Two foreign studies have highlighted why the virus that causes COVID-19 is so infectious to other SARS viruses.
Researchers from the University of Queensland collaborated with colleagues from the UK and Europe in the studies, who also showed a way to prevent the virus from infecting cells.
The SARS-CoV-2 virus uses a protein called Spike to enter host cells by binding to a receptor in human cells, called ACE2, and does so as a gateway.
In a new study published in Science, Dr. Giuseppe Balistreri of the University of Helsinki in Finland and Professor Mikael Simons of the Technical University of Munich in Germany collaborated with UQ researchers to demonstrate that the virus can also introduce some other receptor, called neuropiline, into cells.
In collaboration with Professor Frederic Meunier of the UQ Queensland Brain Institute, they discovered that neuropiline receptor, NRP1, is discovered in a variety of human cells, adding upper respiratory cells, possibly explaining why SARS-CoV-2 is more infectious and more widely invasive than similar viruses.
Dr. Balistreri stated that the fact that antibodies that block NRP1 are able to block infection by up to 40% strongly advises that this pathway is the key to infection of the virus.
Professor Meunier said there is no doubt that SARS-CoV-2 affects our brain cells and that the long-term consequences are still known.
“The discovery that NRP1 is linked to Spike opens the door to in-depth studies on the neurotropism of the virus, its ability to infect nerve tissue, such as new healing pathways. “
Meanwhile, in a study also published in the same Science factor, Dr. Yohei Yamauchi and Professor Peter Cullen of the University of Bristol worked with other UQ researchers to examine the interaction between the virus and this receptor.
Dr Kai-En (Kevin) Chen and Professor Brett Collins of the UQ Institute of Molecular Bioscience were going to accurately show how the virus joins a host mobile through modeling the site where they interact.
“We now know that in addition to the well-known ACE2 receptor, Spike joins a mobile receiver at the time of the neuropiline host,” Professor Collins said.
“We use X-ray crystallography to see the arrangement of proteins at the atomic point and visualize binding sites with an impressive point of detail. “
The University of Bristol team tested the possibility of breaking the link between the virus and the cells.
“We found that by preventing viral protein from sticking to cells, it was imaginable to decrease the virus’s infection rate,” Dr. Yamauchi said.
“If we can make a drug that prevents the virus from joining the cells, it may be a new treatment to treat COVID-19. “
The COVID-19 series that causes the SARS-CoV-2 virus that joins the receptor is discovered in other pathogenic human viruses such as Ebola and HIV-1, but also in SARS-CoV.