A mosquito under the microscope.
The association between climate and infectious disease is poorly understood, says Irina Tezaur, a computational scientist at Sandia National Laboratories. “Correlations have been observed but it’s not known if these correlations translate to causal relationships.”
To make accurate longer-term predictions, scientists need more empirical data, multiple datasets specific to locations and diseases, and the ability to calculate risks that depend on unpredictable nature and human behavior. Another obstacle is that climate scientists and epidemiologists are not collaborating effectively, so some researchers are calling for a multidisciplinary approach, a new field called Outbreak Science.
Climate scientists are far ahead of epidemiologists in gathering essential data.
Earth System Models—combining the interactions of atmosphere, ocean, land, ice and biosphere—have been in place for two decades to monitor the effects of global climate change. These models must be combined with epidemiological and human model research, areas that are easily skewed by unpredictable elements, from extreme weather events to public environmental policy shifts.
“There is never just one driver in tracking the impact of climate on infectious disease,” says Joacim Rocklöv, a professor at the Heidelberg Institute of Global Health & Heidelberg Interdisciplinary Centre for Scientific Computing in Germany. Rocklöv has studied how climate affects vector-borne diseases—those transmitted to humans by mosquitoes, ticks or fleas. “You need to disentangle the variables to find out how much difference climate makes to the outcome and how much is other factors.” Determinants from deforestation to population density to lack of healthcare access influence the spread of disease.
Even though climate change is not the primary driver of infectious disease today, it poses a major threat to public health in the future, says Rocklöv.
The promise of predictive modeling
“Models are simplifications of a system we’re trying to understand,” says Jeremy Hess, who directs the Center for Health and the Global Environment at University of Washington in Seattle. “They’re tools for learning that improve over time with new observations.”
Accurate predictions depend on high-quality, long-term observational data but models must start with assumptions. “It’s not possible to apply an evidence-based approach for the next 40 years,” says Rocklöv. “Using models to experiment and learn is the only way to figure out what climate means for infectious disease. We collect data and analyze what already happened. What we do today will not make a difference for several decades.”
To improve accuracy, scientists develop and draw on thousands of models to cover as many scenarios as possible. One model may capture the dynamics of disease transmission while another focuses on immunity data or ocean influences or seasonal components of a virus. Further, each model needs to be disease-specific and often location-specific to be useful.
“All models have biases so it’s important to use a suite of models,” Tezaur stresses.
The modeling scientist chooses the drivers of change and parameters based on the question explored. The drivers could be increased precipitation, poverty or mosquito prevalence, for instance. Later, the scientist may need to isolate the effect of one driver so that will require another model.
There have been some related successes, such as the latest models for mosquito-borne diseases like Dengue, Zika and malaria as well as those for flu and tick-borne diseases, says Hess.
Rocklöv was part of a research team that used test data from 2018 and 2019 to identify regions at risk for West Nile virus outbreaks. Using AI, scientists were able to forecast outbreaks of the virus for the entire transmission season in Europe. “In the end, we want data-driven models; that’s what AI can accomplish,” says Rocklöv. Other researchers are making an important headway in creating a framework to predict novel host–parasite interactions.
Modeling studies can run months, years or decades. “The scientist is working with layers of data. The challenge is how to transform and couple different models together on a planetary scale,” says Jeanne Fair, a scientist at Los Alamos National Laboratory, Biosecurity and Public Health, in New Mexico.
Disease forecasting will require a significant investment into the infrastructure needed to collect data about the environment, vectors, and hosts a tall spatial and temporal resolutions.
And it’s a constantly changing picture. A modeling study in an April 2022 issue of Nature predicted that thousands of animals will migrate to cooler locales as temperatures rise. This means that various species will come into closer contact with people and other mammals for the first time. This is likely to increase the risk of emerging infectious disease transmitted from animals to humans, especially in Africa and Asia.
