Millions of people across the globe are continuing to suffer from long-term symptoms after recovering from common infections like COVID-19, influenza, and Epstein–Barr virus. Chronic fatigue, brain fog, muscle pain, gut problems, and a disturbing reaction to exercise are becoming alarmingly common—yet the biological explanation has remained elusive. Now, new research suggests a shocking possibility: your blood vessels may be under attack from within, thanks to virus-induced “zombie” cells.
These long-lasting symptoms, collectively known as long-COVID or myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), have long puzzled scientists. The World Health Organization officially classifies ME/CFS as a post-viral fatigue syndrome and a brain disorder. While such conditions have existed for decades, COVID-19 has triggered an explosion in cases, with an estimated 400 million people now affected by long-COVID since 2020.
Despite extensive investigation, no widely accepted explanation has fully accounted for the biological mechanisms behind these illnesses—until now. A team of international researchers has proposed a new and disturbing theory: that certain viruses transform healthy blood vessel cells into “zombies” that confuse the immune system, impair blood flow, and trigger cascading dysfunction throughout the body.
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At the heart of this theory is a process known as endothelial senescence—a condition where the cells lining the inside of blood vessels stop functioning normally, refusing to die while still releasing inflammatory and clot-promoting signals. These senescent cells become half-dead, half-alive entities that wreak havoc on surrounding tissues and immune responses.
The team’s review explores how viral infections, particularly from viruses like SARS-CoV-2 and influenza A, can push endothelial cells into this dangerous state. Infected cells stop dividing but begin releasing biochemical signals that thicken the blood, promote microclots, and narrow blood vessels—disrupting circulation and reducing oxygen delivery throughout the body.
This could explain why patients with long-COVID or ME/CFS experience debilitating exhaustion after exercise. Instead of relaxing and allowing more blood to flow, these compromised vessels constrict, depriving muscles and organs of oxygen and causing symptoms to worsen the day after physical activity. In the brain, reduced blood flow and leaky vessels could cause cognitive issues and dizziness. In the gut, weakened vascular barriers may allow bacteria and toxins to enter the bloodstream, triggering widespread inflammation.
Even more troubling is the role of the immune system—or rather, its failure. Normally, the body’s natural killer cells, macrophages, and complement proteins would target and remove these senescent cells. But in long-COVID and ME/CFS, these immune functions are impaired. Senescent endothelial cells may even emit signals to repel immune attack, allowing them to persist unchecked and sustain the disease process.
This could lead to a vicious cycle: viruses initiate endothelial senescence, the immune system fails to eliminate the damaged cells, and the resulting inflammation and vascular dysfunction feed back into the progression of symptoms. What begins as a viral infection spirals into a long-term, self-sustaining illness.
Current research is now focused on proving this theory. In the U.S., a clinical trial is underway to study cellular senescence in long-COVID. Researchers are testing how patient blood samples affect healthy endothelial cells in the lab and are developing imaging techniques that may one day detect senescent cells inside the body. If successful, these methods could unlock a new era of diagnosis and treatment.
The goal is clear: identify and target these “zombie” cells before they can inflict lasting damage. By directly addressing the cellular aging process within the vascular system, scientists hope to develop therapies that reduce symptoms, restore function, and finally offer relief to millions living with long-COVID and ME/CFS.
What was once a mysterious and misunderstood condition may now be on the verge of a breakthrough—one that begins not in the lungs or brain, but in the blood vessels quietly deteriorating after a viral storm.
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