Even a mild respiratory infection, whether it’s COVID-19 or the seasonal flu, can leave lasting effects on the body. However, new research from Tulane University suggests the long-term impacts on the brain differ significantly between the two viruses. The study, published in Frontiers in Immunology, reveals that while both infections can cause lingering lung damage, only SARS-CoV-2 – the virus that causes COVID-19 – is associated with persistent brain inflammation and injury to small blood vessels, even after the virus is no longer detectable. This research offers crucial insights into the neurological symptoms frequently reported by individuals experiencing long COVID, such as brain fog, fatigue, and mood changes.
The findings underscore a critical distinction in how these common respiratory viruses affect the body. While influenza is more often linked to respiratory complications, COVID-19 appears to uniquely target the brain, leading to a distinct set of long-term neurological challenges. “Influenza and COVID-19 affect large populations worldwide and carry a significant public health toll, yet the mechanisms behind their long-term effects remain poorly understood,” explained Dr. Xuebin Qin, lead author of the study and professor of microbiology and immunology at the Tulane National Biomedical Research Center.
Distinct Impacts on Lung and Brain Tissue
To disentangle the effects common to respiratory infections from those specific to COVID-19, researchers utilized a mouse model to examine lung and brain tissue after the infections had cleared. The study found that in the lungs, both viruses triggered a similar response: immune cells that didn’t fully deactivate and an increase in collagen, a protein associated with scarring. This collagen buildup can stiffen lung tissue, potentially explaining the persistent shortness of breath some individuals experience after a respiratory illness. However, a key difference emerged when researchers examined the lungs’ ability to recover.
Following influenza infection, the lungs demonstrated a robust repair mechanism, activating epithelial progenitor cells to rebuild the airway lining. This repair response was largely absent after COVID-19 infection, suggesting the virus may interfere with the lung’s natural healing processes. But the most striking differences were observed in the brain. The research, similarly highlighted by Neuroscience News, revealed that COVID-19 caused persistent brain inflammation and small blood vessel injury, even when the virus was no longer present.
Vascular Injury and Neurotransmitter Disruption
The study identified tiny areas of bleeding and inflammation in the brain’s small blood vessels following SARS-CoV-2 infection – a finding not observed after influenza. This vascular component aligns with growing evidence linking COVID-19 to endothelialitis (inflammation of the blood vessel lining) and thrombotic complications (blood clot formation), potentially fueling the persistence of neurological symptoms. The research showed that SARS-CoV-2 infection alters gene expression related to serotonin and dopamine regulation, neurotransmitters crucial for mood, cognition, and behavior. This disruption could explain the persistent cognitive and mood changes experienced by individuals with long COVID.
Researchers also found that gene expression profiling of brain tissue following SARS-CoV-2 infection revealed ongoing activation of inflammatory signaling cascades, coupled with disruption of neurotransmitter regulation pathways involving serotonin and dopamine systems, as reported by Bioengineer.org. This supports clinical observations of neurological dysfunction following COVID-19.
Implications for Long COVID and Future Research
These findings, supported by an American Heart Association award focused on understanding the long-term cardiovascular and cerebrovascular effects of COVID-19, are critical for developing targeted therapies for long COVID. Understanding the distinct mechanisms by which COVID-19 impacts the brain could lead to interventions aimed at reducing inflammation, protecting blood vessels, and restoring neurotransmitter balance. The Tulane study builds on previous research, including a 2026 study that also highlighted the unique neurological effects of SARS-CoV-2.
As research continues, it’s becoming increasingly clear that COVID-19’s impact extends far beyond the initial respiratory infection. The long-term neurological consequences, particularly the persistent brain inflammation and vascular injury, require further investigation to fully understand the scope of the problem and develop effective strategies for prevention and treatment. The ongoing efforts to unravel the cardiovascular and cerebrovascular dimensions of post-COVID syndrome are vital for improving the lives of those affected by this complex condition.
Disclaimer: This article provides informational content and should not be considered medical advice. Please consult with a qualified healthcare professional for any health concerns or before making any decisions related to your health or treatment.
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