The authors used a VSV pseudotype system. This is where the S protein from nCoV2019 is expressed on the surface of another virus called VSV. Inside the virion (viral particle), most of the VSV genome has been replaced by a reporter gene.
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In fact, the most interesting part of the study (to me) is their last experiment, showing that serum from a SARS patient can block entry. This suggests that maybe people with preexisting immunity to SARS might be more resistant or SARS antibodies could be used to treat nCoV2019.
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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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