What’s Next and How Does This End?

What’s Next and How Does This End?

Introduction

What’s next and how does this end? A somewhat philosophical look at our future. Indeed, if it doesn’t happen with this variant, it’ll happen with the next one, or maybe the next. Some version of this coronavirus is bound to flummox our vaccines and cause harm. In the past two years, SARS-CoV-2 has hopscotched across the globe, rejiggering its genome to better coexist with us. The latest contender, Omicron, has more than 50 mutations, making it the most heavily altered variant of concern that researchers have identified to date. Even in the fully vaccinated, at least a few antibodies will likely be stumped, and at least a few cells infected. Our collective defences may soon bear an Omicron-shaped dent. But the dent and data look much better now in terms of disease severity, this showing this now, with the usual qualifications about S African weekend reporting:

https://twitter.com/pieterstreicher/status/1469743320092102659?s=24 

So is it over? Endemic is now often used to describe the point where the virus’s danger fades to the levels of the flu or, better yet, the common cold. In its technical definition, though, endemic describes an equilibrium, a point where the immunity gained in a population is balanced by the immunity lost. Immunity can be gained through vaccination or infection, and it can be lost through waning immune response, new variants, or population turnover as susceptible babies are born. A pathogen’s impact becomes a lot more predictable and stable when it’s endemic. During their long coexistence with us, the viruses that cause the common cold and flu have all found this equilibrium with some seasonal fluctuation; we are first infected or vaccinated as young children and then frequently reinfected as immunity fades and viruses evolve. The coronavirus that causes COVID is new, though; it is still trying to infect large swaths of adults for the very first time. China is largely uninfected, for example, ironically.

So, we might approximate the start of endemic COVID as the point where nearly everyone has been vaccinated or infected. Reinfections or breakthroughs will happen, but we hope they will be milder, which seems to be true thus far with Omicron. This blanket of immunity might be enough to head off big surges that overwhelm hospitals. But whether the endemic COVID actually becomes as benign as the common cold, or as bad as the flu, or worse, depends on both our changing immunity and the virus’s continued evolution. We just don’t know; and we don’t know how long it will take to reach endemicity.

But, a dose of humility now: we are not very good at predicting the future of this virus. If you were reading COVID news back in March 2020, you may remember graphs of projected COVID cases that looked like a steep mountain. This is the classic epidemic curve. Cases rise exponentially until they hit a peak, the point of supposed herd immunity, and they start falling exponentially. Then, the pandemic was over. Places as far flung as slums in Delhi to the Amazonian town of Manaus, to me reached herd immunity in the summer of 2020. Wrong.

This is obviously not what happened. Instead, COVID has come in multiple waves and plateaus. Some of these peaks and troughs were probably seasonal, as people spent more or less time indoors. But Europeans and Americans also clearly changed their behaviour in response to the threat of the coronavirus itself. In spring 2020, people stopped going out. Schools closed. We later started wearing masks and socialising more outdoors. Traditionally, models haven’t really incorporated behaviour because we haven’t as populations altered our behaviour in drastic ways to respond to pathogens. The behavioural shifts due to COVID were so profound that they’re forcing epidemiologists to reconsider how to model infectious disease. In particular, they are trying to understand how people may keep modulating their behaviour as cases rise or fall: when the local news reports that hospitals are overwhelmed, does that prompt people to take more precautions in response? Could that explain why the summer Delta surge in the Southern states in the US fell off without drastic interventions?

The path to endemicity might also be bumpy because of how a virus spreads through social networks. A virus is inherently self-limiting in the short term; it induces immunity in those it sickens and eventually runs out of people to infect in a particular social circle. In a recent paper scientists call this “transient collective immunity”; the virus hits this wall and cases fall even without the entire population reaching herd immunity. But the protection has an expiration date. Cracks form in this wall as we start interacting with new people. Perhaps Joe Shmoe stayed at home awhile and then attended a slew of weddings over the summer, where he got exposed. This constant rewiring of our social networks lets the virus find new susceptible people and can lead to new waves.

As we continue on the path toward endemic COVID, we may see more local surges every time the coronavirus finds a pocket of susceptible people. But it may be hard to predict exactly when. You might think of it like a fire: the dry fuel is out there, though precisely when a spark of the coronavirus will find it depends on chance. You can get lucky for so long with this virus, and you can get unlucky. There’s something very erratic about transmission going on.

The more inherently transmissible the virus is though, the quicker it will find the rest of the susceptible population and reach endemicity. The coronavirus has already significantly upped its transmissibility from the original Wuhan strain to Alpha to Delta. We don’t yet know where Omicron sits. The emergence of new variants has been hard to forecast. Early in the pandemic, scientists thought the coronavirus mutated rather slowly, until these variants with a huge number of mutations suddenly appeared and rewrote the rulebook. Nobody had predicted that. That’s totally out of the box.

Immune responses

How our immunity changes over time will also influence the length of this transition period. Thus far, immunity to infection is waning, but immunity to severe disease still looks rather durable. Will immunity to severe disease ever wane? Will multiple exposures to the virus, either through boosters or infections, strengthen immunity permanently? We still don’t fully know today how Omicron affects the elderly with 2 shots, unboosted in the developed world. All this affects the speed at which we reach equilibrium, and where that equilibrium lands. Further complicating matters, the virus is also adapting to evade the immune system. Delta has some ability to do this; Omicron might be even better at it, given its 32 mutations alone in the spike protein. Considering all of the complexity here, the final endemic equilibrium of COVID is hard to describe clearly. We might know we’ve technically reached endemicity only in when we’ve seen COVID follow a regular seasonal pattern year after year.

Instead of trying to gauge how far we are from this still-hazy future, we might turn instead to figuring out how to live through this uncertain transition period. We may be stuck here for a while yet. Even as the long-term picture remains unclear, we can make decisions for the short term based on what’s happening today. This requires a willingness to alter our behaviour, switching precautions on and off as needed. We have a precedent for this. When cases were low over the summer, we felt comfortable going maskless indoors, knowing full well that masks might be needed again if cases went back up. This is a marathon, not a sprint. Given how quickly COVID fortunes have shifted with Delta and might now shift again with Omicron, our strategies also need to evolve to suit the situation at hand. It’s not flip-flopping to change course. It’s facing reality.

