Ann: Trading Halt, page-65

Did some searching just to see if there was any plausible scientific possibility.

Found this less that 3 weeks old

https://link.springer.com/article/10.1007/s00134-020-05985-9

"Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target"

I refer to this section & the reference:

Delivering excessive soluble form of ACE2.Kuba et al. [10] demonstrated in mice that SARS-CoV downregulates ACE2 protein (but not ACE) by binding its spike protein, contributing to severe lung injury. This suggests that excessive ACE2 may competitively bind with SARS-CoV-2 not only to neutralize the virus but also rescue cellular ACE2 activity which negatively regulates the renin-angiotensin system (RAS) to protect the lung from injury [12, 30]. Indeed, enhanced ACE activity and decreased ACE2 availability contribute to lung injury during acid- and ventilator-induced lung injury [12, 31, 32]. Thus, treatment with a soluble form of ACE2 itself may exert dual functions: (1) slow viral entry into cells and hence viral spread [7, 9] and (2) protect the lung from injury [10, 12, 31, 32].

31.Zhang R, Pan Y, Fanelli V, Wu S, Luo AA, Islam D, Han B, Mao P, Ghazarian M, Zeng W, Spieth PM, Wnag D, Khang J, Mo H, Liu X, Uhlig S, Liu M, Laffey J, Slutsky AS, Li Y, Zhang H (2015) Mechanical stress and the induction of lung fibrosis via the midkine signaling pathway. Am J Respir Crit Care Med 192:315–323


I know clutching at straws but could they really pull a massive rabbit out of the hat tomorrow?