Most pathogens are typically specialists in specific regions. This doesn’t necessarily apply to viruses, which tend to be generalists if often gravitating to specific systems like the respiratory system by the way they get in to the body. Hearing, vision, and other systems are affected after the infection. That’s very new, and potentially very dangerous.
COVID-19, however, is showing some very different characteristics to just about all other types of pathogens. Multisystem Inflammatory Syndrome (MIS) is a general systemic phenomenon. It causes inflammation in young kids across a wide spectrum of tissues which looks like a rash.
Also quite worrying enough – Survivors of infections are seeing single or multi-system problems after they’ve recovered. How? How does a respiratory virus cause gastrointestinal and other organ problems after the patient has supposedly recovered? (Note, and subject to confirmation: The recovered patients are assumed to have had classic respiratory infections.)
To access these other systems, There are only so many ways to do that. The bloodstream is the obvious avenue. It may be that processor organs like the kidneys can “spread the joy”, but that’s not quite enough. The gastrointestinal system is a pretty hostile place for pathogens, chemically or biologically. Gate-crashers are not necessarily welcomed. Salk drank a tube of cholera and just got a stomach ache. Infection is definitely not easy.
Yet, COVID-19 seems to be causing significant problems in these systems. Again, how? What’s the correlation?
Before we get started – The information below is speculation and extrapolation from a not-very authoritative, very early stage, knowledge base. The main reason for its existence is that it is a possibly very useful line of approach. Professionals please excuse a bit of over-simplistic expression, but I’m trying to make the ideas easily comprehensible to lay readers.
Does COVID-19 have a multisystem “skeleton key” to the organs?
This question may seem a bit over the top, particularly given the early stages of investigation and need for a lot of hard evidence. The problem is that if we don’t ask it, we’re stuck with a virus which is somehow affecting other systems AFTER it’s supposedly cured. It’s obviously critically important to find out as much as possible about the way the virus continues to do damage after the event. There are any number of possibilities, like a secondary infection from other sources, etc., but the subsequent infections all have a prior COVID-19 infection as common ground.
The smoking gun, such as it is, does have some weight behind it, although it would be nice to have a lot more:
• Multiple recovered patients experiencing post-infection medical conditions.
• All these additionally affected cases are right outside the supposed natural respiratory infection mode.
• MIS indicates the COVID-19 virus can and does access other systems. This might be a migratory phenomenon, or simple “random points of infection”, a scattergun effect of some levels of viral presence.
The physical process of viral infection requires a virus to “lock on” to cells. So if a virus can lock on to multiple types of cells…? Admittedly, it may be that strains of the virus are adapted to do that, but to be able to affect so many types of organs and tissues?
You’d need a skeleton key to do that. Strain mutations or not, or perhaps even adapted second-generation viruses in the body which have developed this capacity, perhaps?
There’s a reason for this question
The point of this speculation is that the virus may well have something very like a skeleton key. An instant lock-on for many, perhaps all, types of tissue. Viruses are theoretically passive in all but the infectious stage. They can’t infect unless they can lock on.
If that’s the case, it may be possible to use it to deliver a whole range of precision-targeted medications, nano-bots, etc. at the cellular level. We can swipe this all-purpose key from the virus. Some payback, at least.
The other, somewhat less enthusiasm-provoking, issue is a bit grim. If a virus can become a general systems attacker, what’s the defence? What if other viruses develop this capability? We need to know what it is, how it works, and how to stop it.
Can the skeleton key be used against the virus? Maybe. If the virus is distracted by dummy antigens aligned to catch the skeleton key, for example, it would lock on to an empty target. The skeleton key would be a liability to it.
Slight qualifier – My thing is solving problems. I work across a vast range of subjects. My experience is that you need to recognize the problem and its scope first. In this case, the methods of the virus are a big problem. I hope these ideas are some use to somebody.