Although this virus and our immunity shape the possible futures of endemic COVID, the ultimate burden of the number of cases and deaths we tolerate is up to us. Will we permanently alter our behaviour to suppress respiratory illnesses? Wear masks in winter? Improve building ventilation? Isolate at the slightest sign of illness and be allowed to take sick days from work and school, no questions asked?  Like herd immunity, endemicity is a bit of technical jargon that has been refashioned as shorthand for the threshold when science supposedly says we can stop worrying about COVID. But that isn’t up to science alone. We decide when we stop worrying about COVID. How far we are willing to go to prevent how many more cases is a question with social and economic trade-offs.

For now, we are truly living through unprecedented times. SARS-CoV-2 is the first virus modern science has ever seen emerge and march toward global endemicity. We’ve never watched this process play out before in such detail. We won’t know what endemic COVID looks like until we get there. But we do have to figure out how to live with the coronavirus, now and into the future.

There are papers like this being published, these 2 from this week alone:

https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-021-06902-1

But immunity isn’t a binary switch that some party-crashing variant can flip off. Even if a wily virus erodes some of the safeguards that our original flavour vaccines have raised, it’s nearly impossible for a variant to wipe them away completely. I don’t think we’re ever going to go back to square one of having no immunity against this virus. Defences, if they drop, should fall stepwise, not all at once: first against infection, then transmission and mild symptoms, and finally the severest disease. And vaccinated immune systems are extraordinarily stubborn about letting go of those last fortifications, this picture remaining incredibly important:

The degree and speed of erosion remain very much up for debate. Our vaccines may turn out to be a meh match for this variant; vaccine makers might rush to update their shots. We should know more soon, though am not sure what to make of all the contradictory neutralisation assays. If I understand it rightly, of the 10% of Danish Omicron cases, 20% have had boosters. The maths becomes easy. But now, actually, is still a pretty good time to sign up for a booster, as the CDC, FDA, Boris and so on have urged, even though they won’t exactly mirror Omicron’s every quirk. A vaccine that’s only a so-so match for a virus variant can still create a stellar shield. Sometimes, dips in immunisation quality can be rescued with a little extra quantity.

Consider, first, what happens when a vaccine trains a body using a near-perfect pantomime of the pathogen that later appears. A COVID-19 shot pumps in a little lesson on coronavirus spike, modelled on the original virus; immune cells study its contents and panic, then scramble to sweep away the interloper. When the actual virus appears, the process repeats itself more swiftly and smoothly. T cells home in on infected cells and annihilate them; antibodies, churned out by B cells, anchor themselves stubbornly all over the spike, gumming on as tightly as superglue. This sticky strategy is particularly powerful: Antibodies can prevent SARS-CoV-2 from using its spike to dock onto vulnerable cells, or earmark the virus for violent destruction. The microbe can be cleared from the body before it even has time to cause symptoms or spread to someone else.

When a new version of the virus shows up, freckled with mutations, certain antibodies may start to lose their grip; 32 of Omicron’s mutations are in the spike. Some could stop tethering to the microbe entirely, while others might slip on and off the pathogen as if slicked with heavy palm sweat. That leaves the virus’s key protein uncovered more frequently, giving the microbe more opportunity to interact with your cells.

That scenario is less than ideal but not necessarily a crisis. Spike’s a big old protein, and some of the antibodies sparked by the original vaccines should still be stage-four clingers. Even antibodies with subpar stickiness can still act in concert. Although each individual antibody might detach fairly frequently, if tons of others swoop in, even noncommittal molecules can keep the virus out of our cells. Antibody levels drop in the months after people get their shots, a natural and expected phenomenon, but boosters buoy them right back up, sometimes to new heights.

Quantity, of course, can’t infinitely compensate for quality. Immunologists and vaccinologists are now trying to get a handle on how bad the current variant-vaccine mismatch might be. One of the most straightforward experiments involves growing some Omicron (or an artificial look-alike), mixing it up with antibodies from immunised people, and seeing if the microbe can still infiltrate cells in a Petri dish. This test assesses antibody neutralisation, how well the molecules waylay viruses outside cells without assistance from other immune defenders. As mentioned, neutralisation assays are imperfect proxies for vaccine effectiveness. A fivefold drop in virus-blocking capacity, for example, doesn’t directly translate to a shot that’s now five times worse at protecting people.

In an actual human body, antibodies don’t have to work alone. Some of them pop onto the virus and flag down hungry cells that want to gobble it down. And the antibodies we have in our blood at any given moment aren’t the ones we’re stuck with. If, for instance, a small contingent of middling antibodies was struggling to pin Omicron in place, the rest of the immune system would notice and reawaken dormant, vaccine-taught B cells to help. Wised up to the mismatch, some of these veteran Bs would hunker down to learn Omicron’s features, then churn out more compatible antibodies. Totally new B cells, ones that didn’t respond to the original-recipe vaccine, would also rally, producing their own custom-made antibodies to hook onto Omicron.

Reinforcements would be marshalled from the T-cell side too, and unlike finicky antibodies, these assassins are tough to confuse. It’s much harder to evade a T-cell response than an antibody response. Faced with mutations, T cells will usually simply ignore them and annihilate their targets all the same. T cells on their own can’t stave off infection entirely. But they do seem able to bring disease under control before it gets too severe.

First vaccinations post up these defences in the body so they’re raring to go when a virus arrives. Boosters then build on that. Each additional dose serves as a scare tactic, terrifying the body into vanquishing a foe it was sure had been defeated before. More immune cells get mobilized. Antibody numbers skyrocket. B cells will manufacture antibodies that are sharper, stronger, and more sophisticated, better able to recognise and trounce coronavirus variants of all kinds, a response that’s expected to keep getting better. Months after vaccination, researchers can still see evidence of B cells trying to turn their antibodies into better weapons, just in case the virus returns. Fighting this variant could be, in many ways, a new and important reason to dose up again.

It’s possible boosters on their own won’t do the trick. Some immunized people will probably still get infected with Omicron, even a bit sick; if that happens too frequently, or if post-vaccination cases are consistently severe, we’ll need to trot out our contingency plans. Moderna is also testing whether a third full dose of its current shot (rather than the standard half-dose booster) might be enough to counteract Omicron’s stealth. It’s also mixing up some tweaked formulations that account for the variant’s mutations; Pfizer says it may do the same. Similar concerns fuelled the development of beta and delta specific boosters earlier this year, but we never actually had to use them. Beta mostly petered out on its own and against both variants, the original vaccine recipe seemed to do just fine.

