Clear Scientific Communication is at the Heart of Public Trust
The continuing COVID-19 pandemic impels the world to question how it will be possible to recover. Leaders attempt to boost confidence with “hopeful” messaging. But poor public understanding is beset by contradictions from public health officials. The tone of ambivalence from experts creates an appearance of half-truths and an approach of half measures. Making sense of the science requires embracing a level of uncertainty and the flexibility to change paradigms as better evidence emerges. Although the complexity of dynamic experimental research may be challenging to convey, poor public communication erodes an already diminished trust in institutions and science.
The public wants to make informed choices about their own health, but information for even the scientifically fluent and information savvy, is scarce and confused. Before getting vaccinated or complying with any number of potentially risky public health recommendations, people want to better understand the scientific rationale behind vaccine policies, the possible trajectory for viral evolution, and risks posed to human health. Navigating the coronavirus pandemic also requires careful helmsmanship through the COVID-19 infodemic. Transparent and unvarnished communication is a start. “This too shall pass” doesn’t work here. Society cannot wait for this one to pass. This article describes the complexity of viruses and attempts to detail elements about the novel coronavirus that may be relevant but ignored in the scientific public discourse.
Viruses are still largely mysteries, even to scientists. It is often debated whether or not they are really living, since they lack many of the characteristics that describe life. Viral genetic diversity is difficult to characterize because viruses lack conserved genetic markers that are often used to understand relatedness in cellular organisms. They infect all forms of living cells, from animals to bacteria, and are significantly represented in symbiotic organisms, such as corals. They have largely been thought of as parasitic, but some do behave as mutualistic organisms. The evolution of placental mammals is attributed to a mutualistic retrovirus. In fact, they are heteronomous, in that they have diverse life cycles, and they can even be advantageous, although they are more often known for their harmful attributes. SARS-CoV-2, the newest notable in a family of notorious RNA viruses, is well recognized as a nasty example. Its most incredible feature, as an RNA virus, is its ability to change.
Viruses Can Jump Into Different Hosts In What Is Known As “Spillover”
In general, hundreds of viruses spillover from other organisms to infect people, but most of these spillover events result in a failure to launch. If viruses do make it, they often take an unremarkable path to rapid obsolescence. Only about half of spillover viruses are even transmissible (the capacity to be passed on to new hosts). Mostly, a virus lies in wait for a viable host, teetering on the brink of extinction and then falling off. The majority die out due to a lack of a compatible host. Viruses need a partner to function since they lack much of their own biological components for replication. Viruses find a host, but if the host is a recluse and hasn’t many friends to introduce to its companion pathogen, it dies out, as well. A successful virus is one that meets a compatible host – and the ideal host candidate is one that is extremely social, existing in continual close proximity to others of its kind so that the virus can jump from one reservoir to the next without much demand for a sophisticated strategy or need to adapt its script. Humans have made the perfect vector for SARS-CoV-2. Our inherent socialization and population-dense habitats, coupled with our technology-boosted mobile lifestyles, make us some of the most efficient viral dispersers known to life.
SARS-CoV-2 superficially appears indistinguishable from legions of other respiratory pathogens, in part because it imparts common symptoms. The potential harm of SARS-CoV-2 has been underestimated by some, its pathogenicity mistaken for superficial similarities of more familiar illnesses such as the flu and the cold. A COVID-19 infected person may experience nothing, or a rattling of the lungs and fever or chills, but for others it is much more deadly. Its variable lethality makes it hard to characterize, leading some to misjudge and make those who have only seen mild cases believe it only badly afflicts a limited demographic. But COVID-19 has proven to be severe or lethal in nearly all demographics, even though predominantly the weak and vulnerable are its most visible targets. Moreover, many infected people, including those with mild cases early on, can experience long-term health consequences from the virus, sometimes with serious effects that do not immediately appear. This seemingly ordinariness to many is part of its maleficence. It is a Trojan horse, hiding in plain sight.
