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I wonder if they actually used human lung cells for this test; the article doesn’t seem to specify. Past tests have used Vero cells, which are apparently the no
by ashtonkem 5y ago
I wonder if they actually used human lung cells for this test; the article doesn’t seem to specify. Past tests have used Vero cells, which are apparently the norm for virology research, but aren’t a good analogue for human cells for Covid infection. This seems to be why some compounds worked well in a Petri dish, but didn’t work in actual humans.
- raphlinus 5y agoHere's the actual paper: https://www.pnas.org/content/118/43/e2108728118 https://www.pnas.org/content/118/43/e2108728118 There's a lot of detailed discussion about different types of cells. Vero cells don't have TMPRSS2, but Calu-3 (human lung epithelial) cells do. To dramatically oversimplify, this compound works on the latter type but not the former. They also did a little safety testing in a mouse model. This is early stage, as you point out there are a lot of things that work well in the lab and not so much in real humans, but still I find it promising.
- ashtonkem 5y agoI’m not the best reader of scientific papers, but it looks like they used human lung cells and Vero cells. I’m not qualified to speak to the rest of the experimental design, but it looks like they’ve at least avoided that old mistake. > We analyzed pseudotype entry driven by the spike protein of SARS-CoV-2 (SARS-2-S) or the glycoprotein of vesicular stomatitis virus (VSV-G) into the TMPRSS2-positive human lung cell line Calu-3 (7, 29). VSV-G was used as a control, as it does not depend on TMPRSS2 for host cell entry. Besides Calu-3 cells, we further used Vero cells (African green monkey, kidney) as a control, as these cells do not express TMPRSS2, and therefore any reduction in SARS-2-Sdriven entry would be related to either unspecific side effects or cytotoxicity.