Omicron’s genetic architecture threatens to combine some of Beta’s and Delta’s most concerning and immunity-elusive traits. Is Omicron going to be worse? Maybe. Although mRNA vaccines can be modified very quickly, they still have to be studied and cleared by the FDA. If that process kicks into gear, it’ll be at least a few weeks before the public can sign up. Everything is a matter of timing. Omicron’s looks very transmissible, not very harmful and let’s face it right now, viral variants will always turn around faster than new vaccines.

But that’s the point, regulation and the whole supply chain will speed up. So if Omicron-with-wings comes along and is harmful in the future, we’ve managed a trial run already.

Boosters alone won’t stop Omicron. Their power is mainly iterative, restorative; they lift what has already been laid down. If anything, the threat of Omicron is a reminder of the potency of first doses. These remain the most important line of defence. The more people who stay unvaccinated, the more difficult it will be for the fully vaccinated, and the boosted, to keep a fast-moving, fast-changing virus at bay. If Omicron’s the super-speedster some worry it could be, the stakes in the race between virus and vaccine just went up. There’s no time to waste.

Looking back and forwards

In hindsight, we clearly could have prepared more seriously, reacted more quickly, communicated more effectively, protected one another more actively and so on. But the next time there’s a public-health threat, we will do better. Right?

Not necessarily. Knowing the many ways that we mishandled COVID-19 is a bit like knowing the number of pages in a textbook to study before an exam. It gives us an idea of the task ahead but not how difficult the work will be. True preparation means studying the problems and working out solutions. There’s a lot of material to cover from this pandemic. And we have no idea when the next test is coming. Thought it interesting that TIME magazine sent a list of about 50 initiatives that could mitigate the next health crisis to experts who could expect to be involved. They asked them to score each strategy’s priority and feasibility on a scale of 1 to 5, with vaccines and drugs, and data scoring most highly:

https://time.com/collection/preventing-next-pandemic-survey/

With this in mind, research from Hopkins, Bloomberg and others considered each country’s ability to prevent, detect, and respond to health emergencies based on publicly available information in addition to other factors, such as public confidence in government. The Washington Post summarises: “The average country score for 2021 was 38.9 out of a possible 100 points, essentially unchanged from 2019. No country scored above 75.9. The United States, with its vast wealth and scientific capability, maintained its top overall ranking, it was also number 1 when the first index was released in 2019. But the United States also scored lowest on public confidence in government, a key factor associated with high numbers of coronavirus cases and deaths.” Other countries in the top 10 include: Australia, Finland, Canada, Thailand, Slovenia, the United Kingdom, Germany, South Korea and Sweden.

Looking back at biology, viruses have been on the planet for millions of years, much longer than Homo sapiens. Not quite technically “alive”, a virus is a strand of genetic code enclosed in a protein sheath and needs a living host to reproduce. We know about only a tiny fraction of the viruses in the world, although the work of finding them has sped up recently with the advent of genetic sequencing. There are about 1.6 million viruses on the planet in mammals and birds, of which about 700,000 could have the potential to infect humans. But of these, only about 250 have been identified in humans. The rest are still out there, they just haven’t made the leap. One of the world’s most prominent virus-hunters is Peter Piot, who co-discovered the Ebola virus in 1976. He explains that viruses are so nimble because they are always looking for their next host. “What is the raison d’être of a virus? It is to find a host to survive,” he tells me. “Because viruses cannot multiply without a living cell…viruses need susceptible plants, animals, humans, so they have to find them and then jump from one to another.”

Viruses typically lurk in a reservoir host, a plant or animal that can harbour them without getting sick, and then become more problematic when they cross into a new species. Many are concerned that coronavirus will not be our last deadly epidemic. “We are living in the age of pandemics,” Piot says, sounding a bit short of breath, a reflection of his own encounter with Covid-19 earlier this year, as reported in the FT. “I think we are going to see more and more of them, and the fundamental reason is that we failed to live in harmony with nature.” He points to the factors that make disease emergence more likely, such as deforestation and the illegal trade in wild animals. Forests cover about a third of land on Earth, but they are being cut down, often to make way for cash crops or cattle farming. Every minute, forests the size of 35 football pitches are cleared.

“This probably started already when we became sedentary, from nomads,” Piot says. “And I’m not saying we should go back and live like nomads. But when you put it all together, population pressure, urbanisation, agricultural practices, deforestation, high mobility… and then climate change is going to make all these things worse.” As the planet warms up, it is changing the patterns of disease. Insects that carry zoonotic ­diseases, such as ticks and mosquitoes, are ­expanding their range and moving into new areas. Lyme disease is spreading into North America and across Europe, recently prompting the European Centre for Disease Control to launch a monitoring programme for the illness, which is carried ­by ticks. Whatever the next event will be, and we know there’ll be another event, it’s already out there. For diseases like dengue fever, heavy rains make its spread more likely by creating breeding grounds for the mosquito that carries it. Last year there were a record number of dengue cases in Latin America, more than three million, amid concerns that climate change will exacerbate the disease.

While these are not new viruses, they are spreading in new areas and interacting with trends such as deforestation in ways that we don’t yet fully understand. As humans impact the planet in both obvious and non-obvious ways, by some counts new viruses are appearing more frequently. The broad outlines of how these diseases emerge are clear: they typically come from animals, spilling over into humans through close contact. And the places where this is most likely to happen are also known: disturbed land, fragmented habitats and wildlife markets. Knowing all this didn’t stop the world from suffering through coronavirus. But maybe, just maybe, it will help us get it right next time, or at least improve our chances. Dennis Carroll from the Global Virome Project certainly thinks so. He has spent nearly his whole life looking for viruses and is leading an ambitious project to find more of them, all of them, in fact. He’s also led a programme called “Predict” at the United States Agency for International Development, which morphed into the Global Virome Project.

The Global Virome Project is basically about going to the viruses before they come to us, and putting together a comprehensive database,” he says. “If we had this data, we would have picked up Covid-19 in October [2019], for instance.” He believes our response to novel viruses is limited because we don’t know about them in advance, before they start infecting humans. “Whatever the next event will be, and we know there will be another event, it’s already out there,” he says. He refers to these unknown viruses as “viral dark matter”. To build this database will be expensive. Carroll estimates it would take about $1.6bn and at least 10 years to find 75% of the 1.6 million viruses. Predict catalogued and sequenced more than 900 novel viruses. But USAID decided to pull its funding for Predict under the Trump administration in 2019, just before the arrival of the Covid-19 pandemic. The Global Virome Project is considered something of a moonshot in the scientific community: even if all those viruses were identified, we might not be able to tell which ones are contagious and threatening to humans. What is key to know is which ones are the viruses that can, for humans, not only infect but have the ability to be transmitted from humans to humans, and science is not yet there.

