Scientists conduct study to understand molecular mechanism behind long COVID-19 symptoms

A team of scientists from the NYU Grossman School of Medicine has conducted a study that provides a better understanding of how the pandemic virus causes depression, anxiety and loss of concentration known as “brain fog” in patients who develop long-term COVID-19.

According to the scientists, SARS-CoV-2 is successfully cleared by the immune system in most people, but some struggle with long-term complications, the cause of which is unknown. During the research, the scientists examined hamsters and human tissue samples and discovered the most profound biological changes that occur in the olfactory system. While a recent study from the same lab showed how SARS-COV-2 infection impairs the sense of smell by altering the activity of certain olfactory proteins (receptors), this latest study reveals how the sustained immune response in olfactory tissue affects the brain centers that control emotion and cognition.

The findings of the study were published Tuesday in Science Translational Medicine. According to the scientists, it is the first study to show that hamsters previously infected with SARS-CoV-2 develop a unique inflammatory response in olfactory tissue.

This chronic inflammatory state seen in SARS-CoV-2 corresponded to an influx of immune cells such as microglia and macrophages, which clear away debris left behind in the wake of the dead and dying olfactory cell lining. They recycle that material, but also cause additional production of cytokines, pro-inflammatory signaling proteins. This biology was also evident in olfactory tissue from autopsies of patients who had recovered from initial COVID-19 infections but had died from other causes.

“Given the systemic scope of the findings, this study suggests that the molecular mechanism behind many long-term COVID-19 symptoms stems from this ongoing inflammation, while describing an animal model close enough to human biology to be useful in designing of future treatments,” Benjamin tenOever, PhD, co-corresponding study author, professor, Department of Microbiology, NYU Langone Health.

In addition, the research team found that due to the idiosyncrasies in how the virus copies itself, SARS-COV-2 likely triggers a stronger immune response than the same amount of influenza A, which may explain the greater scarring caused by SARS-COV-2. in the lungs and kidneys of the hamsters 31 days after the initial infection. The study also confirmed that the prolonged immune responses seen in prolonged COVID-19 occur in tissues where the SARS-COV-2 virus is no longer present.

Whatever the cause, the chronic immune response in olfactory tissue of SARS-CoV-2 infected hamsters was associated with behavioral changes that the study authors tracked with established tests. For example, hamsters from the SARS-CoV-2 group stopped trying to swim more quickly, a degree of depression, or responded more quickly to foreign objects (marbles) in their cages, a behavior linked to fear. Depression and anxiety are common hallmarks of long-term COVID, and these behavioral abnormalities have been shown to correlate with unique changes in brain cell biology, the researchers say.

While conducting the study, the scientists also examined the lungs a month after clearing the virus and after any acute lung infection. They found that airway reconstruction after COVID-19 infection was significantly slower than with influenza A. In addition, examination of tissue slides under a microscope also showed scarring of the lung, which was more widespread in SARS-COV-2 infected lungs. . Meanwhile, the study also found that the inflammatory response to SARS-COV-2 resulted in damage to the kidneys that lasted longer than damage caused by infection with the influenza A virus.

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