Neuroinflammation After Mild SARS-CoV-2 Infection: What Are the Long-Term Effects?

25 Aug 2023 | Back to News, Publications and Annual Reports
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Recent research has already revealed that patients who have died after a severe SARS-CoV-2 infection exhibited brain inflammation. Additionally, there is a growing body of research focused on patients with Long COVID who experience prolonged neurological symptoms such as fatigue and cognitive impairments. These symptoms significantly impact their daily lives.

Approximately 10% of individuals infected with SARS-CoV-2 develop Long COVID, but where does it all begin? Which brain cells potentially play a role in this?

Medical imaging

Non-invasive PET is a method used to depict and monitor inflammation in the body over a specific period of time. In humans, this technique has been extensively utilized to visualize diseases in the brain, such as multiple sclerosis, by capturing inflammation through PET scans. Here at BPRC, we use PET to follow inflammation in non-human primates.

PET-scans of brains of infected macaques

During a SARS-CoV-2 infection, the lungs are initially affected, but other organs, including the brain, can also fall victim to the infection. We have visualized this phenomenon in our SARS-CoV-2 monkey model by conducting PET scans weekly over a period of 7 weeks. Through this approach, we observed a gradual increase in brain inflammation over time following the infection. We also conducted detailed analyses of inflammation in specific brain regions 7 weeks post-infection. We observed a rise in the quantity of activated immune cells, which could potentially be detrimental to the brain.

Possible effects for neurons in the brain

These findings underscore the value of our SARS-CoV-2 monkey model in longitudinally monitoring brain inflammation after a viral infection. This approach enables us to demonstrate that 7 weeks after a mild infection, inflammation persists in the hippocampus and brainstem. This may indicate the occurrence of prolonged inflammatory reactions in the brain, which could potentially be harmful to neurons. While the extent of neuron damage following a SARS-CoV-2 infection has not been thoroughly investigated, it could potentially serve as an explanation for the long-term neurological symptoms observed in Long COVID patients.

With this study, we have illustrated the progression of brain inflammation following a mild infection, revealing that these inflammatory processes persist 7 weeks after infection. Our data provides a basis to further research into neuronal damage in the brain caused by immune cell activation or the virus itself. This work has been published in the Journal of Neuroinflammation.