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Antiviral drug shows efficacy against COVID-19 in human cells and mice

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posted on Apr, 7 2020 @ 05:36 PM
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Ok, I posted this in the big thread, but thought it warranted a thread in itself for more attention.

Apparently, researchers have indicated a broad-spectrum oral antiviral drug shows some signs as both a prophylactic and therapeutic for Covid-19, both in vitro and in vivo, as well as other Coronavirus respiratory diseases.

EIDD-2801 shows efficacy against COVID-19 in human cells and mice


Researchers have demonstrated that EIDD-2801, an oral antiviral drug, can be used as either a prophylactic or a therapeutic for SARS-CoV-2, the coronavirus causing the COVID-19 pandemic. The drug also showed efficacy against related coronaviruses SARS-CoV and MERS-CoV.

Collaborators from the University of North Carolina at (UNC-) Chapel Hill Gillings School of Global Public Health, Vanderbilt University Medical Center (VUMC) and the Emory Institute for Drug Development (EIDD), all US, tested EIDD-2801 in both mice and cultured human lung cells infected with the various coronaviruses. Their findings were published in Science Translational Medicine.


Article:

Science Translational Medicine: An orally bioavailable broad-spectrum antiviral inhibits SARS-CoV-2 in human airway epithelial cell cultures and multiple coronaviruses in mice


Abstract

Coronaviruses (CoVs) traffic frequently between species resulting in novel disease outbreaks, most recently exemplified by the newly emerged SARS-CoV-2, the causative agent of COVID-19. Herein, we show that the ribonucleoside analog β-D-N4-hydroxycytidine (NHC, EIDD-1931) has broad spectrum antiviral activity against SARS-CoV-2, MERS-CoV, SARS-CoV, and related zoonotic group 2b or 2c Bat-CoVs, as well as increased potency against a coronavirus bearing resistance mutations to the nucleoside analog inhibitor remdesivir. In mice infected with SARS-CoV or MERS-CoV, both prophylactic and therapeutic administration of EIDD-2801, an orally bioavailable NHC-prodrug (β-D-N4-hydroxycytidine-5′-isopropyl ester), improved pulmonary function, and reduced virus titer and body weight loss. Decreased MERS-CoV yields in vitro and in vivo were associated with increased transition mutation frequency in viral but not host cell RNA, supporting a mechanism of lethal mutagenesis in CoV. The potency of NHC/EIDD-2801 against multiple coronaviruses and oral bioavailability highlight its potential utility as an effective antiviral against SARS-CoV-2 and other future zoonotic coronaviruses.



I have not read the entire study, however.

edit on 7-4-2020 by Liquesence because: (no reason given)



posted on Apr, 7 2020 @ 05:45 PM
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a reply to: Liquesence

Broad spectrum -- that's even more exciting.

Let's hope it means good things in real life for real people.




posted on Apr, 7 2020 @ 05:52 PM
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a reply to: Liquesence

Just the abstract is good enough for laymen .

Future zoonotic coronaviruses ? It likes tigers , probably all cats . The Longleat safari park owner lord bath , is dead of Corona .


edit on 7-4-2020 by DoctorBluechip because: Park owner rip



posted on Apr, 7 2020 @ 06:02 PM
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a reply to: Liquesence

That looks promising. I havent ready the study yet and wouldn't understand half of it without google, but I think its smart to target the RNA of the coronavirus.

I just wouldn't trust that they arent also provoking host cell RNA mutations as well. This could have bad side effects I imagine.


edit on 7-4-2020 by HelloboysImbackguy because: (no reason given)



posted on Apr, 7 2020 @ 06:57 PM
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originally posted by: HelloboysImbackguy
a reply to: Liquesence

That looks promising. I havent ready the study yet and wouldn't understand half of it without google, but I think its smart to target the RNA of the coronavirus.

I just wouldn't trust that they arent also provoking host cell RNA mutations as well. This could have bad side effects I imagine.



They checked for that, if I read the paper correctly. It doesn't.

According to a microbiologist researcher friend of mine at Stanford, human cells have means of detecting and correcting errors during RNA replication. Most viruses don't and that's how drugs like this and Remdesivir work. They present fake building blocks to the viral RNA, the replication process incorporates those fakes into the RNA, the viruses can't tell the difference between the fakes and the real stuff and they have no way of getting rid of it, so the viral replication stops.



posted on Apr, 7 2020 @ 07:34 PM
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a reply to: 1947boomer

Cool, sounds reasonable enough.




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