Humans are probably becoming infected with viruses from animals all the time but in most cases it is aborted, in the sense that it may cause a problem in one person, but that is it. There is also a huge amount of marketing around this idea that it could stop the next pandemic. The big problem is it is far, far too many viruses to shortlist. It starts to look like a very long list of things that will just never make it into people. But supporters say that the research at Predict has already helped in the fight against Covid-19, and the Global Virome Project will too here: https://www.globalviromeproject.org/. And even if it doesn’t help us prevent, it prepares us to have the data to be ready to jump into action. One thing that scientists agree on is just how little we know about what’s out there. We haven’t identified all the mammals on the planet, let alone all the viruses. And even the viruses we have identified often remain mysterious. Ebola is one example: scientists have not been able to confirm which animal the virus resides in, also known as the reservoir host. Influenza viruses are another: because they mutate so quickly, a broad vaccine has never been possible. Every time we’re out there doing long-term surveillance, we’re finding new species of vertebrates. Take bats: about 1,400 species have been identified so far, and that number goes up each year. Bats are particularly interesting to epidemiologists, because they harbour so many viruses that can be harmful for humans, including Sars and Ebola. Also, monkeys and great apes, often act as sentinels for pathogens that impact humans because of their genetic similarity to us. Sometimes they can pass viruses to humans, HIV crossed over from chimpanzees, but humans can also pass viruses to apes (something of a concern during Covid-19 unless all these zoo animals can get it via some other means which I doubt).

Viruses are even more diverse than mammals, he explains, because they do not have a common origin. Every time we look for viruses, either in vectors or in hosts, we find new things, and they often challenge our understanding of the diversity of the viruses that are out there. Another thing scientists can agree on is that destruction of the natural world makes it more likely that new viruses will emerge and spill over into human populations. Cutting down forests, planting single-crop plantations for palm oil and operating large livestock farms can all increase human contact with emerging diseases. It doesn’t matter if you are a gorilla or a human, if you have a disturbed forest, you have a shift. You suddenly have diseases which become very abundant which were not abundant before. Things come into contact which were not supposed to be in contact. Some things die out, others become superabundant. So you have a higher likelihood of disease being transmitted, that is clear.

Habitat destruction also means that only the hardiest species survive, the very species most likely to carry disease. One example is the multimammate mouse, a common species in west Africa and the carrier of Lassa fever. The mouse appears to thrive in degraded landscapes such as agricultural plantations and around households, and Lassa cases have been increasing over time, killing thousands of people each year. Animals are behaving in very different ways than they normally would just to survive. They’re looking for food. We do not yet know whether a similar dynamic might have contributed to the emergence of Sars-Cov-2, which is believed to reside in a type of horseshoe bat as its reservoir host. From there the virus may have crossed directly into humans, or transferred through an intermediary such as a pangolin, or stored and released by a Chinese lab.

The suspected role of the pangolin in Covid-19, although still unconfirmed, points to another factor which was almost certainly in play: the illegal wildlife trade. Trafficking rare animals also traffics their viruses. With the world in the grip of the Covid-19 pandemic, there is a focus on finding solutions like never before, and not just for this virus but for the viruses to come. Vaccine research is one area already benefiting from this surge in investment, and an area where the hunt for new viruses could help in the long term. One group in this field is the Coalition for Epidemic Preparedness Innovations (Cepi), which was set up with backing from the Gates Foundation to work on vaccines for emerging diseases. This year it is leading the Covax initiative, which is developing a vaccine for Sars-Cov-2. Nine vaccines are under development, of which eight are already undergoing clinical trials. Sars-Cov-2 is an example where things are getting better all the time in terms of vaccine development.

There are a finite number of virus families, 25 or 26, and people do see that some of those families are more likely to have an emerging epidemic so working on viruses in those families you can learn an awful lot, even if that isn’t an exact match of what will come in the future. When Sars-Cov-2 came along, previous research on Mers (Middle East Respiratory Syndrome), which is also caused by a type of coronavirus, helped accelerate vaccine development. Cepi and others are also trying to develop vaccines that could target entire families of viruses, though that goal has been elusive so far. Sometimes the barriers to development are not just scientific: pharmaceutical companies have been reluctant to invest in vaccines for diseases that impact poor and remote populations. One example is Lassa fever, which has been around for 50 years but with no vaccine developed yet. Part of the reason Cepi was set up is to address these gaps; it has six vaccines in progress for Lassa fever. Developing futuristic broad vaccines and cataloguing every zoonotic virus on the planet are both compelling ideas, but many years away from becoming reality.

What else can be done in the meantime? Addressing the environmental destruction at the root of many new diseases is one option, albeit a difficult one. The logging of the Amazon rainforest, another hotspot for disease emergence, is of particular concern right now for ecologists and epidemiologists. But two approaches stand out that may be able to make a difference in the near term. One is to monitor human health more closely in hotspot areas so that new diseases can be spotted and treated more quickly. Another is to incorporate ecology more closely into public health decisions. Tying human health programmes together with wildlife monitoring is already starting to happen in some areas. In some parts of Brazil, for example, primates are tested for yellow fever, so that humans living nearby can be vaccinated if necessary. Climate patterns and seasonal weather variations can be used to predict the timing and intensity of diseases such as dengue and cholera.

I don’t think the next pandemic is going to be predicted by some machine learning or some algorithm. You have to be on the ground. What is needed is to set up a very solid and strong surveillance system that enables people to detect these pathogens in real time, and then make this information available. A recent paper in Science estimated that spending about $30bn annually on measures such as reducing deforestation and curbing wildlife trafficking would pay for itself many times over by decreasing the risk of the next pandemic. “A major effort to retain intact forest cover would have a large return on investment, even if its only benefit was to reduce virus emergence events,” it stated. As the world fights on against Covid-19, researchers say that there are some silver linings. It has triggered a huge amount of investment and research. Scientists are collaborating more across fields, critical for an area such as zoonotic disease, which cuts across ecology, epidemiology and molecular biology. Advances in genetic sequencing could arm us better when the next virus arrives. And there is a fresh acknowledgment that human health is deeply connected to the health of our ­planet.

