Nikhil Prasad Fact checked by:Thailand Medical News Team Jun 01, 2026 48 minutes ago
Medical News: A new study has uncovered compelling evidence that a persistent immune system malfunction may be driving one of the most debilitating forms of Long COVID. Researchers found that patients suffering from Long COVID Postural Orthostatic Tachycardia Syndrome (LCPOTS), a condition marked by a rapid rise in heart rate when standing, appear to have ongoing immune activation fueled by oxidative stress and chronic inflammation.
Researchers uncover evidence that persistent immune activation and oxidative stress may be driving
Long COVID POTS symptoms
The research was conducted by scientists from Vanderbilt University Medical Center, the Center for AIDS Health Disparities Research, the Veteran's Health Administration Tennessee Valley Healthcare System in Nashville, Tennessee, and Horus University-Egypt in New Damietta, Egypt.
A Debilitating Long COVID Condition
Postural Orthostatic Tachycardia Syndrome, or POTS, affects the body's ability to properly regulate blood flow and heart rate when a person stands up. Since the COVID-19 pandemic, doctors around the world have reported a dramatic rise in cases linked to previous SARS-CoV-2 infections.
People with Long COVID POTS often experience dizziness, racing heartbeats, fatigue, shortness of breath, chest discomfort, digestive problems, brain fog, and exercise intolerance. The condition disproportionately affects women and can persist for years, severely reducing quality of life.
In this study, researchers compared 25 patients with Long COVID POTS to 15 individuals who had recovered from COVID-19 without developing POTS.
Immune Cells Found Stuck in Inflammatory Mode
One of the most striking discoveries was that a type of immune cell called a monocyte appeared to be under intense oxidative stress. Oxidative stress occurs when harmful molecules known as reactive oxygen species overwhelm the body's natural antioxidant defenses.
The researchers found that monocytes from Long COVID POTS patients contained more mitochondria, the energy-producing structures inside cells, and produced significantly higher levels of damaging oxygen-related molecules. At the same time, several genes responsible for antioxidant protection were switched down. This combination created ideal conditions for ongoing cellular damage and immune activation.
Damaged Proteins May Be Triggering Persistent Immune Attacks
The study also revealed unusually high levels of compounds called isolevuglandins, or IsoLGs. These highly reactive molecules are produced during oxidative stress and can attach themselves to normal proteins, effectively transforming them into targets that the immune system may mistakenly view as dangerous.
Researchers believe these altered proteins may act like "false alarms," continuously stimulating immune responses long after the original coronavirus infection has resolved.
This
Medical News re
port highlights that these abnormal protein changes may represent one of the clearest biological explanations yet for why some Long COVID patients remain ill for years.
Evidence of Ongoing Immune Battle
Another major finding involved the discovery of large numbers of T cell-monocyte complexes circulating in the blood of Long COVID POTS patients. These cellular pairings were roughly three times more common than in recovered individuals without POTS.
Scientists found that these immune cell pairs were not random. Instead, they formed active immune synapses, specialized communication structures that allow immune cells to exchange signals and coordinate attacks.
The T cells within these complexes were highly inflammatory and produced elevated amounts of immune molecules including interferon-gamma and IL-17A. Importantly, higher levels of these inflammatory cells were linked to more severe symptoms and larger increases in heart rate when standing.
Inflammation Appears Connected to Nervous System Dysfunction
The researchers also discovered elevated levels of inflammatory cytokines circulating in the blood. These included interferon-gamma, tumor necrosis factor-alpha, and IL-17A, all of which have been associated with nerve inflammation and neurological disorders.
Patients with Long COVID POTS showed evidence of impaired parasympathetic nervous system activity, the branch of the nervous system responsible for slowing heart rate and promoting recovery. The findings suggest that persistent inflammation may be interfering with normal autonomic nervous system function.
The researchers propose that oxidative stress, immune activation, and autonomic dysfunction may reinforce one another in a self-perpetuating cycle.
Conclusions
The study provides some of the strongest evidence so far that Long COVID POTS is not simply a lingering aftereffect of infection but may involve an ongoing biological process driven by immune dysfunction. The discovery of oxidative stress in monocytes, abnormal IsoLG-modified proteins, elevated inflammatory cytokines, and active immune cell interactions offers a potential explanation for the persistent symptoms experienced by many patients. These findings also open the door to future treatments aimed at reducing oxidative stress, blocking harmful immune activation, or restoring normal autonomic nervous system function. While additional studies are needed to confirm these mechanisms, the research represents an important step toward understanding one of the most challenging complications of Long COVID.
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.medrxiv.org/content/10.64898/2026.05.08.26352776v2
For the latest on Long COVID, keep on logging to Thailand
Medical News.
Read Also:
https://www.thailandmedical.news/articles/long-covid
Share
Tweet
Share
