Galectin-3 in Long Covid is emerging as a key factor in abnormal clotting, inflammation, and persistent symptoms.
Two leading scientists, Prof. Resia Pretorius and Dr. Douglas Kell, have uncovered key insights into why long COVID causes blood clotting issues. Their groundbreaking research highlights abnormal clots, the role of a protein called galectin-3, and potential treatment options for the millions living with long COVID worldwide.
What’s Happening in the Blood of Long COVID Patients?
People with long COVID often experience symptoms like fatigue, brain fog, and shortness of breath. Prof. Pretorius and Dr. Kell’s research shows these could be caused by unusual blood clots that disrupt circulation.
The Two Types of Clots
- Amyloid Fibrin Microclots
- These clots are made from fibrinogen, a protein in your blood. In long COVID, fibrinogen becomes misfolded, turning into sticky clumps, similar to tangled hair.
- These microclots trap inflammatory molecules, making it hard for your body to break them down and worsening symptoms.
- Hyperactive Platelet Clumps
- Platelets, the blood cells that stop bleeding, become overactive in long COVID. They form clusters that can block blood flow, like a traffic jam on a motorway.
How Do Scientists Detect These Clots?
The researchers used advanced tools to study blood from long COVID patients:
- Flow Cytometry: This tool works like a blood traffic monitor, counting and analyzing blood cells to reveal abnormal clotting patterns.
- Fluorescent Microscopy: A technique that uses dyes to make clots glow, showing their amyloid-like structure.
These tools provide clear evidence that these clots are biologically different from normal clots.
What’s the Role of Galectin-3?
Galectin-3 is a protein found in the body, but in long COVID, it acts like superglue, making clots stickier and harder to remove.
- Galectin-3 also triggers inflammation and tissue scarring (fibrosis), creating a vicious cycle that worsens long COVID symptoms.
- High levels of galectin-3 in long COVID patients make it a promising target for treatment.
Potential Treatments Based on These Findings
Pretorius and Kell’s work opens the door to several new treatment possibilities:
- Anti-Galectin-3 Drugs
- Drugs targeting galectin-3 are already being tested for other conditions, like heart disease. These could help reduce inflammation and dissolve clots in long COVID.
- Amyloid-Busting Therapies
- Medicines used to treat Alzheimer’s disease, which also target amyloid clumps, could be repurposed for long COVID.
- Anti-Inflammatory Treatments
- Reducing overall inflammation could stop these clots from forming. Lifestyle changes, anti-inflammatory diets, and specific medications might help.
- Improved Diagnostics
- Tools like flow cytometry and fluorescent microscopy could help identify patients with these clotting issues earlier, leading to faster and more effective treatment.
Challenges and What We Don’t Know Yet
Despite these exciting findings, many questions remain:
- Who is at risk?
Not everyone with long COVID develops these clots. Why some do and others don’t is still unclear. - Reinfection Concerns
Can getting COVID again worsen these clots? More research is needed. - Treatment Risks
Anti-clotting therapies need to be carefully balanced to avoid increasing the risk of bleeding. - Lingering Virus Fragments
Some evidence suggests fragments of the virus might remain in the body, fueling ongoing inflammation. This theory needs further investigation.
Why This Research Is Important
This groundbreaking research validates the experiences of long COVID patients, proving their symptoms are real and rooted in measurable biological changes. The findings also highlight the urgent need for more funding, research, and attention to long COVID—an issue still affecting millions globally.
What This Means in Real Life
The idea of microclots and galectin-3 can feel abstract, but it helps explain something many people with Long Covid experience.
Symptoms often do not behave like a typical respiratory illness. Breathing feels difficult even when oxygen levels are normal. Fatigue does not improve with rest. Muscles feel weak or heavy after minimal effort.
If microcirculation is impaired even subtly tissues may not receive oxygen efficiently, particularly during exertion. This does not always show on standard tests, but it can still affect how the body functions.
This is one reason symptoms can feel disproportionate to what scans or blood tests show. The issue may not be large, visible damage, but small-scale dysfunction happening across multiple systems at once.
This also helps explain why symptoms fluctuate. If circulation, inflammation, and clotting activity change from day to day, capacity changes with them.
What is galectin-3 and why is it relevant in Long Covid?
Galectin-3 is a protein involved in inflammation, immune response, and tissue repair. In Long Covid, emerging research suggests it may play a role in amplifying inflammation and stabilising abnormal clot structures, including microclots.
This matters because it connects two key features seen in Long Covid — persistent inflammation and impaired microcirculation. Rather than being a standalone issue, galectin-3 may act as a bridge between these processes, helping explain why symptoms like fatigue and breathlessness can persist even when standard tests appear normal.
Does targeting galectin-3 offer a real treatment option?
t is a promising idea, but still experimental.
Drugs that target galectin-3 are already being studied in other conditions, particularly those involving fibrosis and chronic inflammation. In theory, reducing galectin-3 activity could help break the cycle of inflammation and abnormal clot stability seen in some Long Covid patients.
In practice, these treatments are not yet approved or widely available for Long Covid. Clinical trials and further research are needed to determine whether targeting galectin-3 leads to meaningful symptom improvement, and for which group of patients it might be most relevant.
Is there strong evidence that microclots and galectin-3 cause Long Covid symptoms?
The evidence is growing but not yet definitive.
Studies from researchers like Resia Pretorius and Douglas Kell have identified abnormal clot structures and associated inflammatory markers in Long Covid patients. Galectin-3 has been proposed as one of the factors that may contribute to their persistence.
However, this is still an active area of research. Not all studies find the same results, and the exact role of microclots and galectin-3 in driving symptoms is still being clarified. At present, it is best understood as a plausible and increasingly supported mechanism, rather than a confirmed single cause.
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Disclaimer: This blog is for informational purposes only and does not replace professional medical advice. Always consult your healthcare provider if you have concerns about your health.