Other things can happen too. Global warming could precipitate viral mutations or new infectious diseases that don’t respond to antimicrobial treatments. Insecticide-resistant mosquitoes could evolve. Weather-related food insecurity could increase malnutrition and weaken people’s immune systems. And the impact of an epidemic will be worse if it co-occurs during a heatwave, flood, or drought, says Hess.
The devil is in the climate variables
Solid predictions about the future of climate and disease are not possible with so many uncertainties. Difficult-to-measure drivers must be added to the empirical model mix, such as land and water use, ecosystem changes or the public’s willingness to accept a vaccine or practice social distancing. Nor is there any precedent for calculating the effect of climate changes that are accelerating at a faster speed than ever before.
The most critical climate variables thought to influence disease spread are temperature, precipitation, humidity, sunshine and wind, according to Tezaur’s research. And then there are variables within variables. Influenza scientists, for example, found that warm winters were predictors of the most severe flu seasons in the following year.
The human factor may be the most challenging determinant. To what degree will people curtail greenhouse gas emissions, if at all? The swift development of effective COVID-19 vaccines was a game-changer, but will scientists be able to repeat it during the next pandemic? Plus, no model could predict the amount of internet-fueled COVID-19 misinformation, Fair noted. To tackle this issue, infectious disease teams are looking to include more sociologists and political scientists in their modeling.
Addressing the gaps
Currently, researchers are focusing on the near future, predicting for next year, says Fair. “When it comes to long-term, that’s where we have the most work to do.” While scientists cannot foresee how political influences and misinformation spread will affect models, they are positioned to make headway in collecting and assessing new data streams that have never been merged.
Disease forecasting will require a significant investment into the infrastructure needed to collect data about the environment, vectors, and hosts at all spatial and temporal resolutions, Fair and her co-authors stated in their recent study. For example real-time data on mosquito prevalence and diversity in various settings and times is limited or non-existent. Fair also would like to see standards set in mosquito data collection in every country. “Standardizing across the US would be a huge accomplishment,” she says.
Understanding how climate change contributes to the spread of disease is critical for thwarting future calamities.
Jeanne Fair
Hess points to a dearth of data in local and regional datasets about how extreme weather events play out in different geographic locations. His research indicates that Africa and the Middle East experienced substantial climate shifts, for example, but are unrepresented in the evidentiary database, which limits conclusions. “A model for dengue may be good in Singapore but not necessarily in Port-au-Prince,” Hess explains. And, he adds, scientists need a way of evaluating models for how effective they are.
The hope, Rocklöv says, is that in the future we will have data-driven models rather than theoretical ones. In turn, sharper statistical analyses can inform resource allocation and intervention strategies to prevent outbreaks.
Most of all, experts emphasize that epidemiologists and climate scientists must stop working in silos. If scientists can successfully merge epidemiological data with climatic, biological, environmental, ecological and demographic data, they will make better predictions about complex disease patterns. Modeling “cross talk” and among disciplines and, in some cases, refusal to release data between countries is hindering discovery and advances.
It’s time for bold transdisciplinary action, says Hess. He points to initiatives that need funding in disease surveillance and control; developing and testing interventions; community education and social mobilization; decision-support analytics to predict when and where infections will emerge; advanced methodologies to improve modeling; training scientists in data management and integrated surveillance.
Establishing a new field of Outbreak Science to coordinate collaboration would accelerate progress. Investment in decision-support modeling tools for public health teams, policy makers, and other long-term planning stakeholders is imperative, too. We need to invest in programs that encourage people from climate modeling and epidemiology to work together in a cohesive fashion, says Tezaur. Joining forces is the only way to solve the formidable challenges ahead.
This article originally appeared in One Health/One Planet, a single-issue magazine that explores how climate change and other environmental shifts are increasing vulnerabilities to infectious diseases by land and by sea. The magazine probes how scientists are making progress with leaders in other fields toward solutions that embrace diverse perspectives and the interconnectedness of all lifeforms and the planet.
