SARS-CoV-2 Protein Fuels Lung Inflammation by Hijacking Macrophages
The SARS-CoV-2 protein ORF8 reprograms macrophages to promote viral replication and lung inflammation. Blocking the ORF8-linked receptor IL-17RA reduced inflammation and fibrosis in mice, pointing to a potential therapeutic target. The post SARS-CoV-2 Protein Fuels Lung Inflammation by Hijacking Macrophages appeared first on GEN - Genetic Engineering and Biotechnology News .
Scientists are unraveling how the SARS-CoV-2 virus causes lasting lung damage in severe COVID-19 cases. While infected airway cells play a role, immune cells called macrophages ultimately become part of the problem. In a study published in Science Advances, researchers at Gladstone Institutes and UCSF found that a viral protein called ORF8 is a key driver of this process.
ORF8 increases macrophage expression of ACE2, the receptor that SARS-CoV-2 uses to enter cells. Infected macrophages lose their antiviral function, undergo inflammatory cell death, and release signals that promote lung inflammation, making surrounding lung cells more susceptible to viral replication. The presence of macrophages can override ORF8's previously reported inhibition of lung epithelial cell infection, leading to more severe disease.
Mice infected with SARS-CoV-2 carrying ORF8 experienced greater lung inflammation, viral load, and scarring compared to those infected with the unaltered virus. The researchers suggest that ORF8 may be a potential therapeutic target, highlighting brodalumab, an FDA-approved IL-17RA antibody, as a possible treatment.
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