We’re so focused on these high-tech solutions because they appear to be what a high-income country would do. And indeed, the Biden administration has gone all in on vaccines, trading them off against other countermeasures, such as masks and testing, and blaming “the unvaccinated” for America’s ongoing pandemic predicament. The promise of biomedical panaceas is deeply engrained in many of our psyches, but COVID should have shown that medical magic bullets lose their power when deployed in a profoundly unequal society. There are other ways of thinking about preparedness. And there are reasons those ways were lost.

History lessons to the present

In 1848, after investigating a devastating outbreak of typhus in what is now Poland, the physician Rudolf Virchow wrote, “The answer to the question as to how to prevent outbreaks … is quite simple: education, together with its daughters, freedom and welfare.” Virchow was one of many 19th century thinkers who correctly understood that epidemics were tied to poverty, overcrowding, squalor, and hazardous working conditions, conditions that inattentive civil servants and aristocrats had done nothing to address. These social problems influenced which communities got sick and which stayed healthy. Diseases exploit society’s cracks, and so “medicine is a social science,” Virchow famously said. Similar insights dawned across the Atlantic, where American physicians and politicians tackled the problem of urban cholera by fixing poor sanitation and dilapidated housing. But as the 19th century gave way to the 20th, this social understanding of disease was ousted by a new paradigm.

When scientists realized that infectious diseases are caused by microscopic organisms, they gained convenient villains. Germ theory’s pioneers such as Robert Koch put forward an extraordinarily powerful vision of the pathogen as an entity that could be vanquished. And that vision, created at a time when European powers were carving up other parts of the world, was cloaked in metaphors of imperialism, technocracy and war. Microbes were enemies that could be conquered through the technological subjugation of nature. The implication was that if we have just the right weapons, then just as an individual can recover from an illness and be the same again, so too can a society. We didn’t have to pay attention to the pesky details of the social world or see ourselves as part of a continuum that includes the other life-forms or the natural environment.

Germ theory allowed people to collapse everything about disease into battles between pathogens and patients. Social matters such as inequality, housing, education, race, culture, psychology, and politics became irrelevancies. Ignoring them was noble; it made medicine and science more apolitical and objective. Ignoring them was also easier; instead of staring into the abyss of society’s intractable ills, physicians could simply stare at a bug under a microscope and devise ways of killing it. Somehow, they even convinced themselves that improved health would “ultimately reduce poverty and other social inequities,” wrote Allan Brandt and Martha Gardner in 2000:

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC1446218/

This worldview accelerated a growing rift between the fields of medicine (which cares for sick individuals) and public health (which prevents sickness in communities). In the 19th century, these disciplines were overlapping and complementary. In the 20th, they split into distinct professions, served by different academic schools. Medicine, in particular, became concentrated in hospitals, separating physicians from their surrounding communities and further disconnecting them from the social causes of disease. It also tied them to a profit-driven system that saw the preventive work of public health as a financial threat. “Some suggested that if prevention could eliminate all disease, there would be no need for medicine in the future,” Brandt and Gardner wrote.

This was a political conflict as much as an ideological one. In the 1920s, the medical establishment flexed its growing power by lobbying the Republican-controlled Congress and White House to erode public-health services including school-based nursing, outpatient dispensaries, and centres that provided pre- and postnatal care to mothers and infants. Such services were examples of “socialised medicine,” unnecessary to those who were convinced that diseases could best be addressed by individual doctors treating individual patients. Health care receded from communities and became entrenched in hospitals. Decades later, these changes influenced America’s response to COVID-19. Both the Trump and Biden administrations have described the pandemic in military metaphors. Politicians, physicians, and the public still prioritize biomedical solutions over social ones. Medicine still overpowers public health, which never recovered from being “relegated to a secondary status: less prestigious than clinical medicine [and] less amply financed,” wrote sociologist Paul Starr. It stayed that way for a century.

During the pandemic, many of the public-health experts who appeared in news reports hailed from wealthy coastal universities, creating a perception of the field as well funded and elite. That perception is false. In the early 1930s, the U.S. was spending just 3.3 cents of every medical dollar on public health, and much of the rest on hospitals, medicines, and private health care. And despite a 90-year span that saw the creation of the CDC, the rise and fall of polio, the emergence of HIV, and relentless calls for more funding, that figure recently stood at … 2.5 cents. Every attempt to boost it eventually receded, and every investment saw an equal and opposite disinvestment. A preparedness fund that was created in 2002 has lost half its budget, accounting for inflation. Zika cash was cannibalised from Ebola money.

In May this year, the Biden administration said that it would invest $7.4 billion in recruiting and training public health workers, creating tens of thousands of jobs. Last year, America’s data systems proved to be utterly inadequate for tracking a rapidly spreading virus. Volunteer efforts such as the COVID Tracking Project had to fill in for the CDC. Academics created a wide range of models, some of which were misleadingly inaccurate. But public health’s long-standing neglect means that simply making the system fit for purpose is a mammoth undertaking that can’t be accomplished with emergency funds, especially not when those funds go primarily toward biomedical countermeasures.

But here is public health’s bind: though it is so fundamental that it can’t (and arguably shouldn’t) be tied to any one type of emergency, emergencies are also the one force that can provide enough urgency to strengthen a system that, under normal circumstances, is allowed to rot. When a doctor saves a patient, that person is grateful. When an epidemiologist prevents someone from catching a virus, that person never knows. Public health is invisible if successful, which can make it a target for policy.

Biden’s new pandemic plan contains another telling detail about how the U.S. thinks about preparedness. The parts about vaccines and therapeutics contain several detailed and explicit strategies. The part about vulnerable communities is a single bullet point that calls for strategies to be developed:

https://www.whitehouse.gov/wp-content/uploads/2021/09/American-Pandemic-Preparedness-Transforming-Our-Capabilities-Final-For-Web.pdf

This isn’t a new bias. In 2008, Philip Blumenshine and his colleagues argued that America’s flu-pandemic plans overlooked the disproportionate toll that such a disaster would take on socially disadvantaged people. Low-income and minority groups would be more exposed to airborne viruses because they’re more likely to live in crowded housing, use public transportation, and hold low-wage jobs that don’t allow them to work from home or take time off when sick. When exposed, they’d be more susceptible to disease because their baseline health is poorer, and they’re less likely to be vaccinated. With less access to health insurance or primary care, they’d die in greater numbers. These all came to pass during the H1N1 swine-flu pandemic of 2009.