The COVID-19 virus’ stealthiness and its ability to disguise itself as benign or mild in a vast number of cases, or not presenting at all for pre-symptomatic and asymptomatic cases, allows it to silently jump into new carriers without alerting the host of its presence. It is extremely competent at replication, creating unwitting super-spreaders. This allows the virus to continue circulating through the population, silently replicating, exploiting human weakness, readily adapting, and spreading all the more. This is in contrast to its close cousin SARS-CoV-1 (sometimes referred to as just SARS or SARS “classic”), which during its own pandemic moment in 2002-2004, was so evidently virulent that it was easily identifiable. SARS classic was so conspicuous, it made it relatively facile to suppress, much like a heavy-footed hobbling assassin who lacks any element of surprise.
Viral Fitness Is Characterized By Transmissibility And Virulence
Understanding viral evolution can help predict the trajectory of a pathogenic virus in order to develop useful management strategies. But given the diversity among viruses and selective pressures provided by the host environment, it is hard to generalize. Transmissibility (discussed above) and virulence, or the virus’ ability to cause harm to the host, are two important factors that govern outcomes for the host. How to measure virulence is still debated, particularly with respect to teasing out theory and empiricism in viral evolution. From a theoretical position, virulence is usually captured in models as mortality, while experimental formulations exist within a range of sublethal measures that are much harder to quantify and unite in analyses. This creates a gap between observed versus theoretical knowledge of virus virulence, particularly between species. Generalizing whether a virus will become more or less lethal on the basis of inputs and interventions from what is known of other viruses is disputed.
The term “trade-offs” between different aspects of viral fitness was first introduced to explain various patterns in severity of pathogenicity. A classic view originally held by biologists was that virulence should decrease over time, reaching an equilibrium preserving optimum fitness for the virus, based on the evolutionary reasoning that the virus would not benefit from being too harmful to its hosts, because exterminating the host would inhibit its spread. This would result in a die-out of the virus. The logic makes a reciprocal assumption, where increased transmissibility, or a more infectious virus, should result in a milder virus, because if viral hosts are less sick, they are more likely to be moving around and exposing the virus to new potential hosts. Therefore, viruses that spread more easily, or are more transmissible, should leave more descendants, or be more evolutionarily fit. Likewise, those that too easily kill off their hosts will not replicate as readily and be less fit. The argument follows that a virulent virus should tend towards less virulence over time. This would mean that viral pandemics would eventually resolve through a natural lethal recession, leaving people sick but not dead, or not sick at all.
This cost-benefit trade-off is thought to be exemplified by theoretical models in animals for malaria. There are several examples where human pandemics were lethal but then receded towards a more benign illness. Some use SARS-CoV-1 as an example of such a case, but recession in many cases, like SARS classic, had more to do with containment strategies and other behavioral interventions which led to eventual viral suppression. Moreover, in experimental settings for vaccine development, SARS-CoV-1 regained fitness, becoming more virulent after a period of recession. In other cases where virus virulence was reduced over time, such as the flu, a level of host immunity had developed after continued long term exposure or with polio, from widespread vaccination. In the specific case of the flu, a lifetime of exposure has built up immunity for almost everyone today from continual exposure since birth.
Trade-offs could be a function between several fitness factors, although evolutionary geneticists argue that the transmission-virulence trade-off has little empirical support. There is still limited understanding of trade-off dynamics. What is known is that virulence does evolve in pathogens. This means that viruses can become more or less lethal due to environmental conditions that drive the evolutionary process. In several experimental evolution studies, serial passage of viruses increases virulence in new hosts from intra-host competition, meaning that viruses can evolve to become more dangerous within hosts. One postulate is that increasing lethality in hosts is due to competition with new viral strains existing within the host.
If there is no selective pressure on a host to “self-limit” its virulence, a virus will remain virulent and can become even more lethal. Hypothetically, an abundance of excess vectors – or the abundance of available hosts, could eliminate the pathogen’s need for hosts to survive and maintain the virus’ lethality. Humans can seed the environment with conditions that optimize viral fitness if the virus is capable of adapting. In the case of a disease like COVID-19, it is postulated that if enough people exist for the virus to easily pass from one host to the next, especially if they are moving around a lot and in close proximity to one another, then there is no selective pressure for the virus to reduce its virulence. The virus might not have to become milder in order to transmit well. Some argue the virus risks losing its own competitive advantage to a more aggressive viral strain, better at siphoning resources from the host, optimizing replication; therefore, maintaining its virulence may be more advantageous.
