Vice-Dean: Research and Postgraduate Students, Faculty of Science, Stellenbosch Univ; Honorary prof: Univ of Liverpool Research: coagulation, inflammation
Stellenbosch, South Africa
Joined April 2011
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@dbkell and I have a new preprint out. Watch this space also for proteomics data on plasma enriched with microclot complexes. Please see summary by @drwwalter in the link below.
What a fantastic paper - as a functional medicine doctor and member of CluB-12.org with a deep love for all the clinical and scientific aspects of Vitamin B12 I was on cloud 9 reading this landmark publication. Gemini has created notebooklm.link.google/RdBCP…
@FScholkmann and @dbkell This is of great importance as we believe that amyloidogenic platelet debris forms the seeding areas for one of our main microclot complex phenotypes.
Serotonin-driven platelet hyperactivation directly promotes extensive fibrin deposition in the microvasculature (Marotta et al., 2026: science.org/doi/10.1126/scii…)
This finding could be relevant to explain the formation of persistent fibrinaloid microclots. @resiapretorius
For those interested in PEM, see our perspective with lead author @fcowester.
link.springer.com/article/10…
PEM has traditionally been viewed as symptom exacerbation and/or emergence of new symptoms following exertion. This perspective proposes that PEM may instead reflect disrupted coordination across interconnected physiological systems operating over distinct post-exertional timescales.
Key questions
•Does PEM reflect disrupted coordination across physiological systems and timescales?
•Can distinct post-exertional physiological trajectories define patient subgroups?
•Does recurrent post-exertional physiological dysregulation contribute to cumulative cardiometabolic burden?
•How do the timing of assessment and disease heterogeneity influence the identification of post-exertional physiological trajectories?
•Can longitudinal cardiometabolic profiling identify biomarkers associated with distinct post-exertional trajectories?
Together, addressing these questions may help determine whether PEM represents disruption of the coordinated physiological responses that shape post-exertional physiological trajectories, and how these alterations contribute to the multisystem and cardiometabolic manifestations of ME/CFS and Long COVID.
Ultimately, advancing our understanding of PEM may require moving beyond symptom characterization toward the longitudinal investigation of post-exertional physiological trajectories across interconnected physiological systems and timescales, while integrating cardiometabolic health as an important source of biological heterogeneity, particularly in individuals with obesity and T2D, in future mechanistic and interventional studies.
It would be fascinating to see if drugs can be designed to prevent proteins to fold into an amyloid structure. @dbkell
Many drugs work by binding to a specific target in the body and blocking or changing what it does. An important first step in the drug development process is designing a molecule that can bind tightly to its target. Traditionally, that's meant weeks or months of expert work per target, sifting through a large number of candidates to identify the few that work.
We wanted to test if Claude could successfully design novel protein binders from scratch (also called de novo design). With a protein design prompt written by a human expert, Claude autonomously designed protein binders against 14 out of 15 targets.
We then worked with Adaptyv Bio and Twist Bioscience, who independently built and tested the proteins Claude designed.
Thank you @RenegadeRes! These are the types of patient/researcher/clinician engagements we need. Patients speak, researchers and clinicians thinks deep into what we might have seen in the lab and in the clinic. Sometimes aha moments might happen precisely when we share opinions and examples.
Thank you to everyone who attended our August 14, 2026 webinar ""Patients to Researchers: Lived Experience"! Such great and informative discussions
If you couldn't make it, here's the recording on our YouTube channel: youtube.com/watch?v=kxlUUgO4…
I am so happy to be involved in this wonderful initiative of @CODA_research. Together with leading researchers and clinicians in the field we will bring together a competent team of people to find ways to study and to treat damaged blood vessels, and the accompanying inflammatory, immune and clotting-related pathologies that so many patients with complex diseases suffer from.
Meet @resiapretorius Professor Resia Pretorius, Professor, Vice-Dean: Research and Postgraduate Students, and Program Chair of CODA's Vascular Initiative.
Professor Pretorius is helping lead research into how blood vessel health, circulation, and inflammation may contribute to complex chronic disorders and advance our understanding of shared disease biology.
