An Alternative to Vaccination for COVID-19.

Jun 2, 2020
3
2
15
A Competitive Disease Propagation Model as an Alternative to Vaccination for the Protection of Humanity from COVID-19.
Draft 2 June 2020, 2000 GMT
Form rules prevent me from showing my Gmail address.
Abstract
This unfinished paper is to start a discussion on an alternative model for protecting humanity from COVID-19. By itself COVID-19 poses enormous moral and ethical challenges. The model presented in this paper poses its own additional moral and ethical challenges, some of which will be addressed herein. One of the most critical challenges of all is the time required until the World’s population is sufficiently protected from COVID-19. The time required impacts lives and suffering not only from the disease itself but also from the social and economic consequences of our current efforts to protect the World’s population. The economic consequences are not merely an abstract construct, but impact lives and suffering by the loss of the ability to meet basic human needs for food, shelter and education.
Most COVID-19 research focuses on the production of antivirals and vaccinations. An alternative approach is to infect the population with a different disease, such as one of the common human coronaviruses, 229E, NL63, OC43 or HKU1. This could allow people to produce the helper T cells that would fight COVID-19, creating immunity on a faster timeline than vaccination production and distribution.
The COVID-19 challenges far exceed the abilities of any one group or person. As a Systems Engineer, Computer Scientist and Applied Mathematician this is a request for collaboration from people and teams with the expertise and resources to address these unique challenges.
A Comparison of Competitive Disease Propagation and Vaccination Models
Inoculating a sufficient portion of the World’s population with a vaccine to directly and indirectly, through herd immunity, protect humanity against COVID-19 is the gold standard but is not the only approach. One can imagine multiple ways to inoculate humanity for protection from COVID-19. Another approach would be to infect a sufficient portion of the World’s population with a minor disease that as a side effect provided some immunity to COVID-19.
Vaccination with its individual delivery to each person provides greater control over the inoculation process and consequently lower risks. But this control comes at the cost of producing and distributing individual vaccines. Vaccination has at best a linear time, O( n ), production rate limitation to inoculate humanity. Infecting the World’s population with a disease gives up the individual control over the process with consequently higher risks. In exchange, it can at best achieve exponential spreading through the population and thus a Log time, O(Log( n )) complexity.
A Vaccination Model
At a high level Vaccination against COVID-19 consists of Discovering or developing a vaccine, Testing in animal models, Testing in humans, Clinical trials, Developing a production process, Constructing factories and supply chains to produce the vaccine, and Developing world-wide transportation and distribution systems to inoculate a sufficient portion of the World’s population to protect humanity against COVID-19.
A Competitive Disease Propagation Model
At a high level Competitive Disease Propagation against COVID-19 consists of Discovering or developing a disease, Testing in animal models, Testing in humans, Clinical trials, Developing an infection process, and Developing world-wide education and infection networks to inoculate a sufficient portion of the World’s population to protect humanity against COVID-19.
A Comparison of the Models
Comparing these two models shows many similar steps, with the similar steps taking comparable amounts of time. The key differences are that the Vaccination Model requires Constructing factories and supply chains, and Developing world-wide transportation and distribution systems, while the Competitive Disease Propagation Model requires Developing world-wide education and infection networks. These key differences affect how the two models scale to inoculate a sufficient portion of the World’s population to protect humanity against COVID-19. For the Vaccination model, the complexity of producing inoculations scales linearly, O( n ), for the number of inoculations required. The complexity of the transportation and distribution system is O(nLog( n )) or higher. For the Competitive Disease Propagation model, the complexity is O(Log( n )) for the number of inoculations required.
To put numbers to this, conservatively assume that 6 Billion people or 75% of the World’s nearly 8 Billion population, need inoculations for adequate protection. A total combined global factory production capacity of 1 Million doses per day requires 6000 days or nearly 16.5 years to produce the inoculations. A competitive disease with a duration of one week and an R0 of 10 would require 10 weeks to produce the inoculations. While these numbers are arbitrarily chosen, they illustrate the way linear vaccine production and exponential disease spreading could possibly scale.
To see this from another point of view, consider the number of inoculations produced per week for the two models.
Week
1
2
3
4
5
6
7
8
9
Vaccination
7x10^6​
14x10^6​
21x10^6​
28x10^6​
35x10^6​
42x10^6​
49x10^6​
56x10^6​
63x10^6​
Competitive Disease Propagation
10^1​
10^2​
10^3​
10^4​
10^5​
10^6​
10^7​
10^8​
10^9​

