Lucy: If he hadn’t discussed it, media would have accused him of hiding the info. Some media already had canned interviews with Medical types days ago (longer?) ready to broadcast. Some started two days ago. Today’s world…
You can inhibit replication though. This family of virus has been very responsive to anti-malarial agents.
To determine whether the antiviral effects of LAAs could be observed with avian strains and a swine strain isolate of the 2009 pandemic influenza, plaque inhibition assays were carried out with the highest non-toxic concentration of the various compounds. For the swine strain (A/Swine/OTH-33-2/2009 (H1N1)), chloroquine, amodiaquine and quinacrine were most effective in inhibiting replication (more than 60% inhibition) compared to primaquine (less than 20% inhibition) ( Figure 5 ). At equivalent concentrations of LAAs, the swine OTH-33-2 isolate and the human pH1N1/2009 ( Figure 5 and Table 1 ) seemed to have comparable sensitivities although the swine isolate was slightly less sensitive. This might be attributable to possible genetic variations between isolates. Interestingly, amodiaquine was the most potent compound at inhibiting the replication of the highly pathogenic avian influenza H5N1 (HPAI; A/Domestic Goose/Germany/R1400/2007 (H5N1)) rather than the low pathogenic avian influenza strain (LPAI; A/Teal/Germany/WV632/2005 (H5N1)) ( Figure 5A ). In contrast, chloroquine, primaquine and quinacrine seem more effective at inhibiting the low pathogenic avian influenza stain rather than the highly pathogenic ( Figure 5B–D ). All LAAs were only capable of inhibiting Emu-Tx avian strain (A/Emu/Texas/39924/1993 (H5N2)) replication by less than 40% ( Figure 5 ). Overall, we demonstrated that the swine isolate (H1 subtype) appears to be generally more sensitive to inhibition of endosomal acidification induced by LAAs than the avian strains (H5 subtype), except for the primaquine. Again, in accordance with the study by Di Trani et al. that used only chloroquine, LAAs were less effective against human than avian strains suggesting that endosomal pH dependence is more associated with human viral adaptation than avian viruses [37]. Taken together, our observations support the evidence that a lower pH is necessary for influenza replication and that targeting endosomal acidification in host cells can be considered as a potential avenue for inhibiting replication of different influenza strain.
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Keep in mind this is petri dishes at levels just below being toxic; the results are centered around how these drugs change cellular pH.
Personally I would much prefer a qualified person to provide clear and succinct information about what clinical trials have been done. Important information like that rather than it may be or it may not be useful.
Oh I am well aware of it, I am just saying it has been studied in this family of viruses and has demonstrated some effects on cell replication. Not saying it will work, just that it is not completely out of left field if some real research is showing results.
Interesting read. I wonder what it is about the specific MOA (in regards to inhibiting replication) that helps with the coronavirus, being an anti-parasitic drug?
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Interesting…I have to agree.
■■■■■■■■■ just ■■■■■■■ happen.
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Meh.
He was Trump being Trump.
It’s been approved by the FDA to use in a clinical trial.
In his usual mangling way, Trump managed to mess that message up.
Stephen Hahn clarified just fine when he spoke about it.
Seriously, stop listening when Trump speaks.
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In the original linked story:
Sounds like the FDA has not even tested its efficacy. Why would the President of the US be touting something that hasn’t even been tested? It makes no sense whatsoever.
I’ll rescind my criticism. After further googling it appears there is some hope around this drug. I’m fine with Trump’s statement now since there does seem to be some medical opinion favoring it.
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There have been tests - not official clinical trials.
See post above yours.
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He should sound like more of an authority than my mom does when she texts me something she just heard is maybe true.
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This doesn’t target the virus, it targets the host cells through endosomal acidification. Which impedes viral replication.
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So that some can complain about him being a bully?
remdesivir may work on a cellular level to stop viral replication. This drug was used on the first US patient in Everett, WA. It proved effective. I hope this gets on the fast-track for treatment.
Do you have a report on that?
From what I have seen, the results in direct virus replication impedance has been so so. Which is why I find targeting the host cells (human cells) a novel approach which may have promise.
