Jason Yeung

No, haven’t seen any. I vaguely remember a few professional level dancers posting about lingering issues years ago on Instagram but that’s the extent

As someone who previously knew little about Orientia tsutsugamushi, it was surprising to learn how many cases there are: "Within endemic regions, commonly known as the tsutsugamushi triangle, there are an estimated one million cases annually[...]". Currently working on something related

The preprint is out! Congratulations to @ywangapril.bsky.social on this investigation into leading DENV drugs. Possible in large part due to the AViDD center grants…

Mechanistic insights into dengue virus inhibition by a clinical trial compound NITD-688 | PNAS Dengue, caused by the dengue virus (DENV), presents a significant public health challenge with limited effective treatments. NITD-688 is a potent p...

Happy to share our recent study on the mechanism of a clinical #DENV inhibitor, NITD-688. For someone with a background in biophysics, it's also a learning journey into #virology, #antiviral, and academia/industry collaboration. Thanks Xuping, Pei-Yong and all the collaborators at UTMB/Novartis!

The furin cleavage site is required for pathogenesis, but not transmission of SARS-CoV-2 https://www.biorxiv.org/content/10.1101/2025.03.10.642264v1

Druggable genome screens identify SPP as an antiviral host target for multiple flaviviruses

www.pnas.org/doi/10.1073/...

Unfortunately, persistent SARS-CoV-2 seems to be confined to tissues. If a good cell/animal model for SARS-CoV-2 persistence was available, parameters from models could be adapted to understand dynamics and feedback loops required for persistence. Until then, the focus is understandable.

A lot of discussion re: assay development and tissue-level sampling for persistence. To really get at how persistence is generated needs measurable longitudinal markers amenable to mathematical modeling akin to viral load for HIV. Modeling was transformational for treatment strategies there.

This gene and PLSCR1 keep showing up in host factor CRISPR screens. Still ambiguous what they exactly do but definitely act early before interferon. Interestingly, DAZAP2 KO largely shows up as a hit when the screen has an earlier end point (shorter than 4-7 days)

Will the choroid plexus be sampled alongside other CNS tissue being examined? Despite substantial evidence for potential infection, most non-LC autopsy studies skip sampling it.

I've actually been learning Rust over this past year in large part because I kept seeing you post about it on twitter lol. Your evangelizing is working

I find it remarkable how SARS-CoV-2 remains out-of-phase with the other respiratory viruses. Hasn’t settled down to being a mainly winter infection yet.

Thoughts?

People keep telling me I should monetize it but I have no idea where I want to go with this now. Ballet was 10 years ago now. As I get more into medicine and try to wrap up my PhD, I'm finding I have less and less time and I'm finding it hard to let it die.

I love the quote "You can just do things." This was the biggest shift in thinking from this. I felt like this was my first step from being a consumer to a do-er.

In roughly 3 years, I was a leader in this niche thing of ballet analytics because no one else really did it. I've met tons of people online and it's helped my science career directly. The project website popped off and receives way more traffic than any journal article I've written (so far 🙃).

Once I learned R, I decided I was going to study ballet trajectories as a side project. To be honest, it felt trivial at the time. I learned shiny, the tidyverse, and Quarto because of it.

I just kept doing it for years and people started to notice. I shared the data freely, making some friends.

After some injuries, I read the signals--moved back home, loafed around for a year, and went to college. Yet, I had this idea that I had mismanaged my short ballet career. When I was in, I didn't research companies well and generally had no real sense of what my chances of progression were.

6 years ago, I started a data science project that landed me a board position at a non-profit featured in the NY Times.

My first career was as a professional ballet dancer straight out of high school. I was good enough to stick around and keep jobs but not to advance quickly. ->

Thrilled to share our latest work identifying that #SARSCoV2 #Omicron variants harboring an L260F mutation in NSP6 have enhanced replication and pathogenesis. A not so brief thread 🧵

A One Health Investigation into H5N1 Avian Influenza Virus Epizootics on Two Dairy Farms In early April 2024 we studied two Texas dairy farms which had suffered incursions of H5N1 highly pathogenic avian influenza virus (HPAIV) the previous month.