Learn more about the CODA Vascular Initiative and CODA's Neuroimmune Research Portfolio:
hubs.la/Q04qxNwH0
#ComplexDisorders #Research #LongCOVID #MECFS #VascularResearch #NeuroimmuneResearch #MedicalResearch #PatientsCantWait
After some comments on biomarkers, I thought to add further thoughts.
I do not believe there is a single one and novel biomarker for #LongCOVID.
This is a multi-system disease, affecting different organ systems. Sometimes the organs that have already been vulnerable before acute infection(s), will be most affected.
By looking at various pathology lab biomarkers (e.g the list shared in a previous post), we can identify possible treatment targets.
Another point is that microclot complexes are definitely not unique to LongCOVID. The processes driving their presence, is circulating inflammatory molecules, immune dysfunction and vascular damage. Therefore we have been looking at their content, and searching for various modifications on proteins associated with them.
Something to keep in mind:
Each disease will have specific types of inflammatory molecules in circulation. We now know that even every patient will have a unique inflammatory molecule load.
We need to determine which inflammatory molecules, which post-translation modifications, and thus which pathways we should look at, to eventually decide on treatment.
Why is it so difficult?
There is not 1 single symptom or organ that is affected. Some patients will develop a diabetes profile, some will have an immune driven disease. The list goes on. Some will have viral persistence.
Because of this heterogeneous picture, we need personalised treatment, multiple biomarker panels and a clear understanding what each dysregulated lab result means.
To my X followers, including the fake and catfish accounts:
For some time I have been the target of sustained personal harassment on this platform, much of it from anonymous and impersonating accounts. I have stayed quiet and kept working. I am addressing it now, once, and then returning to the science.
I am not the only one. A number of researchers working on the biological basis of this illness, including collaborators of mine, have faced the same pattern of harassment. Much of it appears coordinated and comes from a small number of accounts whose interest is clearly not the science: their aim is not scientific debate; it is to intimidate people for doing research they do not like.
Targeting scientists for studying a disease is not scepticism; it is intimidation.
On the facts: the claim that our work "has not been replicated" is untrue. Independent groups have confirmed or applied these findings:
- the same aggregates were confirmed in pulmonary embolism (Baker et al., Communications Medicine, 2023);
- amyloid-fibrinogen aggregates predicted disseminated intravascular coagulation and mortality in sepsis (Schofield/Toh et al., Blood Advances, 2024);
-increased fibrinaloid microclots were found in Long COVID by an independent UK group (Dalton et al., Sheffield Hallam, preprint, 2024);
- and the methods have been taken up in paediatric Long COVID (Steifman, Yonker et al., Pediatric Research, 2026).
This is now a field with dozens of independent papers.
One thing to make very clear: I have no involvement in any apheresis or plasmapheresis treatment for these conditions. Why? It is simply not my field of expertise. I cannot control how others use published methods, and it is wrong to attribute their choices to me.
On Biocode, our start-up company: public universities have a clear responsibility to translate research into public benefit, and commercialising discoveries through spin-out companies is a core part of that mandate. That is precisely what Biocode was created to do. It is an early-stage university spin-out, it is not profitable, and repeated insinuations that I am personally enriching myself are false.
I welcome robust scientific criticism; that is how science works, and II have actively reached out to colleagues who see the field differently.
Harassment, account stalking, impersonation and personal attacks are not criticism. I am documenting it, I am taking advice on my options, and I will not be engaging with it further.
Just because biological researchers are targeted in this way does not mean we will stop. If anything, it strengthens our resolve to understand diseases and to serve the millions of patients who are waiting for answers.
There has been a discussion on X lately about biomarkers for #LongCOVID, so I thought I would share some blood markers available that might point to immune, clotting and endothelial dysfunction. Encouragingly, all of them are available at specialised pathology labs worldwide.
These are also the molecules we keep finding trapped in fibrinaloid microclot complexes across our various (proteomics) analyses: fibrinogen, von Willebrand factor, Factor VIII, serum amyloid A, complement proteins (C3, C4, C5, C1q, factor B), platelet factor 4, P-selectin, myeloperoxidase, neutrophil elastase, transforming growth factor beta-1, endothelin-1, vascular endothelial growth factor, Serum Amyloid A, and many more. We also know that many of our collaborators have also find these molecules in the soluble fraction of plasma, when when they have done proteomics and ELISA tests.
