID origins, I think I'm here these days as a casual obvserver of the debate:

Extremely unlikely:
* Bioweapon unleashed intentionally

Unlikely:
* Bioengineered, released by accident

1/5
Plausible:
* Natural virus collected from bats and brought to the lab for study, escaped by accident

Very plausible:
* Zoonotic origin

Both of the the plausible scenarios above should inspire thought and action to reduce future risk, imho.

2/5
But, as I've said, I am not following this closely and I'm far more concerned about all the evolution that has occurred since SARS-CoV-2 started spreading in humans.

It just seems like the debate is a mess, and the claims are way too strong both ways.

3/5
Read 5 tweets
Apr 1
I should be clearer about this one as well. It's not that children don't mount any immune response (they do, and vaccines work in kids too).

It's that it's not obvious that just exposing kids to SARS-CoV-2 means it'll become no big deal as adults.



1/
We don't know enough about the strength and duration of immunity conferred by infection in kids, especially relative to risk. Vaccines seem to work pretty well in children (vs. severe acute illness at least), but is that long-term? How much does it wane and how quickly?

2/
What is the significance of the fact that children seem to exhibit a much lower adaptive immune response to SARS-CoV-2 infection than adults? Remember, minimizers said this was good because children clear the virus effectively. It's not obvious how one can have it both ways.

3/
Read 5 tweets
Apr 1
Ok, I was pretty glib and imprecise about ACE2 binding of SARS-CoV-2 being one possible distinguishing factor, so to be clearer:

🧵

* The question was whether there is nothing special or different about SARS-CoV-2 other than the fact that it's new in humans.

1/
* Three of four common cold coronaviruses known so far don't use ACE2. Two of the three very bad ones from the past 20 years do (SARS1 and SARS2 do, MERS doesn’t).

2/
* One of the common coronaviruses, HCoV-NL63 does use ACE2.

* So, obviously, simply binding to ACE2 is neither necessary (MERS doesn't) nor sufficient (NL63 does) for being very bad. I'm not claiming that it's just about ACE2.

3/
Read 8 tweets
Apr 1
If the only factor that determines whether a new coronavirus will kill and disable millions of people is simply that it's new, and nothing about the virus itself, that's quite concerning given that there will be more of them coming.
We've had three very bad coronaviruses come from bats in the last 20 years. One of them reached pandemic level. Not only are climate change and habitat encroachment allowing more zoonoses, our activities are also increasing viral abundances in bats.

science.org/doi/10.1126/sc…
On the other hand, if SARS-CoV-2 is notably different in some way (e.g., the sheer number of organs it can damage, how transmissible it is, how fast it evolves, etc.) and that's why it was fast worse overall than SARS1 or MERS, that would be a less terrible scenario in some ways.
Read 4 tweets
Mar 31
People who claim that repeated SARS-CoV-2 infections in children will result in them building up immunity such that infections in adulthood will be mild need to explain how this occurs when children do not develop adaptive immune memory to SARS-CoV-2.

news-medical.net/news/20230126/…
Read 4 tweets

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