Trade-off models typically assume that a virus can evolve unbounded, but viral evolution is limited to maximal rates of entry, replication, viral assembly, and spread within the host. Defense responses within the host should bound the virus’ virulence and ultimately impact a virus’ success on a population level. This is not a certainty, however, and many factors change these variables. If the virus is allowed to mutate freely within the host because it has learned to bypass the immune surveillance of the host, or if it is exposed to selective pressures from competition of more aggressive mutant variants that may have evolved, then the virus may be less bounded and become more virulent. There is still little known about these evolutionary boundaries, but empirical observations reveal the complexity of some of these controls, including adaptations adjusted to optimize within-host competition, an interplay with host immunity, and changes in transmission. There is a misconception that a more virulent virus is more threatening than one with greater transmissibility. But a more transmissible virus allows for a greater abundance of mutants to arise, enriching a pool of potentially new variants that are better adapted to evade the human immune system or become more lethal. Trying to understand which direction the virus will go—more or less virulent and more or less transmissible—is a conundrum at the moment. The only certainty is uncertainty for this problem. Andrew Read, an evolutionary microbiologist at Penn State University, comments on the trajectory of SARS-CoV-2 evolution: “It (the virus) can get nicer, and it can get nastier.” Edward Holmes, an evolutionary virologist at the University of Sydney, Australia, reflects similarly: “One thing you learn about evolution is never to generalize.”
How RNA Viruses Are Optimized To Adapt: Quasi-Species Theory
Viruses reproduce asexually with ruthless efficiency by hijacking a host’s cellular apparati, bypassing the need to make or support their own costly metabolic investments. Due to the lack of biological overhead, they can replicate with unparalleled celerity and change evolutionary course without too much drag on their system. RNA viruses are even more evolutionarily competent at facing operational challenges. Instead of existing as a single genotype, they function as a collection of related genetic sequences, termed “quasi-species”, where fitness is determined by an increased ability to mutate rather than efficiency at replication.
Mutation and selection are what enable evolution to take place, but high mutation rates are typically unfavorable for most organisms because they often result in nonviable offspring. Classic biological “fitness” optimizes existing genetic variation through natural selection, rather than runaway mutation. Increasing mutation rates can be lethal in sexually reproducing organisms, but for RNA viruses, it may enhance diversity. This is accomplished by a critical threshold where RNA viruses exist known as “error catastrophe,” defined as the upper boundary between the genetic stability of a population and fidelity of replication, or the error rate enabling mutations. For RNA viruses, high mutation rates of RNA replication drive genetic evolution by readily manufacturing new variants, consequent to a lack of “proofreading activity” of the virus’ replicating apparatus. The thin boundary between genetic variants enables RNA viruses to be “cooperative”— profiting from a pool of mutations and allowing quasi-species mutants to rapidly select against environmental pressures. The quasi-species theory supposes that the short-term cost of individual mutation is benefited by population-level adaptability. High mutation rates have allowed for the proliferation of RNA viruses, arguably rendering them the most successful biological organisms. Virulence is believed to be enhanced when there is quasi-species diversity.
SARS-CoV-2 is an RNA virus, which describes how it replicates. RNA viruses are advantaged to readily proliferate and adapt. Replicability, transmissibility and adaptability are what make SARS-Co-V-2 so powerful. It is unclear how the evolution of viral quasi-species will develop for the COVID-19 pandemic. The big danger is whether the virus will evolve to become more transmissible and/or more virulent. Evolution is the COVID-19 virus’ weapon. Misappropriated focus is sometimes placed solely on morbidity rates of the virus’ victims, causing some critics to downplay the pandemic. Death rates are, of course, extremely important, but it is also important to reimagine the real threat of the virus and how it is publicly framed. Morbidity is not the only signal-variable to consider.
