bioRxiv: ... ACIS KEPTIDETM Prevents SARS-CoV2-Induced Acute Toxicity in K18-hACE2 Humanized Mouse Model... 2020, Gottschalk et al

[Ravn]

Full title:
Intranasal Administration of ACIS KEPTIDETM Prevents SARS-CoV2-Induced Acute
Toxicity in K18-hACE2 Humanized Mouse Model of COVID-19: A Mechanistic Insight for
the Prophylactic Role of KEPTIDETM in COVID-19
Gunnar Gottschalk, James F Keating, Kris Kesler, Konstance Knox and Avik Roy
https://doi.org/10.1101/2020.11.13.378257

pre-print, in a few mice

Abstract:

Previously, we have demonstrated that ACIS KEPTIDETM, a chemically modified peptide, selectively binds to ACE-2 receptor and prevents the entry of SARS-CoV2 virions in vitro in primate kidney Cells. However, it is not known if ACIS KEPTIDETM attenuates the entry of SARS-CoV2 virus in vivo in lung and kidney tissues, protects health, and prevent death once applied through intranasal route.

In our current manuscript, we demonstrated that the intranasal administration of SARS-CoV2 (1*106) strongly induced the expression of ACE-2, promoted the entry of virions into the lung and kidney cells, caused acute histopathological toxicities, and mortality (28%). Interestingly, thirty-minutes of pre-treatment with 50 μg/Kg Body weight ACIS normalized the expression of ACE-2 via receptor internalization, strongly mitigated that viral entry, and prevented mortality suggesting its prospect as a prophylactic therapy in the treatment of COVID-19. On the contrary, the peptide backbone of ACIS was unable to normalize the expression of ACE-2, failed to improve the health vital signs and histopathological abnormalities.

In summary, our results suggest that ACIS is a potential vaccine-alternative, prophylactic agent that prevents entry of SARS-CoV2 in vivo, significantly improves respiratory health and also dramatically prevents acute mortality in K18-hACE2 humanized mice.

 

[Ravn]

Posting mainly because of this: inactivated virus causes major damage - Can this be a real finding?

Interestingly, intranasal inoculation of that inactivated virus (1 *106) significantly caused mortality in 28% of treated animals (2 out of 7) just after 24 hrs. The death was observed only in female mice. In addition to that, we observed reduced body weight, lowered body temperature, dropped oxygen saturation, and decreased heart rate in surviving animals. This dramatic and unexpected toxic effect after 24 hrs of inoculation with inactivated virus offered a paradigm shift in the molecular action of virus. Bpl-treated Inactivated virus does not have abilities to infect, replicate and spread, even though our results have demonstrated that it can cause substantial toxicity. Hence, our study identifies that the binding and modulation of ACE-2 receptor with spike protein seem to be the most critical step of SARS-CoV2-mediated death and toxicity. Upon binding, SARS-CoV2 might alter the physiological activity of ACE-2 receptor that potentially cause cytotoxicity and death. Our current report suggests that SARS-CoV2 does not require its traditional infective property to cause death.

Cort's Simmaron blog about it: https://www.simmaronresearch.com/blog/covid-19-keptide-ace2-chronic-fatigue-simmaron

 

[roller*]

dead virus kills ??? ...females...

true = "no, you dont have virus in serum"
true = "yes, you are half-dead from that virus"