When SARS-CoV-2 arrived a decade later, history repeated itself. The new coronavirus disproportionately infected essential workers, who were forced to risk exposure for the sake of their livelihood; disproportionately killed Pacific Islanders, Latino, Indigenous and Black Americans; and struck people who’d been packed into settings at society’s margins, prisons, nursing homes, meatpacking facilities. Such patterns are not inevitable. That should just be a political given, and it is not. You have Democrats who don’t even say this, let alone Republicans. Our ethos of rugged individualism pushes people across the political spectrum to see social vulnerability as a personal failure rather than the consequence of centuries of racist and classist policy, and as a problem for each person to solve on their own rather than a societal responsibility. And our biomedical bias fosters the seductive belief that these sorts of social inequities won’t matter if a vaccine can be made quickly enough.

But inequity reduction is not a side quest of pandemic preparednesss. It is arguably the central pillar, if not for moral reasons, then for basic epidemiological ones. Infectious diseases can spread, from the vulnerable to the privileged. “Our inequality makes me vulnerable,” Mary Bassett, who studies health equity at Harvard, said. “And that’s not a necessary feature of our lives. It can be changed.”

In this light, the American Rescue Plan, the $1.9 trillion economic-stimulus bill that Biden signed in March, is secretly a pandemic-preparedness bill. Beyond specifically funding public health, it also includes unemployment insurance, food-stamp benefits, child tax credits, and other policies that are projected to cut the poverty rate for 2021 by a third, and by even more for Black and Hispanic people. These measures aren’t billed as ways of steeling us against future pandemics—but they are. Also on the horizon is a set of recommendations from the COVID-19 Health Equity Task Force, which Biden established on his first full day of office.  Some of the American Rescue Plan’s measures are temporary, and their future depends on the $3.5 trillion social-policy bill that Democrats are now struggling to pass, drawing opposition from within their own party. Health equity requires multiple generations of work, and politicians want outcomes that can be achieved in time to be recognized by an electorate. That electorate is tiring of the pandemic, and of the lessons it revealed.

Last year, for a moment, we were able to see the invisible infrastructure of society. Socially privileged people now also enjoy the privilege of immunity, while those with low incomes, food insecurity, eviction risk, and jobs in grocery stores and agricultural settings are disproportionately likely to be unvaccinated. Once, they were deemed “essential”; now they’re treated as obstinate annoyances who stand between vaccinated America and a normal life.

The pull of the normal is strong, and our metaphors accentuate it. We describe the pandemic’s course in terms of “waves,” which crest and then collapse to baseline. We bill COVID-19 as a “crisis”, a word that evokes decisive moments and turning points, and that, whether you want to or not, indexes itself against normality. The idea that something new can be born out of it is lost, because people long to claw their way back to a precrisis state, forgetting that the crisis was itself born of those conditions.

Better ideas might come from communities for whom normal was something to survive, not revert to. The panic-neglect cycle is not irresistible. Some of the people I spoke with expressed hope that we can defy it, just not through the obvious means of temporarily increased biomedical funding. Instead, they placed their faith in grassroots activists who are pushing for fair labour policies, better housing, health-care access, and other issues of social equity. Such people would probably never think of their work as a way of buffering against a pandemic, but it very much is, and against other health problems, natural disasters, and climate change besides. These threats are varied, but they all wreak their effects on the same society. And that society can be as susceptible as it allows itself to be.

One of the best-studied examples, a seasonal coronavirus called 229E, infects people repeatedly throughout their lives. But it’s not clear whether these reinfections are the result of fading immune responses in their human hosts or whether changes in the virus help it to dodge immunity. To find out, Bloom got hold of decades-old blood samples from people probably exposed to 229E, and tested them for antibodies against different versions of the virus going back to the 1980s.

The results were striking. Blood samples from the 1980s contained high levels of infection-blocking antibodies against a 1984 version of 229E. But they had much less capacity to neutralize a 1990s version of the virus. They were even less effective against 229E variants from the 2000s and 2010s. The same held true for blood samples from the 1990s: people had immunity to viruses from the recent past, but not to those from the future, suggesting that the virus was evolving to evade immunity. Variants such as Omicron and Delta carry mutations that blunt the potency of antibodies raised against past versions of SARS-CoV-2. And the forces propelling this ‘antigenic change’ are likely to grow stronger as most of the planet gains immunity to the virus through infection, vaccination or both. Researchers are racing to characterise the highly mutated Omicron variant. But its rapid rise in South Africa suggests that it has already found a way to dodge human immunity.

How SARS-CoV-2 evolves over the next several months and years will determine what the end of this global crisis looks like, whether the virus morphs into another common cold or into something more threatening such as influenza or worse. A global vaccination push that has delivered nearly 8 billion doses is shifting the evolutionary landscape, and it’s not clear how the virus will meet this challenge. Meanwhile, as some countries lift restrictions to control viral spread, opportunities increase for SARS-CoV-2 to make significant evolutionary leaps.

Scientists are searching for ways to predict the virus’s next moves, looking to other pathogens for clues. They are tracking the effects of the mutations in the variants that have arisen so far, while watching out for new ones. They expect SARS-CoV-2 eventually to evolve more predictably and become like other respiratory viruses, but when this shift will occur, and which infection it might resemble is not clear.

An early plateau

Scientists tracking the evolution of SARS-CoV-2 are looking out for two broad categories of changes to the virus. One makes it more infectious or transmissible, for instance by replicating more quickly so that it spreads more easily through coughs, sneezes and wheezes. The other enables it to overcome a host’s immune response. When a virus first starts spreading in a new host, the lack of pre-existing immunity means that there is little advantage to be gained by evading immunity. So, the first and biggest gains a new virus will make tend to come through enhancements to infectivity or transmissibility.

Genome sequencing which we’ve led in the UK early in the pandemic showed the virus diversifying and picking up 2 single letter mutations per month. This rate of change is about half that of influenza and one-quarter that of HIV, thanks to an error-correcting enzyme coronaviruses possess that is rare among other RNA viruses. But few of these early changes seemed to have any effect on the behaviour of SARS-CoV-2 or show signs of being favoured under natural selection.