Emerging evidence and the appearance of mutant variants cropping up all over the globe provide evidence that the COVID-19 virus is, indeed, changing, it is changing faster than many expected, and the various mutants are readily being distributed far and wide. It is also "learning" from hosts, raising concerns for immune escape, a process that allows viruses to bypass immune surveillance and avoid detection. Recent findings of an immune-compromised patient who cultivated SARS-CoV-2 viral cultures within his body for 154 days helped researchers get a different view of how the virus is changing. Rather than representing a case of reinfection, where the patient is infected, clears the virus, and is infected again, this patient harbored the virus, where it intermittently attacked and receded, giving the virus insight into the weakness of human immune systems and letting it adapt. The patient eventually died. Genetic sequence of the virus over time using molecular amplification technologies showed that the COVID-19 virus evolved inside the patient, acquiring at least 20 mutations, a significant adaptive capacity. These mutations, if passed on, might help variants develop more sophisticated strategies to evade the human immune system.
Global movement (travel, trade, etc.) has vastly improved virus vectorization and helped give rise to new COVID-19 variants. This is unprecedented, as this is the first pandemic where technology has amplified the ability for global spread at present speed and magnitude, coupled with the enormous density of potential vectors inhabiting every biome. A mix of optimal Goldilocks conditions for the virus multiply the capacity for this pandemic to develop beyond the normal biological capacities that have driven past pandemics.
Even more troubling is our lack of understanding for how this virus behaves. New strains are the culprits in revisited pandemic hotspots that had already been devastated by COVID-19. Manaus, Brazil, located along the rainforests of the Amazon, had been ravaged by the disease earlier in 2020 with three-quarters of the city’s inhabitants infected by SARS-CoV-2. Again, a new wave is devouring the area. This reemergence of deadly outbreak in communities assumed to have developed immunity is concerning and raises doubt about immune durability, reinfection, and whether new variants are evolving escape mechanisms from immune defenses.
Vaccines have been heralded as the panacea to pandemic woes, but researchers wonder if new strains will become vaccine resistant. COVID-19 is a totally novel virus and humans are a naïve population without immune defense. Even if humans build up some level of durable immunity against SARS-CoV-2, it is not clear how long it will last, how strong it will be, and whether a full complement of immune defenses can be built to outpace the virus’ ability to learn the immune system and adapt against it. Humans have had no previous relationship with the virus, therefore it is impossible to know exactly how the immune response will develop. In addition to vaccine resistance or a lack of long term immunity, there could be other physiological effects, such as Antibody Dependent Enhancement, where previous exposure to viral antibodies could enhance a severe response upon new infection. ADE is possible in coronaviruses, but it is not clear that this is yet a problem for SARS-CoV-2. Due to the many ways in which the virus could change for the worse, policies to immediately reduce transmission have been prioritized, even if it is unknown if they are yet fully effective.
While it would appear understandable that much of society believed the barrier to controlling the pandemic would be technological, with the development of a viable vaccine being the key step, the main issues are largely logistical. Distribution management has impeded a speedy public health policy response, with other factors that are case-specific challenges. Governments, markets, and poor scientific communication are part of this impasse, which is being addressed. Such delays have prompted some health officials to consider extending second dose intervals to reach more people for those vaccines requiring multiple doses. Public health officials argue that unchecked spread of the virus poses the greatest risk, particularly in light of its capacity to mutate and its high mortality rates. Therefore, it is better to offer some immunity sooner rather than stronger immunity to a smaller segment of society. Many believe that upgrades and boosters will help where initial doses leave off. Vaccine optimists see multivalent vaccines effective against potential emerging variants. Criticism about changing dosing regimen has left the scientific community divided. This science becomes confusing due to the quantity of different vaccines and the variances in efficacies, defined experimentally before results are published.
Many scientists argue that quantity does not equal quality. A large portion of public health scientists have vigorously argued against altering a known effective dosing regimen. They argue that changes are risky in the absence of knowledge of vaccine durability and its efficacy under these modifications. Some argue that recommendations to government are based on assumptions rather than from trial data, such as those given by the Joint Committee on Vaccines and Immunization (JCVI) and the UK Chief Medical Officers in Great Britain. Biologists warn that mRNA, used in the genetic vaccines by Moderna and Pfizer, is quickly degraded by cellular enzymatic systems (RNAases), and that although alterations have been made to the molecules to improve the delivery and longevity of the vaccines, there are no data on how long a clinically effective immune response induces after just a single injection.