Dr. Soumya Swaminathan, Chief Scientist for the World Health Organization, believes an optimistic scenario is a vaccine produced in the tens of Millions in 2021, as quoted by Ars Technica.
In addition to the time required for protection, these models also differ vastly in the type of resources required from the World’s health-care systems. A competitive disease propagation model literally replaces the bioreactors and purifiers from the vaccine factories with people. It replaces the world-wide transportation and distribution systems with people. The impact of this difference in countries with weaker health-care systems is enormous. A competitive disease propagation model works with the resources we have.
What Characteristics Would a Competitive Disease Require?
A Competitive Disease would need to meet a few Goldilocks requirements. It must have sufficiently mild symptoms to minimize direct harm to people. It must be sufficiently contagious to spread rapidly through the World’s population. It must then convey sufficient protection against COVID-19 to make COVID-19 no longer an overbearing threat to humanity.
Shane Crotty and Alessandro Sette, Immunologists at The La Jolla Institute for Immunology, as well Andreas Thiel’s team at the Charité University Hospital in Berlin both have identified the presence of helper T cells that recognize and target the SARS-CoV-2 spike protein. The La Jolla team has detected a similar presence in approximately 50% of blood samples collected between 2015 and 2018, while the Berlin team found 34% of analyzed blood samples from uninfected people also contained these helper T cells. The La Jolla researchers speculate these helper T cells were triggered by past infection with one of the other four coronaviruses that cause colds. One or more these four common cold coronaviruses could be candidates for a competitive disease.
The infectiousness of a pathogen can vary greatly with the behavior of a host. Just as social distancing and isolation can reduce the infectiousness of COVID-19, a cooperative effort between infected and uninfected people could boost R0 enormously. For a common cold type disease with respiratory droplet transmission, an R0 of 10 or even 100 is not out of the question.
How Do We Spread the Disease?
There are a range of possibilities. One method might be using throat swabs from an infected to an uninfected person. Another method might be for an infected person to intentionally cough on another, perhaps coughing into an open mouth or while the other person is inhaling.
What Could Possibly Go Wrong?
At the scale discussed herein, the question is how could anything not go wrong? The following is a short list of things that could go wrong and some possible mitigations. Expanding this list and mitigating these problems is a crucial part of making a competitive disease model ethically, morally and practically possible.
The Spread of the Competitive Disease Could be Contaminated with COVID-19.
Mitigating this risk will require testing, monitoring and tracking. This is a massive quality control issue that must be carefully addressed.
The Spread of the Competitive Disease Could be Contaminated with other Diseases.
As above, this is a massive quality control issue. One approach would be to isolate the desired disease and seed populations around the World. From there the disease can be spread from human to human. The smaller the infection hot spots are, the fewer diseases we inadvertently carry along.
The Competitive Disease Could Mutate into a More Dangerous Strain.
We are fortunate that coronaviruses mutate at a lower rate than other human pathogens, such as influenza. Maximizing R0 and minimizing the size infection hot spots would both reduce the number of and risk from mutations. The idea is to keep the family tree of the disease as wide and as flat as possible. Mutations are most significant on long paths from the root to the leaves of the tree. Perhaps we should call this “Flattening the Tree”?
Seeding populations with the competitive disease allows a tradeoff between the performance and risks of the two models. At one extreme, large hot spots provide the pure competitive disease model, with its higher risks and higher speed. At the other extreme, small hot spots provide the lower risks and lower speed of the vaccination model.
What Comes Next?
How Do We Start?
Using an existing disease, such as one of the common human coronaviruses, endemic to the population, with mild symptoms simplifies some of the moral and ethical challenges. We are not releasing an unknown pathogen. We are, however, intentionally increasing the probability of people’s exposure. Weighing the pros and cons of such a proposal should consider that spreading an existing disease is a lesser risk to the population than letting COVID -19 continue along its course until a vaccine can be produced and distributed in sufficient quantities.
Where Do We Go?
We need to confirm the assumed safety and efficacy of such an approach with one of the common human coronaviruses. We need to quantify the logistics requirements. There are vulnerable groups that must be protected, just as there are with COVID-19. But the potential costs and savings in human lives requires attention.
A discussion between people and teams who have the potential resources and interest in this model should begin. Please consider this proposal and share your comments on the challenges and opportunities presented by a Competitive Disease Model for protecting humanity from COVID-19.
References
Scientists vs politicians: The reality check for “warp speed” vaccine research, Ars Technica, 25 May 2020, Hannah Kuchler.
T cells found in COVID-19 patients ‘bode well’ for long term immunity, ScienceMag.org, 14 May 2020, Mitch Leslie.
Presence of SARS-CoV-2 reactive T cells in COVID-19 patients and healthy donors, https://doi.org/10.1101/2020.4.17.20061440.
 

MMohammed

Assistant Community Manager
Staff member
Nov 12, 2019
32
5
65
To be sure, as you said, there are massive ethical considerations here. However, even the science of fighting this disease by forcing T-cell responses to another disease feels like there's more to lose than gain. I don't even have an issue with anything you've written here. On the contrary, you present a carefully worded and nuanced proposition. My only problem with any such course is the frustrating unpredictability of the COVID-19 immune responses.

That being said, again, this is well written and lends plenty of weight to the potentially life-threatening ramifications involved.
 
Jun 25, 2020
7
0
30
A Competitive Disease Propagation Model as an Alternative to Vaccination for the Protection of Humanity from COVID-19.
Draft 2 June 2020, 2000 GMT
Form rules prevent me from showing my Gmail address.
Abstract
This unfinished paper is to start a discussion on an alternative model for protecting humanity from COVID-19. By itself COVID-19 poses enormous moral and ethical challenges. The model presented in this paper poses its own additional moral and ethical challenges, some of which will be addressed herein. One of the most critical challenges of all is the time required until the World’s population is sufficiently protected from COVID-19. The time required impacts lives and suffering not only from the disease itself but also from the social and economic consequences of our current efforts to protect the World’s population. The economic consequences are not merely an abstract construct, but impact lives and suffering by the loss of the ability to meet basic human needs for food, shelter and education.
Most COVID-19 research focuses on the production of antivirals and vaccinations. An alternative approach is to infect the population with a different disease, such as one of the common human coronaviruses, 229E, NL63, OC43 or HKU1. This could allow people to produce the helper T cells that would fight COVID-19, creating immunity on a faster timeline than vaccination production and distribution.
The COVID-19 challenges far exceed the abilities of any one group or person. As a Systems Engineer, Computer Scientist and Applied Mathematician this is a request for collaboration from people and teams with the expertise and resources to address these unique challenges.
A Comparison of Competitive Disease Propagation and Vaccination Models
Inoculating a sufficient portion of the World’s population with a vaccine to directly and indirectly, through herd immunity, protect humanity against COVID-19 is the gold standard but is not the only approach. One can imagine multiple ways to inoculate humanity for protection from COVID-19. Another approach would be to infect a sufficient portion of the World’s population with a minor disease that as a side effect provided some immunity to COVID-19.
Vaccination with its individual delivery to each person provides greater control over the inoculation process and consequently lower risks. But this control comes at the cost of producing and distributing individual vaccines. Vaccination has at best a linear time, O( n ), production rate limitation to inoculate humanity. Infecting the World’s population with a disease gives up the individual control over the process with consequently higher risks. In exchange, it can at best achieve exponential spreading through the population and thus a Log time, O(Log( n )) complexity.
A Vaccination Model
At a high level Vaccination against COVID-19 consists of Discovering or developing a vaccine, Testing in animal models, Testing in humans, Clinical trials, Developing a production process, Constructing factories and supply chains to produce the vaccine, and Developing world-wide transportation and distribution systems to inoculate a sufficient portion of the World’s population to protect humanity against COVID-19.
A Competitive Disease Propagation Model
At a high level Competitive Disease Propagation against COVID-19 consists of Discovering or developing a disease, Testing in animal models, Testing in humans, Clinical trials, Developing an infection process, and Developing world-wide education and infection networks to inoculate a sufficient portion of the World’s population to protect humanity against COVID-19.
A Comparison of the Models
Comparing these two models shows many similar steps, with the similar steps taking comparable amounts of time. The key differences are that the Vaccination Model requires Constructing factories and supply chains, and Developing world-wide transportation and distribution systems, while the Competitive Disease Propagation Model requires Developing world-wide education and infection networks. These key differences affect how the two models scale to inoculate a sufficient portion of the World’s population to protect humanity against COVID-19. For the Vaccination model, the complexity of producing inoculations scales linearly, O( n ), for the number of inoculations required. The complexity of the transportation and distribution system is O(nLog( n )) or higher. For the Competitive Disease Propagation model, the complexity is O(Log( n )) for the number of inoculations required.
To put numbers to this, conservatively assume that 6 Billion people or 75% of the World’s nearly 8 Billion population, need inoculations for adequate protection. A total combined global factory production capacity of 1 Million doses per day requires 6000 days or nearly 16.5 years to produce the inoculations. A competitive disease with a duration of one week and an R0 of 10 would require 10 weeks to produce the inoculations. While these numbers are arbitrarily chosen, they illustrate the way linear vaccine production and exponential disease spreading could possibly scale.
To see this from another point of view, consider the number of inoculations produced per week for the two models.
Week
1
2
3
4
5
6
7
8
9
Vaccination
7x10^6​
14x10^6​
21x10^6​
28x10^6​
35x10^6​
42x10^6​
49x10^6​
56x10^6​
63x10^6​
Competitive Disease Propagation
10^1​
10^2​
10^3​
10^4​
10^5​
10^6​
10^7​
10^8​
10^9​

