Australian researchers discovered a protein in the lungs that adheres to the COVID-19 virus-like velcro and immobilize it, which could explain why some individuals never get sick with the virus while others suffer severe disease.
Greg Neely, a professor of functional genomics at the University of Sydney’s Charles Perkins Centre, led the study alongside Dr. Lipin Loo, a postdoctoral researcher, and Matthew Waller, a Ph.D. student. On Friday, their findings were published in the journal PLOS Biology.
COVID-19 Immunity
The researchers employed tissue-cultured human cells to examine the entire human genome for proteins that can bind to Sars-CoV-2, the virus that causes Covid-19.
This was accomplished using the CRISPR genetic engineering tool, which allows them to activate all genes in the human genome and then determine which of those genes allow human cells to bind to the Sars-CoV-2 spike protein. The spike protein is required for the virus to infect human cells.
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LRRC15 Protein
The researchers searched the complete human genome for proteins that can attach to the SARS-CoV-2 virus using human cells in tissue culture and the genetic engineering tool CRISPR.
The procedure enabled them to discover a new receptor protein known as LRRC15, which appears to be part of a new immunological barrier that aids in the prevention of serious COVID-19 infections.
While COVID-19 patients produced LRRC15, the researchers believe that not enough of the protein was made to be protective, or that it was produced too late to help.
A separate study from London discovered that LRRC15 levels in blood samples were lower in patients with severe COVID-19 compared to individuals with mild COVID-19, lending credence to the notion that higher levels of LRRC15 might result in less severe disease.
The discovery that LRRC15 is expressed in fibroblast cells, which drive lung fibrosis, could have ramifications for extended COVID-19.
There are currently no effective treatments for pulmonary fibrosis, but Neely hopes that the identification of LRRC15 may change that.
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