The predominant argument is that the faster more people can be immunized, irrespective of vaccine efficacy, the lower the probability for new variants to proliferate since replication is a necessity for new variants to develop. Partial protection is satisfactory if it meets the goal to eliminate deaths and reduce hospitalizations and severe cases, which the vaccines are purported to do if dose regimens from clinical trials are followed. But incomplete protection can also provide an environment for new strains to adapt to become more dangerous and thrive. It is not clear if current strategies will succeed at slowing viral transmission before more dangerous mutants take root and uncontrollably spread.
While it is still unclear what the long term effects of the vaccines are, they have thus far demonstrated to be relatively safe, according to data from trials and rollouts. Many health care professionals argue that vaccines are much safer than contracting COVID-19. But a lack of clarity about the many vaccines on the market has the public reticent to enroll. How the vaccines provide protection varies and their relative efficacies are confusing. While some of the confusion about efficacy has more to do with technical aspects of clinical trial protocols and metrics for end points rather than absolute efficacies, there are mechanistic differences between different vaccines that may carry different long term risks. Moreover, it has yet to be established that all vaccines stop the chain of transmission, which counters the predominant belief that vaccines provide complete personal protection. Some biologists warn that seeding a pool of millions of people with weakened antibodies providing only a meager immune response will accelerate the creation of variants that will learn how to mutate around defense systems. Moreover, mutations can proliferate due to poorly executed policy half-measures. New, more virulent or vaccine resistant strains are realistically probable outcomes.
Pandemic management requires consideration for individuals and populations. Minimizing individual deaths and protecting hospitals from ICU overwhelm has been a primary concern for public health experts. Public health strategies have also attempted to control population-wide transmission with lockdowns, vaccine strategies and a variety of other pandemic policies based on the rationale that the more the virus is given free rein to transmit widely, the more chances it has to develop its evolutionary fitness and mutate. This argument is nuanced rather than a binary debate because strategies need to tailor to specific conditions. The pandemic requires swift action based on partial information with many confounding variables for which much cannot be fully controlled. There will not be immediate scientific certainty for long-term risks. Ultimately, things will be boiled down to tradeoffs—where the risk of unknown outcomes will be weighed against known catastrophes.
Herd Immunity: Real World Versus Theory
Another part of the rationale to vaccinate as many people as possible is to create herd immunity. The term is regularly thrown into optimistic projections about a post-pandemic return to normality, often without full understanding of what it means, its potential and its limits. Herd immunity is a key component of epidemic control, in that only a certain percentage of the population needs to be immune to provide a protective effect to the whole community if herd immunity is reached. That quantity of immunized population varies from disease to disease and has been realized in the past artificially through vaccination. It creates a “shield,” or indirect protection, so that transmissibility becomes reduced and large outbreaks are controlled as fewer people are infected and unable to pass on the disease, with the goal of a natural die-out of the pathogen. It reduces the number of vaccinated people needed to protect the population, but it also provides alternative protection for the ineligible to receive vaccines.
“Natural herd immunity” is often conflated with “artificial herd immunity.” Natural herd immunity occurs over time—usually over the course of many lifetimes. The theory that natural herd immunity could be stimulated for COVID-19, promoted by fringe thinkers, advocacy think tanks and a few governments, created much confusion about the realistic possibility for such a suggestion. Trying to create natural herd immunity by unconstrained transmission is largely viewed as a dangerous proposition with no data to support it, historically or contemporaneously, with what we know of COVID-19 by the global scientific community. Yet the prospect of it circulated widely, even in scientific journals, in part due to a highly derided proposition put together by three scientists accused of “advocacy science,” captured in a manifesto known as “The Great Barrington Debate.” Countless scientific groups from around the world condemned this proposition and said that this is not a debate within the scientific community.
Artificial herd immunity (through vaccination), a demonstrated methodology for pandemic control, and natural herd immunity as a theoretical pandemic intervention, are confused in the media and scientific journals because they are not clearly distinguished as two separate phenomena and are sometimes both just referred to as “herd immunity.” When scientific debate occurs around “herd immunity” for vaccinations, it can be confused for natural herd immunity. Natural herd immunity, before COVID-19, was discussed mainly in regard to livestock disease and laboratory experiments. For humans, herd immunity became popularized when some protection was afforded to unvaccinated children during the measles outbreak from the majority of vaccinated population. The ability for herd immunity to function in the absence of a strong vaccine campaign is still uncertain. Even if it were to work, it requires several important variables to operate in an expected manner, beginning with long-term, durable immunity against the various strains of extant virus. This is far from being a clear case for COVID-19.