An early mutation called D614G within the gene encoding the virus’s spike protein, the protein responsible for recognising and penetrating host cells, seemed to offer a slight transmissibility boost. But this gain was nothing like the leaps in transmissibility that researchers would later observe with the variants Delta and Alpha. The virus’s evolution as like walking in a landscape, where higher elevations equate to improved transmissibility. When SARS-CoV-2 began spreading in humans it seemed to be on a ‘fitness plateau’ surrounded by a landscape of many possible evolutionary outcomes. In any given infection, there were probably thousands of viral particles each with unique single-letter mutations, but Otto suspects that few, if any, of these made the virus more infectious. Most changes probably reduced transmissibility.

If the virus entered at a reasonably high point, any one-step mutation would take it downhill; summiting higher peaks required the combinations of several mutations to make more-significant gains in its ability to spread. In late 2020 and early 2021, there were signs that SARS-CoV-2 had scaled some distant peaks. Researchers in the UK spotted a variant called B.1.1.7 that contained numerous mutations in its spike protein:

That variant, Alpha, spread at least 50% faster than earlier circulating lineages. UK public-health officials linked it to a mysterious rise in cases in southeast England during a national lockdown in November 2020. Around the same time, virus hunters in South Africa linked another mutation-laden variant called B.1.351, now known as Beta, to a second wave of infections there. Not long after, a highly transmissible variant, now called Gamma, was tracked to Amazonas state in Brazil.

These three ‘variants of concern’ share some mutations, particularly in key regions of the spike protein involved in recognizing the host-cell ACE2 receptors that the virus uses to enter cells. They also carried mutations similar or identical to those spotted in SARS-CoV-2 in people with compromised immune systems whose infections lasted for months. This led researchers to speculate that long-term infections might allow the virus to explore different combinations of mutations to find ones that are successful. Typical infections lasting days offer fewer opportunities. Super-spreading events, where large numbers of people are infected, might also explain why some variants flourished and others fizzled out.

Whatever their origins, all three variants seemed to be more infectious than the strains they displaced. But Beta and Gamma also contained mutations that blunted the potency of infection-blocking ‘neutralizing’ antibodies triggered by previous infection or vaccination. This raised the possibility that the virus was beginning to behave in the ways predicted by studies of 229E.

The 3 variants spread around the world, particularly Alpha, which sparked new waves of COVID-19 as it came to dominate in Europe, North America, the Middle East and beyond. Many researchers expected that a descendant of Alpha, which seemed to be the most infectious of the bunch, would pick up additional mutations, such as those that evade immune responses, to make it even more successful. That absolutely proved not to be the case: Delta came out of left field.

The Delta variant was identified in India’s Maharashtra state during a ferocious wave of COVID-19 that hit the country in the spring of 2021, and researchers are still taking stock of its consequences for the pandemic. Once it arrived in the UK, the variant spread quickly and epidemiologists determined that it was about 60% more transmissible than Alpha, making it several times as infectious as the first circulating strains of SARS-CoV-2. Delta is kind of a super-Alpha; the virus is still looking for solutions to adapt to the human host.

Studies from labs suggested that Delta made significant gains in fitness by improving its ability to infect human cells and spread between people. Compared with other variants, including Alpha, Delta multiplies faster and to higher levels in the airways of infected individuals, potentially outpacing initial immune responses against the virus. Yet researchers expect such gains to become ever smaller. Scientists measure a virus’s inherent ability to spread in an immunologically naive population (that is, unvaccinated and not exposed to the virus previously) by a number called R0, which is the average number of people an infected person infects. Since the start of the pandemic this figure has jumped as much as threefold. At some point, I would expect that increased transmissibility will stop happening. It’s not going to become infinitely transmissible. Delta’s R0 is higher than seasonal coronaviruses and influenza, but still lower than that of polio or measles.

Other established human viruses do not make the leaps in infectivity that SARS-CoV-2 has in the past two years, and Bloom and other scientists expect the virus to eventually behave in the same way. Trevor Bedford, the evolutionary biologist at the Fred Hutchinson, says the virus must balance its ability to replicate to high levels in people’s airways with the need to keep them healthy enough to infect new hosts. “The virus doesn’t want to put someone in bed and make them sick enough that they’re not encountering a number of other people,” he says. One way for the virus to thread this needle would be to evolve to grow to lower levels in people’s airways, but maintain infections for a longer period of time, increasing the number of new hosts exposed to the virus. “Ultimately there’s going to be trade-off between how much virus you can produce and how quickly you elicit the immune system.” By lying low, SARS-CoV-2 could ensure its continued spread.

If the virus evolved in this way, it might become less severe, but that outcome is far from certain. “There’s this assumption that something more transmissible becomes less virulent. I don’t think that’s the position we should take,” says Balloux. Variants including Alpha, Beta and Delta have been linked to heightened rates of hospitalisation and death — potentially because they grow to such high levels in people’s airways. The assertion that viruses evolve to become milder “is a bit of a myth. The reality is far more complex.”

The rise of Omicron

Delta and its descendants now account for the vast majority of COVID-19 cases worldwide but it looks like Omicron is rapidly replacing it. Most researchers expected these Delta lineages to eventually outcompete the last holdouts. But Omicron has undermined those predictions. A lot of us were expecting the next weird variant to be a child of Delta, and this is a bit of a wild card. The swift rise in cases of Omicron in South Africa suggests that the new variant has a fitness advantage over Delta. Omicron carries some of the mutations associated with Delta’s sky-high infectivity. But if increased infectivity were the sole reason for its rapid growth, it would translate to an R0; that’s very implausible. Omicron’s rise may be largely due to its ability to infect people who are immune to Delta through vaccination or previous infection.

Scientists’ portrait of Omicron is still blurry and it will take weeks before they can fully assess its properties. But if the variant is spreading, in part, because of its ability to evade immunity, it fits in with theoretical predictions about how SARS-CoV-2 is likely to evolve. As gains in SARS-CoV-2’s infectivity start to slow, the virus will have to maintain its fitness through overcoming immune responses. For instance, if a mutation or set of mutations halved a vaccine’s ability to block transmission, this could vastly increase the number of available hosts in a population. It’s hard to imagine that any future gains in infectivity could provide the same boost.

