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I think its false to say its old news considering it was released 3/4 days ago. ShareSting, your shutting down of discussion where not accordant with your positive view is a sign of your heavy confirmation bias which can be extremely dangerous when one has a cash on the line. One should constantly be re-evaluating their position with an open mind based on the data which is coming out on a daily basis with this fast moving situation
Because they are two different Virus'! As a result will naturally respond, react and operate differently!
Miggy - your approach is admirable. Yes the topic was raised yesterday but as is the reality with these things, until there is a conclusive view either way, which in this case is not possible given the research itself is in flux, the discussion will go on. However, again, seems there is no issue with people re-posting all the positives but not happy when a discussion addressing potential risks is explored further.
I think the issue here, John, is not whether it's needed or not but that, the research suggests, it is the primary entry point into the cell for the virus, meaning the more of it that there is the more chance the virus gets in and can replicate
Ghia, kind of one sided of you to direct your comment at me considering the one I made my remark to was the one who began the personal attacks and furthermore those personal attacks were infact in response to 'meaningful' research that was being discussed.
Sharesting, sounds like your a little butthurt that your investment is being questioned and your agenda of constantly re-posting the positives only is being disrupted
ShareSting, what are you on about? I don't think its helpful to be making accusations against people on here, your comment itself was a cheap shot. One could just as easily say your comments betray your clear agenda to get the sharepriceup and portray a solely positive picture of the share.
Thanks JM, interesting, will look into this further
Hi Manifesto - yes i did and i even posted my views on the postive aspects i took from it however i have to remain balanced.
Interferons are a cytokine Miggy. A Cytokine Storm is when there is a lot of Cytokines released into the body. SNG001 is pumping Cytokines into the body, the risk of triggering a Cytokine Storm is something that must be considered unless there is some cast iron reason that is known of that categorically states there is 0 risk of it happening with SNG001.
Oranges, I think given we have money at stake here the best we can do is try our best to make sense of the information that is becoming available on a daily basis from the multitude of experiments that are being done on this virus in a daily basis. The new findings over the past couple of days on ACE2 must be evaluated. Surely you are not suggesting we disregard and not discuss it.
Its a double edged sword RW - the more virus entering the lungs the bigger the problem. The other potentially related risk here is what is commonly mentioned - the 'Cytokine Storm' - if the Viral Load is increased (i.e. more Virus entering the lungs) due to increased ACE2 receptors and in turn there is more Interferons being pumped into the body to counter it this could lead to the hyperinflammation which causes serious problems. SO on one hand by pumping Interferons in to the body there are more entry points for the Virus and on the other it potentially risks triggering hyperinflammation.
https://www.newscientist.com/term/cytokine-storm/
The major issue here ofc is that the main thing SNG does is pump Interferons into the body thereby potentially increasing ACE2
RW, from my understanding of those articles ACE2 is the 'window' through which SARS-COV-2 (Covid19) gains entry into cells and once in it multiplies. The issue is that Interferons increase the amount of ACE2 in the body thus making it easier for SARS COV 2 to get into the body and multiply
Shares ting,
My comment had nothing to do with 'wanting the share to fail' I was just pointing out how based on the situation decsribed around the Melton man's circumstances, it would have excluded him from the trial according to the trials own exclusion criteria thus may have been something other than SNG that was given.
Forgot to add on the end of that msg:
'' When his condition stabilised he was approached by two nurses who asked if he would like to take part in a medicine trial''
Suggesting that the trial drug was given to him after 96 hours, atleast
Use of a nebuliser does not necessitate that it was SNG, Oxygen may also have been administered in this way aswell as other drugs. Additionally a couple of points from the video and article suggest that it may not have been SNG that was administered with the Melton/Lancashire man;
- "within 48 hours he had tested positive for Covid-19", he was then put on Oxygen "until he stabilised", per the video, he was on oxygen for 96 hours - per the point discussed yesterday, over 24 hours from confirmation of infection with covid is a key exclusion criteria meaning, given these time frames he would not have met the criteria to be included in the trial per the trial's clinical register
the other thing that's been playing on my mind is, *if* it's indeed true that the team has found they are not getting to patients early enough and that is the reason for the home approach being introduced because that may give them better results, then, given we are c.5 weeks in, to statistically give a better weighting to the home tested set of results (to avoid the "grey" result RM mentioned) means SNG would need to test in the home for either significantly more patients that they have tested in hospitals in the next 3 weeks to stay within the timeline OR have to continue the trial for longer to average it out to the upside. Ofc this is contingent on a. home testing giving more favourable result and b. the ACE2 thing not being a problem generally speaking
"SARS-CoV-2, despite the higher titre, *does not induce interferon secretion* and causes lower upregulation of proinflammatory cytokines than does SARS-CoV."
https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30008-2/fulltext
Emphasis in above quote is my own
"The authors obtained human lung tissue samples from 6 donors who were not infected with
SARS-CoV-2 and divided each sample into two subcultures to compare viral replication and
immune activation caused by experimental infection with SARS-CoV-2 to that for SARS-CoV.
This self-paired design addresses potential random differences between tissue samples that are a
problem for small studies. The investigators found that although these two coronaviruses have
similar cell tropism (types I and II pneumocytes, as well as alveolar macrophages), infection and
viral replication was much more efficient for SARS-CoV-2 than SARS-CoV. The higher viral
levels associated with SARS-CoV-2 infection may reflect an even more striking observation
from this study: SARS-CoV-2 largely failed to induce expression of any IFNs (type I, II or III) in
the infected human lung tissues. While this study does not address how SARS-CoV-2 evades the
innate immune response and suppresses endogenous IFN production, these results suggest that
treatment with exogenous IFN might be effective against SARS-CoV-2."
https://academic.oup.com/cid/article/doi/10.1093/cid/ciaa453/5821272