When doctors first began treating patients hospitalized with COVID-19, a concerning pattern emerged. Many of the sickest patients struggled to breathe and developed dangerous blood clots, strokes, heart attacks, and multi-organ failure. Even months after recovering, some patients continued to face fatigue, brain fog, and circulatory issues, now known as long COVID.
Now, researchers think they have identified a single molecule that may explain the damage caused by COVID infections and how future treatments could prevent it entirely.
This molecule is called P-selectin. Scientists believe it is a major factor in COVID-related clotting and a potential tool against future coronavirus outbreaks.
In a discovery that changes how researchers view viral infections in the bloodstream, scientists found that P-selectin acts like biological Velcro, binding tightly to coronavirus particles. This interaction can lead to harmful clotting, but in controlled settings, it can also stop viruses from infecting human cells.
This finding opens up a new class of mRNA therapies aimed not just at COVID-19 but at future viral pandemics as well.
A Molecule With a Double Life
P-selectin is not new to science. It naturally exists on the surface of blood vessel cells and platelets, which are the components of blood responsible for clotting. Under normal conditions, it plays a crucial role in inflammation by helping direct immune cells to sites of infection or injury.
However, during COVID infections, researchers found that P-selectin acts quite differently.
Instead of just signaling immune responses, this molecule becomes unusually sticky. It binds aggressively to coronavirus spike proteins-these spikes are what the virus uses to invade human cells.
That stickiness turns out to be a double-edged sword.
On one hand, P-selectin can trap viruses in the bloodstream, preventing them from entering cells. On the other, its interaction with platelets can form harmful clusters, which significantly increase the risk of clot formation.
“These virus-platelet complexes are a major cause of severe COVID outcomes,” explained lead researcher Dr. Cesar Moreno, who contributed to the study. “They are strongly linked to organ damage, stroke, and death, and they may also explain many long-term symptoms seen in long COVID.”
Why COVID Clots Were So Severe
Blood clots are not unusual during infections, but COVID was different. Patients developed clots at unusually high rates, even while receiving anticoagulant treatments. Some clots appeared in young and otherwise healthy individuals.
The new findings help clarify why.
During an infection, platelets expressing P-selectin grab onto circulating virus particles. These clusters:
- Increase clot formation
- Block small blood vessels
- Disrupt oxygen flow to organs
- Trigger inflammatory responses
This process helps clarify why COVID is not just a respiratory disease but also a systemic vascular illness affecting the heart, brain, kidneys, and lungs.
Importantly, the same mechanism may stay active long after the virus is gone, contributing to ongoing symptoms in long COVID patients.
Turning a Problem Into a Solution
While P-selectin’s role in clotting initially concerned researchers, its ability to bind to viruses revealed a valuable opportunity.
Researchers discovered that when P-selectin is expressed without inflammation, it acts differently. Instead of forming clots, it captures virus particles in the bloodstream and neutralizes them before they can infect cells.
That insight led to a bold idea: what if P-selectin could be intentionally activated as a defense tool?
Using mRNA technology-the same platform used for COVID vaccines-scientists engineered a therapy that increases P-selectin expression in a controlled and non-inflammatory way. The results were remarkable.
In experimental models, the therapy provided broad protection against multiple coronavirus strains, including:
- SARS-CoV-1
- MERS-CoV
- Early COVID strains
- Delta variants
Rather than targeting a single mutation, the therapy works by trapping viruses in the bloodstream, a strategy that remains effective even as viruses evolve.
Beyond Vaccines: A Complement, Not a Replacement
Vaccines remain one of the strongest tools against infectious diseases, dramatically reducing hospitalizations and deaths globally. However, vaccines are not perfect and may not be appropriate for everyone.
Some people cannot be vaccinated due to medical issues. Others may not build a strong immune response. Additionally, as the pandemic showed, viral mutations can outpace vaccine updates.
That’s where broad-acting mRNA therapies may play an essential role.
“These treatments are not meant to replace vaccines,” said senior researcher Professor Greg Neely. “They are designed to complement them, especially for vulnerable populations and in future outbreaks where vaccines may not yet exist.”
Because mRNA therapies can be designed and produced quickly, they provide a rapid-response option for emerging pandemics.
A Genome-Wide Search for Viral Defenses
The discovery of P-selectin was part of a broader effort to find natural human defenses against viruses.
Using CRISPR genetic screening, researchers systematically tested nearly every gene in the human genome to see which ones could block SARS-CoV-2 infection.
The results exceeded expectations.
In addition to P-selectin, the team identified 33 previously unknown genes that can interfere with coronavirus infections. Many of these genes:
- Disrupt viral entry into cells
- Prevent viral replication
- Improve immune recognition
Researchers believe these genes could lay the groundwork for a new generation of antiviral therapies-not just for coronaviruses but potentially for other viral families as well.
Preparing for the Next Pandemic
The COVID-19 pandemic showed how unprepared the world was for a rapidly spreading viral threat. While vaccines were developed quickly, global supply chains, public health systems, and treatment strategies struggled to catch up.
Scientists say discoveries like P-selectin provide a way to prepare for future pandemics.
Instead of reacting to each new virus strain, broad-acting therapies could offer baseline protection against entire classes of viruses, buying precious time during outbreaks.
“At some point, another pandemic is inevitable,” Professor Neely said. “The question is whether we face it with improvisation or preparation.”
Ethical Oversight and Scientific Transparency
The researchers emphasized that all laboratory and animal experiments followed strict ethical guidelines and approved protocols. Human samples were obtained from consenting donors under established medical ethics standards.
The team has filed a patent for the mRNA technology used in the study, but they stated that no other competing interests exist.
They also noted that while the findings are promising, further clinical trials are necessary before any therapy can reach patients.
What This Means for Long COVID Patients
Perhaps the most hopeful implication lies in long COVID, which affects millions worldwide and remains poorly understood.
If persistent clotting and blood vessel inflammation are key drivers of long COVID symptoms, therapies targeting P-selectin pathways could offer new treatment options, potentially easing fatigue, cognitive issues, and organ damage.
While more research is needed, experts believe this discovery finally connects many of the dots between infection, clotting, and long-term disease.
A Shift in How We Fight Viruses
For decades, antiviral treatments have focused on killing viruses or boosting immune responses. This research suggests a third approach: physically trapping viruses before they can cause harm.
By using the body’s own molecular machinery as a protective barrier, scientists may have found a strategy that works not just for current threats but also for those to come.
As the world looks beyond COVID-19, discoveries like P-selectin remind us that some of the most powerful tools against pandemics may already be within us, waiting to be understood.
