There was extrapulmonary spread reported in SARS patients, which might be relevant to #nCoV2019 if it uses the same receptors. So this study aimed to see if ACE2 and TMPRSS2 also mediated this process.
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To be clear the authors aren't suggesting that. They only state that a TMPRSS2 inhibitor approved for human use in Japan should be considered. They also interpret the data well in the context of the study and do not overstate their results.
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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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