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

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 influenza A virus infection.

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While conducting the study, the scientists also examined the lungs a month after virus clearance and after each acute lung infection. (File)

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

According to the scientists, in most individuals, SARS-CoV-2 is successfully cleared by the immune system, but some struggle with prolonged complications, the cause of which is unknown. During the study, 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 hinders the sense of smell by changing the activity of certain olfactory proteins (receptors), this latest study reveals how the sustained immune reaction in olfactory tissue affects brain centers that govern emotion and cognition.

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

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

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

Moreover, the research team found that SARS-COV-2, because of quirks in how the virus copies itself, likely causes a stronger immune reaction 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 initial infection. The study also confirmed that the prolonged immune reactions seen in long COVID-19 are happening in tissues where the SARS-COV-2 virus is no longer present.

Whatever the cause, the chronic immune response in olfactory tissues of SARS-CoV-2-infected hamsters was accompanied by behavior changes the study authors tracked with established tests. For instance, hamsters from the SARS-CoV-2 group were quicker to stop trying to swim, a measure of depression, or to react to foreign items (marbles) in their cages, a behavior linked to anxiety. Depression and anxiety are common attributes of long COVID, and these behavioral abnormalities were found to correlate with unique changes to the brain cell biology, the researchers say.

While conducting the study, the scientists also examined the lungs a month after virus clearance and after each acute lung infection. They found that after the COVID-19 infection, the re-building of the airways was significantly slower than with influenza A. Moreover, an examinations of tissue slides under a microscope also showed scaring in 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 influenza A virus infection.

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