We have known for a while that these proteins are present in both the soluble and the insoluble fraction of plasma, mostly, we have just been searching inside the insoluble fraction of blood plasma for possible dysregulated inflammatory molecules that might in future, be targeted by treatment regimens. What is new in our approach, is that we have only recently started looking at post-translational modifications (PTMs), on proteins and we have found that some are extensively modified: glycated, oxidised, deamidated, citrullinated.
What is PTMs? A post-translational modification (PTM) is a small chemical change made to a protein after it has been built, that slightly alters the protein without changing its underlying identity.
A simple way to picture it: the protein is the basic product, and PTMs are the stickers, tags and add-ons attached to it afterwards. The item is still the same item, but the additions can change how it looks and behaves, whether other things can grab onto it, and how long it lasts.
In the body, these tags get added in response to conditions like inflammation, high blood sugar or oxidative stress. Common examples are sugar molecules stuck on (glycation), oxygen damage (oxidation), or other small chemical groups. The protein's amount in the blood can look completely normal, while these tags quietly change how it works, which is exactly why a routine test can read "normal" and still miss the problem.
Also note that much earlier work by well-known researchers in the fibrinogen field has found post-translational modifications on fibrinogen in various inflammatory diseases.
More to come from our research group! Please, in the mean time see a the table below. These might be some valuable biomarkers that might to used in clinical investigations and might assist clinicians to target some symptoms.
@dbkell and I have also discussed possible devices like capillaroscopy for detecting vascular damage. @ImmunoFever has recently discussed the applications in numerous posts.
Lastly, this is in no way suggesting that these are the only biomarkers, it is just a small snapshot molecules our lab is finding and studying. There are numerous more biomarkers that can be looked at for neuro-immunology, muscle and many more systems.
1/3 Just another link to one of our latest papers: How do prothrombotic (amyloidogenic) microclot complexes form and what do they tell us once present? Are these complexes the single cause of a particular disease?
nature.com/articles/s41419-0…
Exactly, and if we do not stratify patients according to phenotypes, before enrolling them into trials, we are setting ourselves up for failure.
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@surf4children you are right. We should move on from thinking: “1 biomarker” for complex disorders like #longCOVID. Why would we think “1 medication” would work. We need to understand what exact biological pathway drives the disease in a specific patient. We need personalised and precision care. We need single proteomics analysis for every patient. Even then it will not be 1 magic pill.
I have great respect for the Long COVID and ME/CFS patient communities—for their resilience and for the active role they have played in advancing the recognition and understanding of these illnesses. I always learn a great deal from you.
However, when it comes to having open discussions—which I always welcome—I have to say that at least part of the community can become very aggressive at times, even bullying, and unwilling to accept differing viewpoints.
My point about biomarkers was clear: I myself am involved in ongoing research on them. However, I think it will be difficult to identify a biomarker that is valid for everyone and internationally accepted. If that turns out to be the case, I don’t think things will change dramatically, because it should still be possible to diagnose patients, provided there is the will to do so.
We will not give up 🫶🏻@fidjissimo @CODA_research
Today, I shared with the OpenAI team that I have decided to leave my full-time role at OpenAI and transition to being a part-time advisor.
Three months ago, I had to go on medical leave after a severe exacerbation of a chronic illness I’ve lived with for seven years. During that time, it became clear that the road to recovery would be much longer and more complex than I had anticipated—and that I needed to focus on it fully.
When I went on leave, many people told me I was courageous for prioritizing my health. The truth is that I am only making this decision now because I failed to make it many times before.
Over the years, doctors, friends, colleagues, and loved ones encouraged me to slow down. Two years after I got sick, Facebook offered me the opportunity to take a full year of medical leave. I didn’t even pause to consider it. I immediately said no. At the time, Zuck told me I should play the long game. I wish I had listened.
Looking back, I realize that a lot of what made me successful also made this decision incredibly difficult.
I grew up believing that opportunities were precious and that when they appeared, you grabbed them with both hands. That mindset carried me from a small town in southern France to opportunities I never could have imagined. By the time I turned 40, I had already gotten to do more than I’d ever dreamed possible as a kid growing up in Sète.
I love building. My work has always given me a deep sense of purpose. OpenAI in particular felt like a role that my entire career had been building toward, which made this decision even harder.
