The S-pseudotyped VSV can bind the receptor (in this case ACE2 with TMPRSS2 priming) on a cell and enter, but once inside instead of the virus replicating, it expresses GFP and/or luciferase reporters. Reporter expression is then measured and used to quantify entry.
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To their credit, the authors acknowledge the limitations of using serum from a single patient. They don't make wild assertions about the implications on tropism or what it might mean in terms of pathogenesis. I am impressed that the authors did a well-designed study so rapidly
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However, I wanted to illustrate that critical mechanistic entry work like this is distinct from determining mechanisms of pathogenesis. It is one piece of a larger puzzle. To understand how nCoV2019 causes disease, we need data from animal models & clinical samples from patients.
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The bottom line is that these in vitro studies are critical to establish mechanism of entry, but more detailed studies need to be done with authentic nCoV2019 in vitro and in vivo before we can conclude anything about the significance for disease, treatment, or diagnostics
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5906799/ … Shouldn’t they be able to develop an mRNA vaccine from the serum of the SARS patient?
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