Based on recent research, new therapies could promote a mix of viruses in the intestines to help prevent diseases of aging.
The microbiota and aging
In the early 1970s, scientists discovered that the composition of our gut microbiota changes as we age. Recent studies have found that the changes are remarkably predictable and follow a pattern: The microbiota undergoes rapid, dramatic changes as toddlers transition to solid foods; further changes become less dramatic during childhood as the microbiota strikes a balance between the host and the environment; and as that balance is achieved, the microbiota remains mostly stable during our adult years (ages 18-60). However, that stability is lost as we enter our elderly years, and the microbiome undergoes dramatic reorganization. This discovery led scientists to question what causes this change and what effect it has on health.
Centenarians have a distinct gut community enriched in microorganisms that synthesize potent antimicrobial molecules that can kill multidrug-resistant pathogens.
“We are always eager to find out why some people live extremely long lives. Previous research has shown that the intestinal bacteria of old Japanese citizens produce brand-new molecules that make them resistant to pathogenic — that is, disease-promoting — microorganisms. And if their intestines are better protected against infection, well, then that is probably one of the things that cause them to live longer than others,” said Joachim Johansen, a researcher at the University of Copenhagen.
In 2021, a team of Japanese scientists set out to characterize the effect of this change on older people’s health. They specifically wanted to determine if people who lived to be over 100 years old — that is, centenarians — underwent changes that provided them with unique benefits. They discovered centenarians have a distinct gut community enriched in microorganisms that synthesize potent antimicrobial molecules that can kill multidrug-resistant pathogens, including Clostridioides difficile and Enterococcus faecium. In other words, the late-life shift in microbiota reduces an older person’s susceptibility to common gut pathogens.
Viruses can change alter the genes of bacteria
Although the late-in-life microbiota change could be beneficial to health, it remained unclear what facilitated this shift. To solve this mystery, Johansen and his colleagues turned their attention to an often overlooked member of the microbiome: viruses. “Our intestines contain billions of viruses living inside bacteria, and they could not care less about human cells; instead, they infect the bacterial cells. And seeing as there are hundreds of different types of bacteria in our intestines, there are also lots of bacterial viruses,” said Simon Rasmussen, Johansen’s research advisor.
Centenarians had a more diverse virome, including previously undescribed viral genera.
For decades, scientists have explored the possibility of phage therapy — that is, using viruses that infect bacteria (called bacteriophages or simply phages) to kill pathogens. However, bacteriophages can also enhance the bacteria they infect. For example, they can provide genes that help their bacterial host attack other bacteria or provide new metabolic capabilities. Both of these can change which bacteria colonize the gut and, in turn, protect against certain disease states.
Intestinal viruses give bacteria new abilities
Johansen and his colleagues were interested in what types of viruses centenarians had in their gut and whether those viruses carried genes that altered metabolism. They compared fecal samples of healthy centenarians (100+ year-olds) with samples from younger patients (18-100 year-olds). They found that the centenarians had a more diverse virome, including previously undescribed viral genera.
They also revealed an enrichment of genes supporting key steps in the sulfate metabolic pathway. The authors speculate that this translates to increased levels of microbially derived sulfide, which may lead to health-promoting outcomes, such as supporting mucosal integrity and resistance to potential pathogens.
“We have learned that if a virus pays a bacterium a visit, it may actually strengthen the bacterium. The viruses we found in the healthy Japanese centenarians contained extra genes that could boost the bacteria,” said Johansen.
Simon Rasmussen added, “If you discover bacteria and viruses that have a positive effect on the human intestinal flora, the obvious next step is to find out whether only some or all of us have them. If we are able to get these bacteria and their viruses to move in with the people who do not have them, more people could benefit from them.”
This article originally appeared on Big Think, home of the brightest minds and biggest ideas of all time.
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