Science has made incredible progress developing vaccines. Some public sentiment is concerned that vaccine development occurred at such unprecedented pacing, but many working on the vaccine had begun with a head start working on viral vaccines for other pandemics, including that for SARS-CoV-1. Many elements of the mRNA vaccine had been studied during the first SARS pandemic. Most virologists anticipated some sort of global pandemic at some point in the future – a topic long discussed in science but ignored by the public at large since it was not a palpable and immediate dilemma. Still, concerns with long-term population effects are merited, since Phase III trials were rolled out quickly and were limited to specific criteria and segments of the population.
Understanding viral evolutionary dynamics is key to coordinating a pandemic exit strategy. Viral suppression is effective, as witnessed with the ancient plagues to SARS-CoV-1, Marburg and Ebola, and regional controls for SARS-CoV-2. Suppression reduces hospitalizations and deaths, as well as making contact tracing and isolation strategies more manageable because of a lower viral reproduction. There are a number of different suppression strategies to stop the chain of viral transmission. Their success is dependent upon the characteristics of the virus and behavior of the host community.
Knowing how to navigate some of the more basic problems should be easier in a technologically advanced society, but for COVID-19, this is not proving to be the case. Science communication has always been a challenge but increasing social distrust is making it harder to parse the emerging science. Many science communication initiatives have tried to clear up COVID-19 misinformation, but there is much questionable advice from the infosphere. It is often unclear where to turn to get current, accurate information. No one can reliably predict how the virus will evolve or how it will respond to the many vaccines. But we do know that human actions shape the environment of any virus, providing selective pressures that might modulate the virus either way. There will be no known certainty about long-term effects until we have lived with the virus long term. In the end, most debates will be reduced to risk-benefit trade-offs based on partial information rather than any certainty.
Scientific Misinformation Is Hard To Reverse
Public skepticism in the era of COVID-19 is understandable. Medical racism, early-stage vaccination experiments in developing countries, and a history of ethically questionable practices has understandably fueled distrust for institutionally mandated “for-profit” health interventions. These concerns should not be ignored or patronized, particularly when scientists and medical practitioners apply a “just trust me” attitude, circumventing nuanced explanation when the public has questions—sometimes due to the complexity of the issue, but sometimes from a superiority-complex projection that the public "can’t understand." Improving public messaging will help people make choices, even if they are imperfect choices.
The Path Forward Is Through Social Trust
There is a thin, but critical line between healthy skepticism and paranoid conspiracy leaning. Due to knowledge outsourcing, society is structured in such a way that we relinquish a certain level of understanding to the authorities, providing trust to those to whom we cede this power. This provides a paradox, where society tells us to trust the experts. They have training and experience. But we are warned, there are bad actors attempting to manipulate or harm us—many of them institutional. We must learn to think critically and independently. We must stop being sheeple, we are told.
Trust in institutions, especially for science, is diminishing. Even if society is expected to trust scientists, which scientists should they trust? Social theorist of late modern society, Ulrich Beck, evaluates a modern “risk society” where shared tragedy-of-the-common “threats” are determined to be real, but shared “risks” are formulated by a “manufactured uncertainty,” from government, science, the market, and the media. While we continue to rely on experts to support risk decision-making that should be based on evidentiary practices, society is trending towards ideology and value-driven sentiment steered by politics and culture. There is a dire need for society to embrace an agnostic "culture of uncertainty" to facilitate an open dialogue, but our trained thought leaders need to improve their communications to the public.