In CID, Ismaila Shittu, PhD, and colleagues studied two Texas dairy farms which had suffered incursions of H5N1 highly pathogenic avian influenza virus (HPAIV) the previous month.

Hi Bluesky, just in time for the holidays I am excited to share the latest pre-print from my group! We solved the 3D structure of a mysterious viral RNA that resists degradation by host nucleases. A short 🧵 &link below – please also check out the full video! #RNA #RNAbiology #RNASky #lovevirology

Mechanistic Insights into Dengue Virus Inhibition by a Clinical Trial Compound NITD-688 Dengue, caused by the dengue virus (DENV), presents a significant public health challenge with limited effective treatments. NITD-688 is a potent pan-serotype DENV inhibitor currently in Phase II clin...

It's been a momentous few years for both Dengue and DENV antiviral development - particularly for the JNJ and NITD NS4B inhibitors. New preprint from my thesis lab sheds some light on the differences between the two companies' compounds (they don't work the same way): www.biorxiv.org/content/10.1...

1/ PolyBio’s Dr. Sara Cherry asserts: “Treating [the lung] with either nirmatrelvir (Paxlovid) or molnupiravir, we clear the [SARS-CoV-2] infection by 10,000-fold… while nirmatrelvir clears the infection in intestinal cultures, molnupiravir has no activity.”

Doing adventofcode.com to build up those Rust skills! 🎄🦀 Joined late but it's resolving my "I have no reason to use Rust" dilemma

Letter sent in to the Editor of the Guardian on brain microbiome nonsense.

Our study describing inherited DBR1 deficiency leading to SARS-CoV-2 brainstem encephalitis in @jexpmed.bsky.social made the cover! DBR1-mutated hindbrain neurons are susceptible to SARS-CoV-2. Great collaboration with the Rice, Studer, Casanova, Ekwall & Zhang teams.

doi.org/10.1084/jem....

A picture of organized text. The text reads: - Do homologous, non-homologous, and sgRNA non-homologous recombination all involve the same copy-choice process? - I'm leaning towards some aspects are shared but sgRNA production is generally a more "regulated" process. - Can the frequency of de novo non-sgRNA, non-homologous recombination events be explained by polymerase processivity? - Recombination frequency for SARS-CoV-2 is much higher than other human coronaviruses (MERS-CoV, OC43). Is polymerase processivity correlated with recombination frequency for these viruses? The presence of hotspots already suggests a more complex mechanism than the traditional "fall off, reattach" copy-choice model but this would also. Measurement of processivity is complicated by to processivity-improving proteins nsp7 and nsp8. - Multiple potential mechanisms for promotion of inflammation in nsp15 mutant - Increased dsRNA-induced signaling pathways - Accumulation of DVGs may itself be immunomodulatory - How much of the transcriptomic signal is due to each component? - > "This ~2-3 fold reduction in recombination JFreq indicates that the in vivo environment restricts accumulation of recombination events." - Wonder if this is true in bats as well? Host cells that tolerate high recombination frequencies and multiple coronaviruses could be sites that allow for novel coronavirus emergence through recombination

A picture of organized text. The text reads: - Comparing recombination breakpoints from cell culture vs virions vs *in vivo* vs genomic surveillance has information - A sort of deep mutational scanning dataset for deletions - Comparison of virion enriched sequences and intracellular sequences could support packaging sequence for SARS-CoV-2 (believed to be in nsp12-nsp13) - Terasaki K, Narayanan K, Makino S: **Identification of a 1.4-kb-Long Sequence Located in the nsp12 and nsp13 Coding Regions of SARS-CoV-2 Genomic RNA That Mediates Efficient Viral RNA Packaging**. *Journal of Virology* 2023, **97**:e00659. - Another UTMB lab ☺ - Comparison of cell culture with *in vivo* indicates which are subject to additional (likely immune) selective pressures in hamsters - Comparison of virions with genomic surveillance could indicate which are replication viable and demonstrate sufficient amounts of fitness

What a paper. I somehow missed all of the UTMB seminars about this work. There sorely needs to be an updated review article on the molecular basis for coronavirus recombination because I keep getting lost in the weeds. Some thoughts: