The next pandemic: Is there a way to predict and prevent it?
I asked her if the Covid pandemic could have been prevented, from where the next one could emerge, is there a way to predict and stop it.
Orsolya, more than a year since the onset of the COVID pandemic what are the unknowns? What we still don’t know about the virus?
With newly emerging diseases the problem is always having to hit the ground running. We must always remember that anything we find out about the symptoms, the progress, the spread, we only do so once it occurs in a large enough proportion of the population. And that means a lot of people get sick before we catch up with the events. It is impossible to map all existing mutations, we notice and sequence the ones that have already caused a noticeable difference. And while there are very good studies about which sequences are more likely to change, the nature of this change, a.k.a. the nature of the next significant mutant strain remains and will remain unknown. It is very important that we never forget that evolution can not ever be predicted. Changed happen completely randomly, therefore, once a virus such as this gains access to billions of people, there is absolutely no telling what it will do next. This unpredictability is what makes it so difficult and unsustainable to deal with emerging infectious diseases.
With newly emerging diseases the problem is always having to hit the ground running. We must always remember that anything we find out about the symptoms, the progress, the spread, we only do so once it occurs in a large enough proportion of the population. And that means a lot of people get sick before we catch up with the events. It is impossible to map all existing mutations, we notice and sequence the ones that have already caused a noticeable difference. And while there are very good studies about which sequences are more likely to change, the nature of this change, a.k.a. the nature of the next significant mutant strain remains and will remain unknown. It is very important that we never forget that evolution can not ever be predicted. Changed happen completely randomly, therefore, once a virus such as this gains access to billions of people, there is absolutely no telling what it will do next. This unpredictability is what makes it so difficult and unsustainable to deal with emerging infectious diseases.
How will Covid-19 evolve in the future? Could we expect that it will go away at some point?
For it to ‘go away’ is not an option. If we break it down to a very simple logic of evolution, why would it? It has billions of hosts (people) available, it has no problem spreading through international travel and shipping routes, in high density urban areas, it is airborne, it is not affected by environmental temperature within the ranges we live in, and it has no cure.
Vaccination will be of significant help in reducing severe symptoms and fatal outcomes, but we must keep in mind that being vaccinated does not mean that the virus ‘bounces off’ us. It means we are able to deal with it faster than without the vaccine, but while our immune system is dealing with it, we can still spread it to others, including those not vaccinated. This means that the virus simply spends less time in any given vaccinated human, but it does not become less infectious. Think about the flu as a good example. Symptoms are similar, it also spread with droplet infection, it has been infecting us since at least the early XX. century, we have multiple vaccines that are freely available to large proportions of the population, and still, it has not disappeared. This is the scenario we need to prepare ourselves for with COVID19. It will become a permanent factor in our lives and in the lives of future generations for a long time.
For it to ‘go away’ is not an option. If we break it down to a very simple logic of evolution, why would it? It has billions of hosts (people) available, it has no problem spreading through international travel and shipping routes, in high density urban areas, it is airborne, it is not affected by environmental temperature within the ranges we live in, and it has no cure.
Vaccination will be of significant help in reducing severe symptoms and fatal outcomes, but we must keep in mind that being vaccinated does not mean that the virus ‘bounces off’ us. It means we are able to deal with it faster than without the vaccine, but while our immune system is dealing with it, we can still spread it to others, including those not vaccinated. This means that the virus simply spends less time in any given vaccinated human, but it does not become less infectious. Think about the flu as a good example. Symptoms are similar, it also spread with droplet infection, it has been infecting us since at least the early XX. century, we have multiple vaccines that are freely available to large proportions of the population, and still, it has not disappeared. This is the scenario we need to prepare ourselves for with COVID19. It will become a permanent factor in our lives and in the lives of future generations for a long time.
Could this pandemic have been prevented?
Yes, there is a high chance it could have been prevented. The first scientific description of this viral strain was published in 2005 from samples collected at the place of its recent origin. In that paper, the authors warned that this is a close relative of the SARS and MERS viruses, and that it should therefore be considered as a threat to human health. However, the issue was and still is the lack of fluent communication channels between descriptive and executory fields, in this case, viral taxonomy and public health. The most important lesson the pandemic has taught us is that fundamental research and policy need to work together in an effort to not only identify, but also act against the next potential threat. We cannot afford to wait until the next pathogen emerges, and then construct a plan, because once a virus, bacterium, fungus or parasite has established itself in a human host, there is nothing we can prevent anymore. From that point on, we can only try to control the damages and contain the epidemic. The key to prevention is anticipating beforehand, finding them before they find us.
Yes, there is a high chance it could have been prevented. The first scientific description of this viral strain was published in 2005 from samples collected at the place of its recent origin. In that paper, the authors warned that this is a close relative of the SARS and MERS viruses, and that it should therefore be considered as a threat to human health. However, the issue was and still is the lack of fluent communication channels between descriptive and executory fields, in this case, viral taxonomy and public health. The most important lesson the pandemic has taught us is that fundamental research and policy need to work together in an effort to not only identify, but also act against the next potential threat. We cannot afford to wait until the next pathogen emerges, and then construct a plan, because once a virus, bacterium, fungus or parasite has established itself in a human host, there is nothing we can prevent anymore. From that point on, we can only try to control the damages and contain the epidemic. The key to prevention is anticipating beforehand, finding them before they find us.
Many scientists sound alarm that coronavirus will not be our last deadly epidemic. What’s the reason for that? Which are the factors that make disease emergence more likely?
I am one of those scientists. This is just one of many to come. The explanation lays in disease evolution. The theoretical framework is called the Stockholm Paradigm, let me explain the jist of it. When we think about diseases, be it COVID, the flu, chicken pox or measles, we envision it as a pathogen living in a single host, and picture them as an odd couple living a long-term relationship. But pathogens are unfaithful, they never stay in a monogamous relationship with any of their hosts. They have multiple relationships, constantly switching from one host to the other, from humans to pets to wildlife to domesticated species, anything that suits their needs. And if we think about it, most all microbes we know to have caused disease in people have been described from some other species, just think about rabies, Ebola, Zika, malaria, anything. This means that just because it is currently not causing an outbreak in humans, it is still present in some other species we are not even looking at. All infectious agents have these so called reservoirs, species they can infect, but may or may not cause any symptoms. To put is blankly, we tend to treat diseases as cat that we believe will only sits in our armchair, because that’s the only place we’ve ever looked for it. But if the cat isn’t in the chair, does that mean it’s gone forever? No, it’s just out and about somewhere. Do we know when it will show up in the chair again? No, there is no telling. But will it be back? For sure.
Pathogens are the same, they reside is any species they can survive in, never exclusively in one. Diseases emerge when an existing reservoir or host get in contact with another species, that is suitable, but has not been infected yet. And this brings us to the factors getting species in close contact with each other, making emergence more likely: climate change and globalized lifestyle. Climate change results in changing environments, different temperature ranges, different precipitation rates. These changes will often be intolerable by the species currently living in the area and thus lead to migration. Migratory birds move up north following rising temperature rates, rodents occupy higher altitudes, weeds invade montane crops, etc. And once species have commenced migration, they are taking their parasites with them, and passing them on to naïve species in their new habitats. But it isn’t just wildlife and plants, it is more importantly us. When we travel to exotic places, invade natural habitats, plant our crops and breed our animals in close vicinity of natural areas, that is, when we act like the globalized species we are, we not only expose ourselves for potential pathogens, but we also make it incredibly easy for them to spread. Rust fungus only needs to infect a single wheat, it will then have access to acres and acres more. African swine flu only needs to infect a single pig, it will then sweep through thousand other within the breeding facility. And coronavirus only needs to infect a single human, it will then gain access to a world of people.
I am one of those scientists. This is just one of many to come. The explanation lays in disease evolution. The theoretical framework is called the Stockholm Paradigm, let me explain the jist of it. When we think about diseases, be it COVID, the flu, chicken pox or measles, we envision it as a pathogen living in a single host, and picture them as an odd couple living a long-term relationship. But pathogens are unfaithful, they never stay in a monogamous relationship with any of their hosts. They have multiple relationships, constantly switching from one host to the other, from humans to pets to wildlife to domesticated species, anything that suits their needs. And if we think about it, most all microbes we know to have caused disease in people have been described from some other species, just think about rabies, Ebola, Zika, malaria, anything. This means that just because it is currently not causing an outbreak in humans, it is still present in some other species we are not even looking at. All infectious agents have these so called reservoirs, species they can infect, but may or may not cause any symptoms. To put is blankly, we tend to treat diseases as cat that we believe will only sits in our armchair, because that’s the only place we’ve ever looked for it. But if the cat isn’t in the chair, does that mean it’s gone forever? No, it’s just out and about somewhere. Do we know when it will show up in the chair again? No, there is no telling. But will it be back? For sure.
Pathogens are the same, they reside is any species they can survive in, never exclusively in one. Diseases emerge when an existing reservoir or host get in contact with another species, that is suitable, but has not been infected yet. And this brings us to the factors getting species in close contact with each other, making emergence more likely: climate change and globalized lifestyle. Climate change results in changing environments, different temperature ranges, different precipitation rates. These changes will often be intolerable by the species currently living in the area and thus lead to migration. Migratory birds move up north following rising temperature rates, rodents occupy higher altitudes, weeds invade montane crops, etc. And once species have commenced migration, they are taking their parasites with them, and passing them on to naïve species in their new habitats. But it isn’t just wildlife and plants, it is more importantly us. When we travel to exotic places, invade natural habitats, plant our crops and breed our animals in close vicinity of natural areas, that is, when we act like the globalized species we are, we not only expose ourselves for potential pathogens, but we also make it incredibly easy for them to spread. Rust fungus only needs to infect a single wheat, it will then have access to acres and acres more. African swine flu only needs to infect a single pig, it will then sweep through thousand other within the breeding facility. And coronavirus only needs to infect a single human, it will then gain access to a world of people.
Is there a way to predict the next pandemic?
Yes, this is what my research project is about. The DAMA protocol is a four-step action plan, which aims to synchronize the work and tools of academic research and public health infrastructures, in an effort to prevent diseases. DOCUMENTING is the first step, which involves cataloguing the currently described microbes in the fields of virology, bacteriology, micology and microbiology. These are species that we know exist, some of them our future pathogens, who may not have had access to us yet. This gives us a huge set of strains to investigate, whether or not they are actually dangerous to us. But keeping an eye on every single microbe is impossible and unnecessary, so we need to find those that are actually dangerous. ASSESSMENT is therefore the next step to do so. What happens here is that DNA or RNA analyses reveal their closest known relatives, a.k.a. their ‘family relationships’. Just like in our case, any organism will be more similar to its closer kins than to those distantly related to it. If Microbe X is closer related to ones that we know are harmless, then they are also most likely harmless. If, however, its closest relatives are Ebola and Marburg virus, or SARS and MERS, there is a very good chance that Microbe X is also capable of infecting us. This is what we call phylogenrtic triage. Having identified the dangerous Microbe Xs, we then will need to start MONITORING their movement. Using the studies conducted in evolutionary ecology and population biology, we can determine where hosts of Microbe X are distributed, where they can come into contact with humans, crops and livestock, and then we ACT at those specific locations, before pathogens had the chance to infect the first new host. This is the step I am working on, building high speed communication channels between the above described research fields and those institutions of public health that have the power to act before a single outbreak has happened. This is what I believe actual prevention is, evading the disease to ever show up in us.
Yes, this is what my research project is about. The DAMA protocol is a four-step action plan, which aims to synchronize the work and tools of academic research and public health infrastructures, in an effort to prevent diseases. DOCUMENTING is the first step, which involves cataloguing the currently described microbes in the fields of virology, bacteriology, micology and microbiology. These are species that we know exist, some of them our future pathogens, who may not have had access to us yet. This gives us a huge set of strains to investigate, whether or not they are actually dangerous to us. But keeping an eye on every single microbe is impossible and unnecessary, so we need to find those that are actually dangerous. ASSESSMENT is therefore the next step to do so. What happens here is that DNA or RNA analyses reveal their closest known relatives, a.k.a. their ‘family relationships’. Just like in our case, any organism will be more similar to its closer kins than to those distantly related to it. If Microbe X is closer related to ones that we know are harmless, then they are also most likely harmless. If, however, its closest relatives are Ebola and Marburg virus, or SARS and MERS, there is a very good chance that Microbe X is also capable of infecting us. This is what we call phylogenrtic triage. Having identified the dangerous Microbe Xs, we then will need to start MONITORING their movement. Using the studies conducted in evolutionary ecology and population biology, we can determine where hosts of Microbe X are distributed, where they can come into contact with humans, crops and livestock, and then we ACT at those specific locations, before pathogens had the chance to infect the first new host. This is the step I am working on, building high speed communication channels between the above described research fields and those institutions of public health that have the power to act before a single outbreak has happened. This is what I believe actual prevention is, evading the disease to ever show up in us.
Where do you think novel infectious diseases are most likely to emerge?
The sad answer to that is that wherever people are. We are so numerous and occupy so much land that the best chance of any disease emerging is either in us or in species we harbour. They are lurking in the vegetation surrounding agricultural fields, in the wildlife touching noses with livestock, in exotic species we eat, keep, wear, pet or see on our jungle tour. Diseases will emerge on the interfaces between human and natural habitats, wherever those may be.
The sad answer to that is that wherever people are. We are so numerous and occupy so much land that the best chance of any disease emerging is either in us or in species we harbour. They are lurking in the vegetation surrounding agricultural fields, in the wildlife touching noses with livestock, in exotic species we eat, keep, wear, pet or see on our jungle tour. Diseases will emerge on the interfaces between human and natural habitats, wherever those may be.
How dangerous are the glacial frozen viruses that are understudied? How big is the threat?
As dangerous as any other virus capable of infecting, but not having had access to us. We don’t know which of the viruses that are thawed by increasing temperatures are able to infect something important to us. It is a similar situation to tropical and continental microbes: it is an unknown diversity of viruses, bacteria and many more, that may or may not be able to cause disease. A lot of them are probably harmless, but we only need one that is able to establish itself. Our focus should also be extended to these, and any other latent viruses currently not considered in epidemiology. Anticipating the emergence is the only way to sustainably battle emerging infectious diseases.
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