There are many reasons why scientific communication is so hard. The scientific community has arduously sought to bridge the gap between scientists and the public at large and has largely been unsuccessful. Unfortunately, most approaches to scientific reporting occupy two poles—the inchoate, codified peer-reviewed scientific literature, or overly simplified popular science. Popular science and other forms of scientific communication are limited in their scope to accurately describe the complexities of many scientific systems; therefore, they are incomplete in their ability to inform good decision-making. Some websites and specialty blogs provide excellent brief explainers of certain issues, but they have been criticized for being spectacularly unscientific, scientifically vague or too superficial. The more sophisticated details, (i.e., the data, more complex concepts, nuanced results) which provide the opportunity for individual reflection to parse problems are often omitted. Controversial or disputed topics are rarely informed by both sides slamming the opposition. Synthesis of the varying sides rarely occurs.
Academic journals and renowned scientific magazines like Science, Nature, JAMA and others do a great job of featuring investigative scientific reporting, but are not devoted to the task since their primary focus is peer-reviewed scientific research. Academic journals are also less likely to speculate or report on unproven topics, often (but not always) ignoring compelling arguments that are not empirical, even when evidence provides a good basis of preliminary discussion. Academic journals are space-limited with too much competing science to pursue topics that are not well substantiated, even if the topic is more than a fringe view. The excellent reporting done from prominent academic journals often does not capture the attention of the public.
Scientific Communication Needs To Be More Explicit So That The Public Can Make Informed Choices
Science is also hard to communicate because of the polarization of how scientists are ethically perceived, often either as impervious to error, or indoctrinated, mad and manipulative. Scientists push this stereotype, renowned for claiming that one cannot cheat the data and enshrining science as an infallible methodological practice. This claim is spurious, because even with the best practices, science is still framed and analyzed through the human filter. There is no standard handbook of scientific procedure, even though there are methodological guidelines. Sampling biases and statistical errors often arise from faulty assumptions and missing data, among other factors. Numeracy errors (i.e.,the correct math but incorrect measures, measuring false equivalencies, etc.), miscalculations, unrepresentative reporting of data, omissions, methodological errors, experimental biases, and statistical flaws are all ways in which science can go wrong. Still, the scientific methodology is resiliently reliable. But when scientists assert a superior sense of infallibility, omit explanations, or use too much complicated jargon to render themselves incomprehensible, they lose public trust.
Understanding some key factors that contribute to the earnest misunderstanding of science can help one better assess the scientific argument. Some initial guiding principles are:E3(see Addendum for more detailed explanations and examples)
To Manage Ecosystem-Scale Problems, Cooperation Is Necessary
Managing ecosystem-scale societal issues, such as pandemics, biodiversity collapse, climate change, wildfires, and pollution, and winnowing fact from assumptions that appear as fact, or all-out conspiracy theories, necessitates better understanding of the science governing these processes. Science is arguably one of the most important area for society to comprehend, as it underlies many of our most significant policy issues and determines quality of life for all, yet it is one of the area least understood and most vulnerable to misinformation. Science is a low-yield endeavor, often making wrong turns before hitting on the right path. Society needs to allow scientific knowledge to develop through trial and error. Meanwhile, scientists need to communicate effectively—to root out the fringe opportunistic advocacy campaigns that erode trust generally, and to communicate transparently and clearly to the public. Trust is at the root of this progress.
Civilization can seem infinitely durable, particularly as science and technology accelerate. It often seemed an inevitability that life in the modern era would continue positively trending—until COVID-19 disrupted this notion by exposing societal fragility in everyday life. It is not clear what the right answer is for a strong public health vaccine strategy or how to safely exit this pandemic. Even if some vaccines provide us with hope, they alone won't end the global battle against SARS-CoV-2 and other similar, imminent existential threats. What is apparent is that whatever we do, our collective action will affect our society, despite our individual incentives. Some nations have seen success at mitigating the worst aspects of the pandemic compared to the vast majority of the globe. There is no singular approach to which such successes can be attributed, since each nation differs in demography, culture, governance, economy, and other factors. But in the cases where the pandemic was effectively controlled, there was a preponderance for societal cooperation and compliance to governing policies. This approach need not be authoritarian. In an open society, cooperation comes from effective public communication and institutional trust. SARS-CoV-2 has proven to be robust, in part due to its own ability to cooperate as a quasi-species. Humans need to remember that cooperation is key to our success as a species, too.
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see “III. The culture of scientific reporting leaves a vacuum for misinformation”, on Ioannidis and Gelman in this report. ↩