“A hotter planet could change the relationship among infectious agents, their hosts and the human body’s defense mechanisms”
By Sara Goudarzi
Scientists have long known that the rise in average global temperatures is expanding the geographical presence of vector-borne diseases such as malaria and dengue fever, because the animals that transmit them are adapting to more widespread areas. The link between respiratory illnesses, including influenza and COVID-19, and a warming planet is less clear. But some scientists are concerned that climate change could alter the relationship between our body’s defenses and such pathogens. These modifications could include the adaptation of microbes to a warming world, changes in how viruses and bacteria interact with their animal hosts, and a weakened human immune response.
The immune system is our natural defense against harmful substances. When a respiratory pathogen—such as the new SARS-CoV-2 virus that causes COVID-19—enters the body through the airways, it damages cells by taking over their machinery and making more copies of itself. The injured cells release signaling proteins called cytokines that communicate with other parts of the body to activate an immune response against the foreign invaders.
Mammals have evolved another, more basic defense against pathogens: an elevated body temperature relative to that of their environment. As a result of this change, many microbes that are adapted to cooler temperatures are unable to endure a warm mammalian body.
“A lot of organisms in the environment cannot survive [at] 37 degrees” Celsius, the standard for normal human body temperature, says Arturo Casadevall, chair of molecular microbiology and immunology at the Johns Hopkins Bloomberg School of Public Health. “So our temperature is almost like a thermal barrier that protects us against many organisms.”
The higher ambient temperatures expected with a changing climate could, however, favor pathogens that will be more difficult for people’s body to fight. In a paper published in mBIO in 2019, Casadevall and his colleagues described a drug-resistant fungus—Candida auris—that was first isolated from a person in 2009 and emerged on three different continents in the past decade. The common denominator for these emergence events was temperature, the researchers say. The finding, they note, may be the first example of a fungus adapting to a higher temperature and breaching humans’ thermal barrier.
But a fungus—which does not require a host to replicate—is very different than a virus, such as SARS-CoV-2. That virus is thought to have jumped from bats to humans—both warm-blooded hosts—potentially via an intermediate animal. If cold-blooded creatures start to adapt to warmer conditions, they could unleash a slew of new pathogens to which humans may not have immunity.
“Imagine that the world is hotter and that lizards adapt to live in temperatures very close to yours. Then their viruses adapt to higher temperatures,” Casadevall says. “We have two pillars of defense: temperature and advanced immunity. In a warming world, we may lose the pillar of temperature if the [pathogens] adapt to be close to our temperature.”
This issue could be exacerbated as species move to historically cooler climates and higher elevations while the world warms. In a 2017 study published in Science, researchers estimated that, on average, land species are shifting toward the poles at a rate of 17 kilometers per decade, while marine species are doing so at 72 kilometers per decade. Such a reshuffling of species around the planet could mean that animals that host unique disease-causing microorganisms will live side by side with those that would not normally host them, creating new transmission pathways.
A warming world could also have an effect on humans’ other defense mechanism: the immune system. Researchers have been aware for years that factors such as a lack of sleep and stress could weaken it. Last year, in a study published in the Proceedings of the National Academy of Sciences USA, scientists in Tokyo also discovered that heat reduced mice’s immune response to a flu virus. The researchers infected otherwise healthy, young adult female mice with the influenza A virus, one of two types that cause seasonal flu epidemics in humans. The mice were housed for seven days in one of three temperature-controlled spaces: at four, 22 and 36 degrees C, respectively. The study authors found the immune systems of the mice exposed to the highest ambient temperature did not fight the virus as effectively as the other two groups.
Specifically, the researchers noted that the mice in the hottest room ate less than those in the cooler rooms and lost 10 percent of their body weight in the first 24 hours of being exposed to higher temperatures. “People often lose their appetite when they feel sick,” said study author Takeshi Ichinohe, an associate professor at the University of Tokyo, in a press release. “If someone stops eating long enough to develop a nutritional deficit, that may weaken the immune system and increase the likelihood of getting sick again.” When Ichinohe and his colleague Miyu Moriyama, then at the University of Tokyo, supplemented the mice’s diet with sugar or short-chain fatty acids (which are commonly produced by intestinal bacteria), those animals were able to mount a normal immune response.
Ellen F. Foxman, an assistant professor of laboratory medicine and immunobiology at the Yale School of Medicine, who was not involved in the study, expresses caution about making a direct link between heat and the mice’s immune response. “The temperature had an effect on the animals’ behavior, which had an effect on immunity,” and the mice “didn’t form as good of an antiviral immune response in this particular type of flu infection,” she says. In contrast, Foxman’s own 2015 PNAS study showed that the very first steps of the immune response to fight a cold virus were, in fact, boosted by higher temperatures and depressed by lower ones.
The University of Tokyo researchers question if the weakened immune response seen in their study is the result of a nutritional deficit or the fact that the immune system is hampered by heat altering the activity of certain genes. And they say further experiments are needed. Nevertheless, climate change could potentially disrupt the human immune response—either directly via higher temperature or indirectly via its effects on global food security—a scenario suggested by a 2019 Intergovernmental Panel on Climate Change report.
Foxman, who acknowledges the validity of the Tokyo mouse study, believes it is a leap to conclude from its results that warming makes humans more directly susceptible to viral infections. But she acknowledges that changes in climate could alter the number of host animals, their activity and human exposure to them.
“I think that climate change disrupts a lot of patterns—of human behavior, of insect vectors and even [of] bats”—from which the COVID-19 virus and other deadly coronaviruses likely originated, Foxman says. The disruptions could indirectly alter the interactions between diseases and human defenses in ways scientists have yet to fully understand.