Dr. Soumya Swaminathan, Chief Scientist for the World Health Organization, believes an optimistic scenario is a vaccine produced in the tens of Millions in 2021, as quoted by Ars Technica.
In addition to the time required for protection, these models also differ vastly in the type of resources required from the World’s health-care systems. A competitive disease propagation model literally replaces the bioreactors and purifiers from the vaccine factories with people. It replaces the world-wide transportation and distribution systems with people. The impact of this difference in countries with weaker health-care systems is enormous. A competitive disease propagation model works with the resources we have.
What Characteristics Would a Competitive Disease Require?
A Competitive Disease would need to meet a few Goldilocks requirements. It must have sufficiently mild symptoms to minimize direct harm to people. It must be sufficiently contagious to spread rapidly through the World’s population. It must then convey sufficient protection against COVID-19 to make COVID-19 no longer an overbearing threat to humanity.
Shane Crotty and Alessandro Sette, Immunologists at The La Jolla Institute for Immunology, as well Andreas Thiel’s team at the Charité University Hospital in Berlin both have identified the presence of helper T cells that recognize and target the SARS-CoV-2 spike protein. The La Jolla team has detected a similar presence in approximately 50% of blood samples collected between 2015 and 2018, while the Berlin team found 34% of analyzed blood samples from uninfected people also contained these helper T cells. The La Jolla researchers speculate these helper T cells were triggered by past infection with one of the other four coronaviruses that cause colds. One or more these four common cold coronaviruses could be candidates for a competitive disease.
The infectiousness of a pathogen can vary greatly with the behavior of a host. Just as social distancing and isolation can reduce the infectiousness of COVID-19, a cooperative effort between infected and uninfected people could boost R0 enormously. For a common cold type disease with respiratory droplet transmission, an R0 of 10 or even 100 is not out of the question.
How Do We Spread the Disease?
There are a range of possibilities. One method might be using throat swabs from an infected to an uninfected person. Another method might be for an infected person to intentionally cough on another, perhaps coughing into an open mouth or while the other person is inhaling.
What Could Possibly Go Wrong?
At the scale discussed herein, the question is how could anything not go wrong? The following is a short list of things that could go wrong and some possible mitigations. Expanding this list and mitigating these problems is a crucial part of making a competitive disease model ethically, morally and practically possible.
The Spread of the Competitive Disease Could be Contaminated with COVID-19.
Mitigating this risk will require testing, monitoring and tracking. This is a massive quality control issue that must be carefully addressed.
The Spread of the Competitive Disease Could be Contaminated with other Diseases.
As above, this is a massive quality control issue. One approach would be to isolate the desired disease and seed populations around the World. From there the disease can be spread from human to human. The smaller the infection hot spots are, the fewer diseases we inadvertently carry along.
The Competitive Disease Could Mutate into a More Dangerous Strain.
We are fortunate that coronaviruses mutate at a lower rate than other human pathogens, such as influenza. Maximizing R0 and minimizing the size infection hot spots would both reduce the number of and risk from mutations. The idea is to keep the family tree of the disease as wide and as flat as possible. Mutations are most significant on long paths from the root to the leaves of the tree. Perhaps we should call this “Flattening the Tree”?
