In a groundbreaking study, researchers from Charite-Universitatsmedizin Berlin in Germany challenge the widely held belief that memory problems and fatigue post-COVID-19 infection are directly linked to the virus invading the brain. Instead, their findings suggest that these issues may be rooted in inflammation within the body.
Debunking the Brain Invasion Theory
Contrary to early pandemic assumptions, the researchers at Charite found no conclusive evidence supporting the direct persistence or proliferation of SARS-CoV-2 in the brain. Dr. Helena Radbruch, leading the Chronic Neuroinflammation working group, emphasized, “There has been no clear evidence that the coronavirus can persist in the brain, let alone proliferate.”
The absence of intact virus particles in the brain challenges the hypothesis of direct infection, highlighting that previous indications were based on indirect testing methods, lacking conclusive proof.
A New Perspective: Immune Response and Neurological Symptoms
An alternative hypothesis proposed by the study suggests that the neurological symptoms may be an indirect consequence of the robust immune response triggered by the body to combat the virus.
The research involved a comprehensive analysis of brain tissue from 21 individuals who succumbed to severe coronavirus infections in hospital settings, alongside a control group of nine patients who died of unrelated causes after intensive care treatment.
Unveiling Molecular Changes
The team explored visible changes in tissue, searched for virus indications, and conducted a detailed analysis of genes and proteins within individual cells. Although coronavirus genetic material was found in the brain, the researchers did not identify infected neurons.
Dr. Radbruch explained, “We assume that immune cells absorbed the virus in the body and then travelled to the brain. They’re still carrying the virus, but it doesn’t infect cells of the brain. So coronavirus has invaded other cells in the body, but not the brain itself.”
The Molecular Puzzle: Explaining Neurological Symptoms
The study revealed significant molecular changes in some brain cells of COVID-19-infected individuals. Prof. Christian Conrad, head of the Intelligent Imaging working group at the Berlin Institute of Health, highlighted the activation of the interferon signaling pathway, a typical response to viral infections.
“These molecular reactions could explain the neurological symptoms observed in COVID-19 patients,” said Prof. Conrad. “For example, neurotransmitters emitted by cells in the brainstem, reacting to inflammation in the rest of the body, could contribute to fatigue.”
Temporary Nature of Neuronal Reaction
Interestingly, the team noted that the neurons’ reaction to inflammation is temporary, as evidenced by a comparison between those who died during the acute infection phase and those who passed away at least two weeks later. While molecular changes are most prominent during the acute phase, they normalize afterward in the majority of cases.
In conclusion, this groundbreaking study challenges the conventional narrative, shedding light on the potential role of inflammation in causing memory problems and fatigue post-COVID-19. Understanding these mechanisms not only deepens our comprehension of the virus’s impact but also opens new avenues for targeted interventions in treating lingering symptoms.