But what I’m learning now is that grit and endurance are not the only skills required to have impact over decades. Sometimes the harder thing is to stop, listen, and trust that taking care of yourself today makes it possible to contribute for much longer tomorrow.
This experience has also strengthened my conviction about why this work matters.
It has been a jarring experience to spend my days helping build the future while simultaneously navigating a disabling disease that still has no cure.
Over the last seven years, I’ve spent countless hours in doctors’ offices, dealing with symptoms, treatments, insurance, uncertainty, and all the invisible work that comes with being a patient. Like millions of others living with chronic illness, I’ve experienced firsthand how difficult healthcare can be to navigate, even when you have every possible advantage.
More than ever, I believe that some of the most important opportunities for AI lie in helping people solve real problems in their daily lives: their health, their finances, their time and the everyday burdens that shape human experience.
In particular, curing disease is the most important thing AI could accomplish. I’m excited to continue working towards cures through OpenAI but also through my work with @ChronicleBioAI and @CODA_research.
I’m deeply grateful to @sama, @gdb and the OpenAI board for their support during this time and for offering a way for me to continue contributing to the mission without sacrificing my chances of recovery. I’m also so thankful to my team and the many extraordinary colleagues I’ve had the privilege to build alongside.
For now, my focus is recovery. But my belief in the potential of technology to solve deeply human problems has never been stronger.
We and others looking for fibrinaloid microclot complexes, always do analysis on fresh blood plasma samples or plasma spun and stored at -80. We do not support dried sample analysis and any shipment at room temp. One must also be careful, as tissue paper fibers can show autofluorescence. However, we cannot comment on this exact photo.
Have you ever found one of these fibers that look like textile fibers but that have been stained by fibrinogen antibodies? (sars2.net/clot3.html#Further…) McCairn claims this string-like fiber somehow formed spontaneously when he simply mixed fibrinogen with ThT and shook the mixture:
I am so excited to share that @CODA_research, with CEO @amyrochlin and founder @fidjissimo is supporting collaborative research endeavours between my lab and @ImmunoFever lab. Watch this space! We are focusing on #capillaroscopy and vascular damage in #LongCOVID and complex disorders.
gokocamera.com/en/products/m…
CODA supports international collaboration between Stellenbosch University and Massachusetts Institute of Technology to advance microvascular research in complex chronic disorders, via @EurekAlert! @scienceSUN eurekalert.org/news-releases…
😁😁@angryhacademic “sounds” fascinating
@resiapretorius in case this is near you and you fancy destroying your ear holes 😆
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So excited to publish this paper with @DrMark_Faghy and a wonderful team of dedicated researchers and clinicians. One paper at a time, let us keep on making a difference!
After a slight delay.. our new article:
Current status and future perspectives on the mechanistic and pathophysiological understanding of long COVID
Is here: nature.com/articles/s43856-0…
We are excited to invite abstracts to the @ISLCPAIS conference in Amsterdam, 26 to 29 August 2026! We have a fantastic lineup of researchers and clinicians that will share their latest perspectives.
CALL FOR ABSTRACTS – ISLC-PAIS Conference 2026
Researchers, clinicians & interdisciplinary experts:
Shape the future of Long COVID & PAIS.
🗓 Abstract deadline: 15 May '26
📍 Amsterdam: 26 - 29 Aug '26
#LongCOVID #PAIS #CallForAbstracts #MedicalResearch
islc-pais.org/abstract-submi…
This is great news! Now we need to show that these accumulations are amyloid in nature.
Dr. David Izquierdo and his team developed the novel radiotracer [64Cu]-FBP8 that can identify fibrin accumulation in the lung, brain and heart tissue of Long COVID patients when visualized with PET. “Now the question is; can we [use this technology] with patients that have symptoms, but don’t have any clinical evidence,” said Izquierdo. “What we’re trying to do here is determine if Long COVID has a signal that we can measure, quantify and detect in vivo, noninvasively.”
1/8) We are excited that our paper has been published with lead author @maxinewaters250 and @dbkell
In this study, we investigate Post-Vaccination/Post-Infection Syndrome (PV/PIS) and its underlying biology.
🔗 frontiersin.org/journals/cel…
