Resia Pretorius (@resiapretorius) header
Resia Pretorius (@resiapretorius) profile picture

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
Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)Photo by Resia Pretorius (@resiapretorius)
Replying to @dbkell
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…
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Resia Pretorius retweeted
A new study of more than 1.2M adults found that people with Long COVID had a 14% higher adjusted hazard of developing hypertension. One important question is whether endothelial and microvascular dysfunction contribute to this increased risk. Our smallest blood vessels play a critical role in regulating circulation and delivering oxygen to tissues. Persistent endothelial injury, inflammation, and abnormalities in microvascular blood flow may disrupt these functions, with consequences for both tissue perfusion and cardiovascular regulation. At CODA, we're investigating these mechanisms through our Vascular Initiative, led by Professor @resiapretorius. We're also collaborating with Dr. Mikki Tal's team (@immunofever) at MIT on the CAPRIO study, alongside @mhornig, @technopolymath, @TomerTalVH, and others, as part of the @HHSGov TOPx HHS Tech Sprint for AI and Invisible Illness. (Stay tuned as more info on this out this week!) We're working to better understand what happens in the microcirculation, how immune-mediated clotting and endothelial dysfunction may affect blood flow, and which abnormalities can be measured and targeted with treatments. It's important to connect these biological findings to what patients actually experience, and determine whether restoring microvascular and endothelial function can improve their symptoms, daily functioning, and overall health. Let's take science from the lab and put it into the hands of patients. @CODA_research complexdisorders.org/coda-va… ahajournals.org/doi/10.1161/…
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Resia Pretorius retweeted
One of the many tragedies of ME/CFS is that patients can remain trapped with the same unresolved ideas for years or decades because they lack the health, energy, access, or opportunity to reality-test them. They repeat the same stuff over and over again because nothing ever resolves it, while people with the resources to test these ideas often fail to engage deeply enough to understand what patients are actually saying. Even for the most eugenicist pricks, it must be clear that certain positions confer informational advantages. Patients are not inherently right. Like everyone else, they will often be wrong. But being forced to inhabit a particular reality can expose signals that are extremely difficult to perceive from outside it.
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Resia Pretorius retweeted
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
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Resia Pretorius retweeted
What did we learn at the 2026 ISLC-PAIS Conference? And what does it mean for #LongCovid #MECFS #PAIS patients? Join today’s live Patient Recap Session for an accessible summary of the most important insights, discussions and takeaways Watch online for €15: Please share! 🧡 islc-pais.org/patient-recap
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The CODA Vascular Initiative is advancing research to better understand how changes in blood flow, inflammation, and oxygen delivery may play a role in complex chronic disorders. Help accelerate the CODA Vascular Initiative by making a gift today: complexdisorders.org/researc… #ComplexDisorders #MedicalResearch #BiomedicalResearch #VascularResearch #ChronicIllness #TranslationalResearch #PrecisionMedicine #ResearchMatters
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Resia Pretorius retweeted
Why this new PEM paper matters One of the most disabling features of Long COVID and ME/CFS is post-exertional malaise (PEM) — the “crash” that can happen after doing something that would once have been completely ordinary. For years, PEM has largely been described by what people feel: overwhelming exhaustion, brain fog, pain, flu-like symptoms and worsening of other symptoms after physical or mental exertion. This paper asks us to look at it differently. Imagine the body as a collection of interconnected systems. When a healthy person exercises, those systems are temporarily pushed away from their normal state. Heart rate changes. Metabolism changes. Muscles use more oxygen and energy. Hormones, blood vessels and the nervous system all respond. Then something important happens: The body resets. The different systems gradually return towards their normal state. The researchers propose that PEM may involve something going wrong with that recovery process. Instead of all those systems coordinating their return to normal, some may recover too slowly, some may remain abnormal and others may move in completely different directions. In other words, the PEM “crash” might be what it feels like when multiple physiological systems fail to properly reset after exertion. That’s potentially a very important idea because it changes what scientists should measure. Rather than simply asking someone how they feel after exercise—or taking one blood sample—they could follow people for hours or days afterwards and watch how metabolism, circulation, the autonomic nervous system, immune activity and other systems change over time. And different people may have different patterns. That could eventually help researchers identify different biological types of PEM and, importantly, treatments aimed at whatever part of the recovery process has gone wrong. This paper doesn’t prove this mechanism, and it hasn’t discovered a treatment or diagnostic test. It’s a scientific perspective proposing a framework that now needs to be tested. But I think the question it asks is an important one: Perhaps PEM isn’t simply about what exercise does to the body. Perhaps it’s about what the body fails to do afterwards. And if researchers can work out exactly where that recovery process breaks down, we may finally get much closer to understanding one of the defining features of Long COVID and ME/CFS. AI disclosure: I used AI to help research and draft this post. I reviewed and approved the final content.
