Here is an idea.
Give everyone the flu. That should slow the spread of the disease COVID-19. So how crazy is that?
Given the current knowledge of virology and immunology, not so much. The initial idea of vaccination was to give a weak or dead form of an infectious agent to a host so that the immune system of the host could develop antibodies for it and ward off future attacks from that agent or similar agents.
Giving a live or active form of an infectious agent is more risky, though. What if the live version kills you?
Hmmm. Maybe giving everyone the flu isn’t such a good idea if it will kill some of them. Perhaps we can give different people different versions of the flu, which are nonlethal. For sake of speculation, let’s assume that we have the wherewithal to do that.
Getting people sick so that they won’t die? Why do that?
The current mechanism of replication of the virus SARS-Cov-2 (the disease itself is called COVID-19) is partially understood, and to oversimplify, appears to be: have a virus infect a host, get inside host cells, use these cellular mechanisms to reproduce the virus, and then have the copies of the virus go infect other cells. Oversimplifying some more, the immune system (of which antibodies are just one part) will react in ways that cause symptoms like histamine generation and/or using internally generated fluids to combat the change in system status. When enough of these fluids fill the lungs, the host dies. (This is just one outcome; many other unfavorable outcomes can happen. I focus on strategies that may prevent or delay future deaths, and I choose avoiding filling the lungs with fluid to pick a specific strategy.)
Suppose we use a different coronavirus which starts the disease process, but has been observed to not kill the host. Let’s call this virus Fred (or Freda or Fredx, but I’ll use Fred for now): Fred now infects the host, uses the cellular systems to reproduce, but causes a different set of system responses, and the host survives this set of responses.
What if, while Fred is working over this infected host, we then infect the host with SARS-Cov-2?
Potentially, bad things could happen, but the key point for this idea is that the mechanisms for replicating SARS-Cov-2 are already being used by Fred. Before this novel virus can use the host’s resources to replicate, it may be sensed by some T-cells or some other component of the immune system, and the immune system has more time (but fewer resources) to mount a defense.
To answer the “Why do that?” above, it means to disrupt the mechanism for SARS-Cov-2 replication inside the host, and give the immune system time to develop an antibody for this new virus.
This sounds like a good idea: keep SARS-Cov-2 from replicating fast enough so that it can be controlled. Social distancing is (on a macroscopic level) a form of this kind of control. But what could go wrong?
The first weak point is the assumption that we can do this mechanism disruption safely for everyone, or even for enough people. Having the flu is no fun, and things need to get really bad for people to consider this as a treatment or even a preventative. (On the plus side, if you have the flu, you feel more comfortable with being socially distant.)
A second weak point is that we don’t know yet if we have data about how viruses compete for a host. Most of the understanding I have (and I’m guessing much of the medical community has) is based on a model where there is only one kind of attacker on a system, not two. (Flu shots may have a variety of components resulting from different viral loads, but all of these loads are tested and are weak or dead.) Hopefully the data amassed for COVID-19 is being analyzed to find symptom constellations that indicate which viruses can play the role of Fred in this scenario. However, SARS-Cov-2 might find a way to take over from Fred and make things worse.
There are other potential problems such as: the viruses may combine to cause greater disruption; the lifetime of SARS-Cov-2 may be longer than the disruption caused by Fred (and so when you get over one flu, the second one kills you); SARS-Cov-2 ends up using a different mechanism (or organ or locale) for replication, and so Fred does not do any disruption.
However, it might be possible to find a weak point in the mechanism of SARS-Cov-2 replication other than clogging the system with another virus. Probably more competent people have considered and dismissed this idea already. Maybe instead a combination of flu followed a couple days later by an injection of antibodies to that flu can be given to control the period of mechanism disruption. Or some other adjustment to this idea may prove effective.
The point of this post is to contemplate a model of the spread of COVID-19 that suggests ways to tinker with the model to make it malfunction in as effective a way as possible, or even just effective enough to prevent an increase in the death toll.
I currently have comments disabled. If you leave one, I will be notified, however. Also, there are other blogs which have them enabled and would welcome a discussion of this idea. I encourage those interested to use those blogs to link to this post (my own version of replication) and hold the discussion there.
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