![]() Since 2002, the successive emergence of bat-borne severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV), swine acute diarrhea syndrome coronavirus (SADS-CoV) and SARS-CoV-2 has reinforced efforts in uncovering the molecular and evolutionary mechanisms governing coronavirus cell tropism and interspecies transmission. “While TMPRSS2 is more abundant in the lungs, furin is expressed in other organs, perhaps explaining why SARS-CoV-2 is capable of invading and damaging multiple organs.Coronaviruses are a group of viruses causing disease in a wide range of animals, and humans. “In other words, SARS-CoV-2, unlike other, less pathogenic strains, can more efficiently use both proteases, TMPRSS2 and furin, to start the invasion of host cells,” says Maurizio Pellecchia, a professor of biomedical sciences at the University of California, Riverside, who led the research team. These mutations have given the virus the ability to infect a wider variety of tissues in the body. Second, when the authors of the present study looked at the peptide sequence of the SARS-CoV-2 spike protein, they found evidence that newly acquired mutations allow the virus to exploit both furin and TMPRSS2 cleavage sites. ![]() ![]() The study authors cite two lines of evidence for their argument.įirst, when scientists in the past have genetically engineered host cells so that they were unable to make furin, this has failed to stop the virus from infecting the cells. Alternatively, a cocktail of different protease inhibitors could also work, they argue. In their paper, the scientists argue that further research is needed to develop compounds like theirs that inhibit both proteases, rather than just one. ![]() It may be one factor that helps SARS-CoV-2 spread so easily.Ĭompound 1 inhibits both furin and another protease, called TMPRSS2. Their findings have been published in the journal Molecules.Ī previous study had suggested that one of the proteases, called furin, is used by some of the most pathogenic coronaviruses. Scientists at the University of California, Riverside’s School of Medicine and the Sanford Burnham Prebys Medical Discovery Institute, in La Jolla, wanted to find out whether a compound that inhibits two particular proteases would protect cells from invasion by SARS-CoV-2. The cleavage sites and their respective proteases help determine how pathogenic the virus is, which tissues it can infect, and whether it can jump from species to species. A coronavirus can, therefore, only invade cells that bear the appropriate proteases. ![]() The spikes of coronaviruses contain three “cleavage sites,” where particular proteases can split the proteins. This splitting changes the shape of the spikes, exposing the binding sites that allow the virus to gain entry to the cell. Before the new coronavirus can enter a human cell, enzymes called proteases on the cell’s surface must split open the protein spikes that give the virus its characteristic crown-like appearance. When disease-causing viruses break into their hosts’ cells, it is invariably an “inside job.” Viral pathogens can only invade cells and replicate with the assistance of the cells’ own molecular machinery. ![]()
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