Research news from Bhupesh Prusty

Reference to PG and friends at 6:31 —

"And there is the possibility that auto-recovery is possible within these first couple of weeks to months' time. So when we talk about the Long Covid a few people claim that they were sick for a couple of months, then all of a sudden they did yoga and all the other activities and they are all fine now. So they claim that this is all in the head and things like that. So we say that there is a biological mechanism to explain if there is involvement of these lytic viruses which tend to become latent. So... the body needs some amount of time to make the viruses back to latency again. And this is the time when auto-recovery is possible. But if damage goes to the chronic illness part, then you see all the subsequent events like the fatigue, [???] cell dysfunction and other things..."
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There are now 3 videos up at this site, which are a presentation by Dr. Prusty just split into 3 parts. I found watching the videos to be much more informative than trying to troll through that paper. in the third video he says that he thinks the next steps are to go to mouse models because it’s easier to study natural IGM processes in mice. He clearly separates out the differences in the results between patient populations. I’m certainly not qualified to make any comments on the science viability, but I did find him to be serious, well informed and not self promoting.

I would love to hear other comments on the videos.
 
Perhaps i am wrong about this specific research. But every other animal model of CFS i ever saw was utterly stupid.... believing you can give ME/CFS to animals by exhausting them. As if CFS were exhaustion! So i certainly hope he's not going to fall into that trap.

Surely not.... but nothing would surprise me these days!
 
JemPD said:
Perhaps i am wrong about this specific research. But every other animal model of CFS i ever saw was utterly stupid.... believing you can give ME/CFS to animals by exhausting them. As if CFS were exhaustion! So i certainly hope he's not going to fall into that trap.

Surely not.... but nothing would surprise me these days!
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next they will be subjecting the poor animals to childhood abuse/trauma, then making sure they are 'over achievers' by observing how industrious they are on the wheel, or paper shredding, and giving them some kind of virus just incase.
 
I understand and appreciate your humor, and I initially had the same reaction when I watched the video, but in this case I think these reactions are misplaced.

At about six minutes into the third and final video, Dr Prusty explains that the reason he would go to a mouse model is that the process of creating natural IGM in humans is not understood very well at all (“a black box“) and is much better characterized and understood in mouse models. thus he would go to most models to study the process of the creation of natural IGM (and its relationship to his findings?). I did not get the implication that he was creating a “fatigue” model, rather was going to it for a specific "natural IgM" related purpose. He was was speculating in response to a posed question at this point. Perhaps I understood it incorrectly, you can watch it yourself.

having said that, I personally always remember the bromide, “ mice lie and monkeys exaggerate”.
 
voner said:
At about six minutes into the third and final video, Dr Prusty explains that the reason he would go to a mouse model is that the process of creating natural IGM in humans is not understood very well at all (“a black box“) and is much better characterized and understood in mouse models.
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Yes but it is also significantly different in mice. They have a different range of immunoglobulin classes. Human natural antibodies are actually pretty well characterised in certain respects. That includes a specific VH4 gene called VH4.34 that mice would not have.

I am afraid that the whole idea of using animal models for immune disease (rather than normal immune mechanisms) has been pretty much a waste of time for fifty years now. You can prove that a harebrained idea of how something might cause disease in a mouse does cause disease in a mouse. But you can do it for 100 different harebrained ideas. 99 of those must be wrong for any particular human disease (if one is right) and that makes it a pretty reasonable bet that all 100 are wrong. The suffering caused to animals have been vast.
 
Jonathan Edwards said:
Yes but it is also significantly different in mice. They have a different range of immunoglobulin classes. Human natural antibodies are actually pretty well characterised in certain respects. That includes a specific VH4 gene called VH4.34 that mice would not have.
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@Jonathan Edwards, thanks. that is the kind of response I was hoping to enlicit.

I do wish more people would watch the videos and comment. In the final video Dr. Prusty gets asked “what next.“ that is about five minutes and 30 seconds in and for the next four minutes or so he does his speculation on what he would like to do in the future.
 
Meet Mikus Melderis. Mikus is the first doctoral student to join our new group (http://Prustyab.org) in Riga. Mikus is excited to develop 3D tissue organoids to mimic viral latency and reactivation in complex tissue environments. His primary aim is to develop several complex 3D brain organoid models to recapitulate various regions of the human brain using hiPSCs carrying latent viruses. Once he establishes these models and successfully reactivates latent viruses using different physiological stressors, he will conduct complex systems biology-based experiments to deep phenotype cells that allow virus reactivation. These approaches will allow him to understand the crosstalk between the host and pathogen at the single-cell level within complex tissue architecture. Mikus will collaborate closely with the Philipp Wörsdörfer group at University of Würzburg to achieve his goals. Our ultimate aim is to develop complex 3D tissue models to understand herpesvirus biology and its role in developing post-viral chronic illnesses.
https://twitter.com/user/status/1805905749790298523
 
Meet Liba Sokolovska. Liba is a talented doctoral student at RSU who will finish her doctoral studies soon. She has recently joined our new group (http://Prustylab.org) in Riga. Liba is excited to develop tools to understand calcium signaling within the cells. Calcium channels are deeply connected to mitochondrial biology, and we have a long-standing interest in understanding calcium signaling within human cells during viral infections and reactivation.

Everyone possibly knows how crucial mitochondria are for the cell, particularly during post-viral chronic illness. However, we often forget that other organelles, like peroxisomes, are equally critical for the cell, mainly when mitochondria become dysfunctional. Liba is taking up the challenge of understanding mitochondria and peroxisome crosstalk in post-viral chronic conditions. She will carefully delve into the close nexus of ER, mitochondria, and peroxisomes. Herpesviruses, particularly EBV and HHV-6, target these organelles, leading to a chain of events that affect cell physiology. Liba is also keen to understand the potentially complex role of Spike proteins in these processes.
https://twitter.com/user/status/1806344952634323347
 
Meet Zheng Liu (Stefan), a brilliant doctoral student in our group who has been working with us since 2022. Stefan is funded by ME Research UK and the Gordon Parish Charitable trust, UK. Stefan has been instrumental in our ME/CFS and autoimmunity work (http://Prustylab.org).
He focuses on understanding the proteome of human IgG and IgM within active immune complexes. Stefan has elegantly shown how IgG from ME patients causes mitochondrial dysfunction in specific cell types. We focus our work on understanding molecular mechanisms behind every scientific finding. We know IgG from ME patients contribute to secondary chronic illness. Still, the long-term implications of his research will depend upon knowing the exact pathways these IgG molecules affect.
Stefan has pioneered many experimental tools within the last two years, and he hopes to finish his doctoral work with at least two brilliant papers in the coming months. Stefan continues working in our small group at the University of Würzburg, Germany, under the umbrella of the Niklas Beyersdorf group. We hope that his work will be crucial for the future of our virology and cellular biology research in ME and the long COVID field.
https://twitter.com/user/status/1806612147641745766
 
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