Seeding populations with the competitive disease allows a tradeoff between the performance and risks of the two models. At one extreme, large hot spots provide the pure competitive disease model, with its higher risks and higher speed. At the other extreme, small hot spots provide the lower risks and lower speed of the vaccination model.
What Comes Next?
How Do We Start?
Using an existing disease, such as one of the common human coronaviruses, endemic to the population, with mild symptoms simplifies some of the moral and ethical challenges. We are not releasing an unknown pathogen. We are, however, intentionally increasing the probability of people’s exposure. Weighing the pros and cons of such a proposal should consider that spreading an existing disease is a lesser risk to the population than letting COVID -19 continue along its course until a vaccine can be produced and distributed in sufficient quantities.
Where Do We Go?
We need to confirm the assumed safety and efficacy of such an approach with one of the common human coronaviruses. We need to quantify the logistics requirements. There are vulnerable groups that must be protected, just as there are with COVID-19. But the potential costs and savings in human lives requires attention.
A discussion between people and teams who have the potential resources and interest in this model should begin. Please consider this proposal and share your comments on the challenges and opportunities presented by a Competitive Disease Model for protecting humanity from COVID-19.
References
Scientists vs politicians: The reality check for “warp speed” vaccine research, Ars Technica, 25 May 2020, Hannah Kuchler.
T cells found in COVID-19 patients ‘bode well’ for long term immunity, ScienceMag.org, 14 May 2020, Mitch Leslie.
Presence of SARS-CoV-2 reactive T cells in COVID-19 patients and healthy donors, https://doi.org/10.1101/2020.4.17.20061440.
Well written and well thought out. I appreciate your background especially you being an Applied Mathematician, I feel this adds substance and credibility to your thesis. I also agree with MMohammed regarding some ethical hurdles but your proposal of utilizing the T cells is a method of incorporating existing interactions within the human body allows for faster remediation... worldwide.
 
Jun 2, 2020
3
2
15
Hi...

I don't know what specific part of the SARS-CoV-2 virus was the target of the T cell activity. So I can't say whether it was even to the spike at all, or more specifically to any particular part of the spike.

The only data that I have seen is that blood samples from 30% or more of people (that had not had COVID-19) had T cell activity against the SARS-CoV-2 virus. The researchers speculated that perhaps this was from exposure to one of the four common cold coronaviruses.

It is not known if an immune response, T cell activity, to SARS-CoV-2 means that an individual has some degree of imunity to to COVID-19. If an individual has some immunity, it is not known how much. I personally think that any amount of immunity would be beneficial. I think that seriously ill patients are in a race to develop an acquired imune response before their inate immune response causes too much damage to their lungs and other organs.

This is something that requires further research. If it turns out that exposure to one of the four comon cold coronaviruses give some immunity, that would be good news; good news for the alternative approach I hypothesized and good news for everyone who has previously had a common cold from the right coronavirus.

I hope this helps. I don't know anything more specific.

Karl
 

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