Polish Scientists Expose How SARS-CoV-2 Hijacks the Human Body at the Molecular Level to Sustain Long COVID
Nikhil Prasad Fact checked by:Thailand Medical News Team May 04, 2025 2 weeks, 6 days, 33 minutes ago
Medical News: A new in-depth study by scientists from Adam Mickiewicz University and Poznań University of Medical Sciences in Poland has uncovered a disturbing truth—SARS-CoV-2 doesn’t just cause a temporary illness. It leaves behind a trail of molecular destruction that sets the stage for a chronic, ongoing battle inside the body. This molecular war, as the researchers describe it, is defined by persistent viral reservoirs and a misfiring immune system that continues to attack even after the virus appears to be gone.
Polish Scientists Expose How SARS-CoV-2 Hijacks the Human Body at the Molecular
Level to Sustain Long COVID. Image Shows Persistent SARS-CoV-2 Virus Present in
Certain Deep Tissues.
This
Medical News report unpacks how the virus embeds itself deep within the body’s tissues and rewires essential immune and metabolic systems, giving rise to Long COVID—a debilitating condition affecting millions across the globe.
The Four Hidden Triggers of Long COVID
Long COVID, also referred to as Post-Acute Sequelae of SARS-CoV-2 infection (PASC), manifests as persistent symptoms such as fatigue, brain fog, breathlessness, sleep disturbances, and muscle pain long after the acute phase of COVID-19 ends. The Polish researchers have identified four interconnected causes behind this prolonged condition:
-Immune Autoactivation – SARS-CoV-2 triggers the production of autoantibodies that mistakenly attack healthy tissues.
-Reactivation of Latent Pathogens – Dormant viruses like Epstein-Barr virus (EBV) and cytomegalovirus (CMV) are reawakened due to immune suppression.
-Chronic Viral Reservoirs – SARS-CoV-2 continues to linger in tissues, organs, and even stool samples, undetectable by standard tests.
-Metabolic Lock-In – Even after viral clearance, cells may remain trapped in a diseased state, unable to restore normal function.
How SARSCoV2 Hijacks the Body’s Control Systems
The study highlights how SARS-CoV-2 produces a range of proteins—like ORF3a, NSP13, and spike (S1)—that hijack the body’s immune regulatory systems. One of the most alarming tactics is the virus's ability to sabotage autophagy, the process by which cells clear out damaged proteins and viral particles. Blocking autophagy allows infected cells to persist and fuels chronic inflammation.
At the same time, the virus disrupts the Nrf2 pathway, a critical system that manages oxidative stress and inflammation. Without a functional Nrf2 response, cells suffer from excessive damage caused by free radicals, while inflammation becomes uncontrollable.
Mitochondria—the energy centers of the cell—are also targeted. Viral proteins
damage mitochondrial structures and suppress ATP production, leading to fatigue, cognitive dysfunction, and systemic energy depletion, which are hallmarks of Long COVID.
Persistent Virus Hides in Plain Sight
Contrary to earlier assumptions that the virus is cleared shortly after recovery, evidence now shows that SARS-CoV-2 RNA and proteins persist in various tissues, including the liver, colon, lungs, and even the brain. In some cases, viral components were found in patients who tested negative for months, suggesting that the virus can hide and continue to affect cellular metabolism.
In one study cited, SARS-CoV-2 was detected in stool samples long after respiratory symptoms resolved. Some patients showed active viral replication in the gut even without gastrointestinal symptoms. Others had viral proteins in plasma, urine, or stool weeks after their supposed recovery.
Autoimmunity Adds Fuel to the Fire
The immune system, already weakened and confused by the virus, begins to turn on itself. Autoantibodies against interferons, phospholipids, and mitochondrial components were detected in COVID-19 and Long COVID patients. These immune elements can trigger vascular inflammation, blood clotting, and widespread tissue damage.
Multiple studies show that Long COVID patients exhibit elevated levels of proinflammatory cytokines like IL-6, IL-17A, TNF-alpha, and IFN-alpha, which not only sustain inflammation but also promote autoantibody production. This immune autoactivation is a major driver of chronic symptoms and suggests that Long COVID is not just a lingering infection—it is a full-blown autoimmune-like condition in many individuals.
Why Long COVID Is Hard to Treat
The complexity of the underlying mechanisms makes Long COVID difficult to manage. A single drug targeting inflammation may not be enough. Instead, therapies need to address multiple issues simultaneously—viral persistence, immune dysfunction, mitochondrial failure, and autophagy inhibition.
The study proposes that treatment should be personalized and based on the patient’s dominant molecular imbalances. Restoring proper autophagy, reactivating Nrf2, clearing hidden viral reservoirs, and modulating the immune response are all seen as potential strategies.
Conclusion
This powerful review exposes Long COVID as a silent and complex war raging within the body. It is not a simple case of post-viral fatigue, but a deep disruption of immune and metabolic systems driven by chronic viral reservoirs and immune autoactivation. Without proper intervention, many patients may remain stuck in this pathological loop for years.
Understanding how SARS-CoV-2 alters the body at the molecular level offers new hope for developing effective therapies. Only by addressing the full scale of this molecular war can we truly help those still suffering from the long shadow of COVID-19.
The study findings were published in the peer reviewed journal: Frontiers in Immunology
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1582783/full
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https://www.thailandmedical.news/news/breaking-covid-19-news-australian-scientists-discover-a-microrna-called-cov2-mir-o8-that-is-encoded-by-sars-cov-2-and-is-possibly-pathogenetic
https://www.thailandmedical.news/articles/long-covid
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