When HA15 was tested in the body of mice infected with SARS-CoV-2, the drug largely reduced viral load in the lungs.
A team of researchers at the Keck School of Medicine of USC has revealed that blocking the production of a chaperone protein could largely reduce the replication of SARS-CoV-2.against Covid-19, scientists continue to research ways to treat severe infections, notwithstanding people who cannot get vaccinated or if dangerous new strains of the virus arise and bypass vaccine protection.Led by Amy S. Lee, Ph.D.
"A major problem in fighting SARS-CoV-2 is that it is constantly mutating and adapting itself to more efficiently infect and multiply in its host cells," LeeBinding and inhibiting the activity of the GRP78 proved to be the key step So, the researchers began exploring the role of GRP78 and found that while healthy cells require a fraction of GRP78 to function normally, cells under stress need more GRP78 to cope. In a 2021 paper, the researchers had shown that when SARS-CoV-2 enters the scene, "GRP78 is hijacked to work in tandem with other cellular receptors to bring the SARS-CoV-2 virus inside cells, where it can then reproduce and spread," as per the release.to replicate inside human lung cells.
So, Lee and her team decided to get a special messenger RNA tool in the ring to control the production of the GRP78 protein in human lung epithelial cells in cell culture, without interrupting other cellular processes. Afterward, when those cells were later infected with SARS-CoV-2, they produced a lower amount of the viral spike protein, thereby proving that GRP78 was essential for replication and production.
Along with HA15, Lee and her colleagues are also studying the GRP78 inhibitor, YUM70. They discovered that both HA15 and YUM70 can suppress the production of mutant KRAS proteins—a common mutation that tends to resist drug treatment—and reduce the
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