A remedy to prevent uncontrolled inflammation in patients with severe COVID-19 is a step further following a study by the University of Queensland on how immune cells respond to the virus.
Dr Larisa Labzin and Professor Kate Schroder from the UQ Institute of Molecular Bioscience, together with Dr Stuart. Sarah Londrigan of the Peter Doherty Institute for Infections and Immunity, found that the maximum immune cells that contribute to chronic inflammation do not become inflamed with the SARS-CoV-2 virus that causes COVID-19.
Dr. Labzin said that by causing a protective reaction to eliminate the virus, those uninfected cells called macrophages find damage and death in nearby cells and provoke a strong inflammatory reaction.
There is an imbalance in the immune reaction because most macrophages become inflamed with the virus.
We end up with too many immune cells reaching the site of infection, which causes a lot of collateral damage: too much inflammation and too little fighting the virus.
It is a double-edged sword for the body: the immune formula that attacks an infectious disease early is protective, but when prolonged or exceeded it can cause chronic inflammation. “
The IMB studies team is reading how to selectively target macrophages without compromising the body’s ability to fight the virus, in order for severe COVID cases to occur.
Anti-inflammatory drugs are lately given to hospitalized COVID-19 patients after the virus has peaked, to calm the overactive immune response, but the drugs cause patients to suffer secondary infections.
With the new functioning of macrophages, the researchers intend to design anti-inflammatories that can be administered earlier, to prevent inflammation from getting out of control.
Professor Kate Schroder said a greater understanding of the fundamental biology of the immune formula will help us help our bodies fight infections more strongly.
“We have vaccines and antivirals in the fight against COVID-19, but the virus continues to mutate, so this is a way to protect ourselves from new variants and also from pandemics and infections in the long term. “
Studies funded through the National Health and Medical Research Council and published in Science Signaling.
University of Queensland
Labzin, L. I. , et al. (2023). The ACE2 macrophage is required for SARS-CoV-2 replication and subsequent cytokine responses that restrict the continued functioning of the virion. Signage scientifique. doi. org/10. 1126/scisignal. abq1366.
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