A bit of background on me…​ I’ve been in cyber security for almost 20 years. One of my "go tos" for solving security problems is to find ways to use an attacker’s strength against them. Aikido.

One of the other bits of background…​ I’m not looking for a silver bullet to knock out SARS-CoV-2…​ I’m looking for ways to dampen transmission. Just as almost also security is layered, I’m taking a layered approach to the virus.

At the top level, the goal is to get R (or is it R0…​ I’ve heard that R0 means the natural, non-attenuated transmission rate…​ I’ve also heard R0 used as a generic description of the transmission rate at some point in time)…​ anyway…​ the goal is to get R0 as low as possible. Under 1, is good…​ but the lower we can drive the number, the more normalcy and the fewer deaths.

There exist classes of people for whom they have no choice by to be in high risk situations: mass transit riders, folks in long term care facilities, folks in hospitals, etc. These situations are ones where there is required physical proximity…​ and the proximity and seeing someone’s smile and having their touch (especially in the care of long term care) is part of the engagement.

So, I started asking what can be done to dampen or attenuate (I’m not sure of the right word here) spread in the air in required high risk situations? Yes masks. Yes hygiene. But what else? What else can be done to reduce the parts per billion of SARS-CoV-2 in the air? And, yeah, I get that it’s generally clustered rather than uniformly distributed in air.

I’ve got many cats (yes, this is leading someplace) and in a multi-cat house-hold, the cats can get aggressive with each other. I got this stuff called Feliway…​ it’s a feline pheromone that reduces cat aggression (not entirely) and stress.

So…​ I started thinking, what could we put into the air that’s generally inert, but toxic to SARS-CoV-2?

How can we use the strength of SARS-CoV-2 against it? Or put another way, how do we create a “Candygram for Mongo” oh…​ and, yes, I’m older and Blazing Saddles is part of my era.

As I’ve been reading through the literature, one paper stood out.

As I understand it, SARS-CoV-2 attaches to the ACE2 receptors. Once attached, the ACE2 receptors, the cell releases a Furin which cleaves the virus between the S1/S2 points which releases the RNA into the cell and boom…​ infection.

This article indicates that things that interfere with binding to ACE2 receptors had a material (58% reduction in the study) impact on death rates…​ and yes, I’m aware that this is happening inside the body and I’m suggesting something that happens outside the body…​ but it’s additional evidence of the SARS-CoV-2 and ACE2 receptor relationship.

If a protein shaped like an ACE2 receptor that, once attached to by SARS-CoV-2, releases a Furin, could that cleave open the lipid shell of the virus leaving the enclosed RNA exposed to air or whatever? And I’m presuming the RNA is fairly fragile and exposure to air will cause the RNA to disintegrate.