![]() ![]() The N protein is a central player in viral replication, with roles that include stabilizing and releasing the virus’ genetic material. ![]() One was R203M, a mutation found in Delta that alters the nucleocapsid (N), a protein tucked inside the virus that packages its RNA genome. Next, the researchers tweaked the VLP’s proteins with various mutations. The brighter the cells glow after being infected with the VLPs, the more mRNA the VLPs have successfully delivered. They inserted a snippet of messenger RNA (mRNA) that causes cells invaded by the VLPs to light up and glow. It doesn’t spread,” says Charles Rice, a molecular virologist at Rockefeller University.ĭoudna and her colleagues, including co–senior author Melanie Ott, a virologist and director of the Gladstone Institute of Virology, added a new innovation to the VLP system. But because it is stripped of the virus’ RNA genome, it can’t hijack a cell’s machinery to replicate and burst out of the host cell to infect more cells. It can bind with cells in a laboratory and invade them. From the outside, a SARS-CoV-2 VLP looks exactly like the full-fledged virus. But lentiviruses only express spike, not SARS-CoV-2’s other three structural proteins.ĭoudna and her team made the new tool by tweaking lab constructs called viruslike particles (VLPs), which contain all the virus’ structural proteins but lack its genome. That’s partly because, short of deliberately mutating the virus and testing it-research that requires high-level biosafety facilities-the best tool for probing individual mutations has been what’s called a “pseudovirus,” a construct made from a different virus, often a lentivirus, that can express a coronavirus protein on its surface. Researchers analyzing how mutations in the coronavirus’ genome affect its activity have concentrated on the spike protein, which studs the virus’ surface and allows it to invade human cells. … That can now be studied in a much easier way by a lot more scientists.” “The system she has developed allows you to look at any mutation and its influence on key parts of viral replication. The new system, developed by Nobel Prize winner Jennifer Doudna of the University of California (UC), Berkeley, and her colleagues, is a powerful tool for understanding current SARS-CoV-2 variants and exploring how future variants might affect the pandemic, he says. That discovery, published today in Science, is “a big deal,” says Michael Summers, a structural biologist at the University of Maryland, Baltimore County-not just because it helps explain Delta’s ravages. Now, a new lab strategy that makes it possible to quickly and safely study the effects of mutations in SARS-CoV-2 variants has delivered one answer: a little-noticed mutation in Delta that allows the virus to stuff more of its genetic code into host cells, thus boosting the chances that each infected cell will spread the virus to another cell. Just what drives Delta’s ability to spread so rapidly hasn’t been clear, however. As the world has learned to its cost, the Delta variant of the pandemic coronavirus is more than twice as infectious as previous strains. ![]()
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