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.
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Resia Pretorius retweeted
Whilst every individual’s experience is unique, it is striking how many shared themes emerge across the PEM survey responses. When people from all walks of life describe similar physical experiences, it offers a powerful insights into ME/CFS. tinyurl.com/PEMimpactME
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Resia Pretorius retweeted
Replying to @kadamssl
We believe there is real value in bringing researchers together in the same room, to present new findings, challenge each other's work, build collaborations and allow early-career researchers to meet and learn directly from established experts. Those interactions are an important part of what a scientific conference is designed to achieve. Every name you see on our website will be there in person. islc-pais.org/program
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Resia Pretorius retweeted
This piece was hard to write. It's hard to read. Most importantly, it's hardest to live. @CODA_research and our partners won't accept 400M+ people losing their lives to chronic illness. We've built a model to bring real answers. Please read my latest blog here: 👇 complexdisorders.org/our-ceo…
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Resia Pretorius retweeted
Persistent One-Year Mortality Gradient After STEMI and COVID-19: Long-Term Outcomes From the NACMI Registry 🚨45% one-year mortality( Large North American NACMI registry study). ➡️ST-elevation myocardial infarction (STEMI) + COVID-19 patients had nearly 4× higher death rates than pre-pandemic controls (45% vs 11%), ➡️Even STEMI hospital survivors faced lasting risk, the mortality gradient didn’t stop at discharge, ➡️“The cause is likely multifactorial, including pandemic-era disruptions in care, longer time-to-treatment, and THE UNIQUE PATHOPHYSIOLOGY OF COVID-19 STEMI.” ‼️So, persistent long-term risk in COVID-19-associated ST-elevation myocardial infarction (STEMI)! #AvoidSars #AvoidReinfections jscai.org/article/S2772-9303…
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Resia Pretorius retweeted
I'm so excited for this! Come learn how to look at your microvasculature and maybe even join us in the launch of our upcoming clinical study looking non invasively at your circulation.
🧵 1/2 For 10 years, Project Lyme has brought patients, researchers, clinicians, advocates, and supporters together to help move Lyme research forward. Dr. Michal Tal @ImmunoFever from @MIT will join us at our upcoming Gala to celebrate what collaboration can make possible.
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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.
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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.
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Resia Pretorius retweeted
Never underestimate SarsCoV2, a virus that keeps surprising! 👇
Could fibrinogen be an unexpected accomplice of SARS-CoV-2? ➡️ A striking mechanism suggests that Spike can bind fibrinogen and potentially use this interaction to engage integrins on endothelial cells, providing an alternative route beyond ACE2 and potentially contributing to vascular injury. 1/
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Resia Pretorius retweeted
Could fibrinogen be an unexpected accomplice of SARS-CoV-2? ➡️ A striking mechanism suggests that Spike can bind fibrinogen and potentially use this interaction to engage integrins on endothelial cells, providing an alternative route beyond ACE2 and potentially contributing to vascular injury. 1/
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Resia Pretorius retweeted
The awe factor: the virus may be exploiting a protein normally central to blood clotting as a molecular bridge to the vascular endothelium—potentially linking viral entry, thrombosis and post-COVID vascular disease. 2/2 pubs.acs.org/aptsfn/article-…
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Resia Pretorius retweeted
Looking forward to introducing @resiapretorius and calling out CODA's Vascular Initiative at @ISLCPAIS. Important science needs to move out of the lab and into the hands of patients. Most of all, enhancing expanding testing availability so we can better identify blood vessel and blood flow problems in individual patients and use that information to deliver the right treatments.
The Complex Disorders Alliance (CODA) is a sponsor of the 2026 @ISLCPAIS International Scientific Long COVID & Post-Acute Infection Syndromes Conference. CODA CEO @amyrochlin will introduce Professor @resiapretorius, whose research has advanced our understanding of vascular dysfunction and its potential role in complex chronic disorders. Conferences like ISLC-PAIS create opportunities to share emerging research, strengthen scientific collaboration, and accelerate progress toward better diagnosis and more effective treatments for patients living with complex chronic disorders Learn More: hubs.ly/Q04ssyYN0 #PostAcuteInfectionSyndrome #LongCOVID #MedicalResearch #ComplexDisorders #PatientAdvocacy #TranslationalResearch #ResearchCollaboration
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