Evolving to evade immune responses such as antibodies could also carry some evolutionary costs. A spike mutation that dodges antibodies might reduce the virus’s ability to recognise and bind to host cells. The receptor-binding region of spike, the major target for neutralising antibodies, is relatively small and the region might be able to tolerate only so much change and still perform its main job of attaching itself to host cells’ ACE2 receptors. It’s also possible that repeated exposure to different versions of spike, through infection with different virus strains, vaccine updates or both, could eventually build up a wall of immunity that SARS-CoV-2 will have difficulty overcoming. Mutations that overcome some people’s antibody responses are unlikely to foil responses across an entire population, and T-cell-mediated immunity, another arm of the immune response, seems to be more resilient to changes in the viral genome.

Such constraints might slow SARS-CoV-2’s evasion of immunity, but they are unlikely to stop it. There is clear evidence that some antibody-dodging mutations do not carry large evolutionary costs; the virus will always be able to mutate parts of the spike.

A virus in transition

How SARS-CoV-2 evolves in response to immunity has implications for its transition to an endemic virus. There wouldn’t be a steady baseline level of infections. A lot of people have a flat horizontal line in their head, which is not what endemic infections do. Instead, the virus is likely to cause outbreaks and epidemics of varying size, like influenza and most other common respiratory infections do.

To predict what these outbreaks will look like, scientists are investigating how quickly a population becomes newly susceptible to infection, and whether that happens mostly though viral evolution, waning immune responses, or the birth of new children without immunity to the virus. Small changes that open up a certain fraction of the previously exposed population to reinfection may be the most likely evolutionary trajectory. The most hopeful, but probably least likely, future for SARS-CoV-2 would be to follow the path of measles. Infection or vaccination provides lifetime protection, and the virus circulates largely on the basis of new births. Even a virus like measles, which has essentially no ability to evolve to evade immunity, is still around.

A more likely, but still relatively hopeful, parallel for SARS-CoV-2 is a pathogen called respiratory syncytial virus (RSV). Most people get infected in their first two years of life. RSV is a leading cause of hospitalisation of infants, but most childhood cases are mild. Waning immunity and viral evolution together allow new strains of RSV to sweep across the planet each year, infecting adults in large numbers, but with mild symptoms thanks to childhood exposure. If SARS-CoV-2 follows this path, aided by vaccines that provide strong protection against severe disease, it becomes essentially a virus of kids.

Influenza offers another scenario, in fact two. The influenza A virus, which drives global seasonal influenza epidemics each year, is characterized by the rapid evolution and spread of new variants able to escape the immunity elicited by past strains. The result is seasonal epidemics, propelled largely by spread in adults, who can still develop severe symptoms. Flu jabs reduce disease severity and slow transmission, but influenza A’s fast evolution means the vaccines aren’t always well matched to circulating strains. But if SARS-CoV-2 evolves to evade immunity more sluggishly, it might come to resemble influenza B. That virus’s slower rate of change, compared with influenza A, means that its transmission is driven largely by infections in children, who have less immunity than adults.

How quickly SARS-CoV-2 evolves in response to immunity will also determine whether, and how often vaccines need to be updated. The current offerings will probably need to be updated at some point, says Bedford. His team found signs that SARS-CoV-2 was evolving much faster than seasonal coronaviruses and even outpacing influenza A, whose major circulating form is called H3N2. Bedford expects SARS-CoV-2 to eventually slow down to a steadier state of change. “Whether it’s H3N2-like, where you need to update the vaccine every year or two, or where you need to update the vaccine every five years, or if it’s something worse, I don’t quite know,” he says:

https://www.biorxiv.org/content/10.1101/2021.09.11.459844v3

Although other respiratory viruses, including seasonal coronaviruses such as 229E, offer several potential futures for SARS-CoV-2, the virus may go in a different direction entirely. The sky-high circulation of the Delta variant and the rise of Omicron, aided by inequitable vaccine roll-outs to lower-income countries and minimal control measures in some wealthy countries such as the USA and the UK, offer fertile ground for SARS-CoV-2 to take additional surprising evolutionary leaps. SARS-CoV-2 could become more severe or evade current vaccines by recombining with other coronaviruses. Continued circulation in animal reservoirs, such as mink or white-tailed deer, brings more potential for surprising changes, such as immune escape or heightened severity.

Conclusions

It may be that the future of SARS-CoV-2 is still in human hands. Vaccinating as many people as possible, while the jabs are still highly effective, could stop the virus from unlocking changes that drive a new wave. There may be multiple directions that the virus can go in and the virus hasn’t committed. Should new vaccines be needed, and it’s still unclear, Omicron will present the first true test of how quickly mRNA vaccines can be reprogrammed and redeployed. Both Pfizer-BioNTech and Moderna predict they can have new batches ready for human trials within three months. That ability, has fundamentally changed the calculus for Omicron and any future pandemic against which scientists can readily build an mRNA vaccine; how quickly and how much vaccine can be made.

Of course, researchers don’t know how to build a vaccine against every virus; the Covid-19 shot depended on two decades of academic work on other coronaviruses. Anthony Fauci and others at NIH have championed a multi-billion dollar “prototype pathogen” project to fund early-stage development for vaccines against the roughly 20 bugs known to have pandemic potential, allowing companies and government agencies to hit the gas in the event of any outbreak. It would also have the benefit of keeping alive the clinical trial and mRNA manufacturing networks the world built up over Covid. It’s not easy to maintain infrastructure if it’s not being used. Monoclonal antibody treatments from Regeneron and Lilly will probably lose efficacy, but the antibody from Vir and a “universal” antibody from Adagio likely won’t. Neither will the new antivirals from Merck and Pfizer, because they don’t act on the spike protein. I think. But I don’t know.

As the first at-home treatments for Covid, these pills will likely become a key part of the response to Omicron and Covid-19 going forward, with various authorisations having occurred or pending and both companies having struck deals to make them available around the globe. But they also might become a tool to combat other epidemics and pandemics for decades to come. Do we need them now, do we even need Omicron-specific vaccines now. I don’t know but even with the IFR mentioned here of 0.05%, it has potential to cause major harm if one does the simple maths with huge denominators, in a spikey peak later this month:

https://twitter.com/pieterstreicher/status/1469743320092102659?s=24

Omicron is an interesting test case, and whilst the lack of hospitalisations would lead one to the nice conclusion that this is the end of the pandemic, it’s simply not the last variant, and the next one could be worse. Thus, it’s not the end, not even the beginning of the end, but a step in its evolution to being endemic with us.

 


Justin Stebbing
Managing Director

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