Prolonged Presence of COVID Antigens Disrupts Brain’s Immune Response

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New Mechanism of Long COVID Discovered! New Study: Prolonged Presence of COVID Antigens Disrupts Brain’s Immune Response

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New Mechanism of Long COVID Discovered! New Study: Prolonged Presence of COVID Antigens Disrupts Brain’s Immune Response

As the world experiences another wave of rising COVID-19 infections, attention is increasingly focused not only on the acute phase of the disease but also on the long-term effects, known as Long COVID. This condition has become a significant global public health issue.

Long COVID is now considered a heterogeneous disease affecting multiple organ systems. It persists after the acute phase of infection (around four weeks) and can last for several months or even years in some patients. While the acute phase of COVID-19 can be severe, Long COVID is often debilitating, with an estimated incidence rate of 10% to 35%. Many patients experience neurological issues such as anxiety, depression, brain fog, post-traumatic stress disorder, cognitive impairment, fatigue, and sleep disturbances. Previously, persistent neuroinflammation was thought to be the primary cause of these symptoms, but the underlying neuroimmune mechanisms have remained unclear.

In a recent study published in the journal *Brain, Behavior, and Immunity*, scientists from the University of Colorado Boulder have uncovered new insights into the prolonged effects of COVID-19.

They found that residual viral antigens from COVID-19, which persist long after infection, significantly reduce cortisol levels in the brain, triggering the nervous system and causing immune cells to overreact to subsequent stressors. The researchers believe these findings reveal a critical physiological mechanism that explains many of the symptoms associated with Long COVID.

Previous studies have shown that COVID-19 antigens—immune-stimulating proteins released by the virus—can remain detectable in the blood of Long COVID patients for up to a year after infection. These antigens have also been found in the brains of deceased COVID-19 patients. To investigate the effects of these lingering antigens on the brain and nervous system, the research team injected the S1 antigen, a subunit of the spike protein, into the cerebrospinal fluid of test rats, comparing the results with a control group.

After seven days, the rats exposed to the S1 spike protein showed a 31% reduction in corticosterone levels in the hippocampus, a brain region responsible for memory, decision-making, and learning. After nine days, the levels decreased by 37%. Given that rats have a lifespan of two to three years, a period of nine days represents a significant duration. Cortisol, a crucial anti-inflammatory hormone, plays a vital role in converting nutrients into energy, regulating blood pressure, controlling the sleep-wake cycle, and managing immune responses to infections. A recent study showed that cortisol levels are often lower in Long COVID patients, as well as in those with chronic fatigue syndrome.

To further explore the effects of reduced cortisol in the brain, the researchers conducted another experiment. They exposed different groups of rats to a mild bacterial infection and monitored their heart rates, body temperatures, behaviors, and brain immune cell activity. The results showed that rats previously exposed to the S1 spike protein had a stronger reaction to the stressor. Their changes in appetite, behavior, core body temperature, and heart rate were more pronounced than in the control group, and they exhibited more neuroinflammation and heightened activation of microglial cells (the brain’s immune cells).

The researchers believe this study provides the first evidence that exposure to residual COVID-19 antigens alters the brain’s immune response, making it more reactive to subsequent stressors or infections. This overactive immune response could lead to the wide range of symptoms associated with Long COVID. While this study was conducted on animals, further research is needed to determine if and how low cortisol levels contribute to Long COVID symptoms in humans.

Based on these findings, the researchers propose a possible mechanism: COVID-19 antigens lower cortisol levels, and cortisol is essential for controlling the brain’s inflammatory response to stressors. When stressors arise—such as increased work stress, mild infections, or intense physical exercise—the brain’s inflammatory response can spiral out of control, leading to severe symptoms like fatigue, depression, brain fog, insomnia, and memory problems.

However, the researchers caution that simply supplementing cortisol may not be an effective treatment for Long COVID, as it does not address the underlying cause and could lead to side effects. Instead, they suggest that identifying and minimizing stressors may help manage symptoms. Additionally, they believe that eliminating the source of the antigens—such as lingering virus hiding in tissue reservoirs—could be a promising avenue for treatment exploration.

New Mechanism of Long COVID Discovered! New Study: Prolonged Presence of COVID Antigens Disrupts Brain’s Immune Response

References:

Frank, M. G., et al. (2024). SARS-CoV-2 S1 subunit produces a protracted priming of the neuroinflammatory, physiological, and behavioral responses to a remote immune challenge: A role for corticosteroids. Brain Behavior and Immunity.

(source:internet, reference only)

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