As temperatures rise and climates become warmer, there is concern that certain fungi and their associated diseases may become more prevalent and potentially more dangerous to human health. For example, certain types of fungi that cause infections in humans, such as Aspergillus and Cryptococcus, can grow and spread more readily in warmer conditions. Additionally, changes in temperature and precipitation patterns can also alter the distribution and behavior of insects and other animal hosts that carry fungal spores and spores, leading to an increased risk of exposure to these fungi.
A new study finds that rising temperatures cause a pathogenic fungus called Cryptococcus deneoformans to ramp up its adaptive responses. Heat causes a number of genetic changes, some of which may lead to increased heat resistance and others to increased disease-causing potential.
The world is full of tiny creatures that find us delectable. Bacteria and viruses are the obvious villains, causing deadly global pandemics and irritating infections. Fungi, on the other hand, are pathogens we haven’t had to deal with as much.
Pathogenic fungi (Candida, Aspergillus, Cryptococcus, and others) are well-known killers of immunocompromised individuals. However, most healthy people have not had to worry about them, and the vast majority of the planet’s potentially pathogenic fungi do not thrive in the heat of our bodies. But that could be about to change.
According to a new study from Duke University School of Medicine, increased temperatures cause a pathogenic fungus known as Cryptococcus deneoformans to go into overdrive with its adaptative responses. This increases the number of genetic changes, some of which may presumably lead to increased heat resistance, while others may lead to increased disease-causing potential.
Fungal diseases are on the rise, owing largely to an increase in the number of people with weakened immune systems or underlying health conditions.
Asiya Gusa
Higher heat, in particular, causes more of the fungus’ transposable elements, or jumping genes, to arise and move around within the fungal DNA, resulting in changes in how its genes are used and regulated. The research was published in the Proceedings of the National Academy of Sciences.
“These mobile elements are likely to contribute to adaptation in the environment and during an infection,” said postdoctoral researcher Asiya Gusa Ph.D. of the Duke School of Medicine’s Molecular Genetics and Microbiology. “This could happen even faster because heat stress accelerates the rate at which mutations occur.”
This may sound familiar to fans of the new HBO series “The Last of Us,” in which a heat-adapted fungus takes over humans and turns them into zombies creates a dystopian hellscape. “That’s exactly what I’m talking about — minus the zombie part!” exclaimed Gusa, who had just finished watching the first episode and will join the Duke faculty as an assistant professor later this year.
“These are not communicable diseases; we do not transmit fungi to one another,” Gusa explained. “However, the spores are in the air. We constantly breathe in fungi spores, and our immune systems are prepared to fight them.”
Because fungal spores are larger than viruses, your existing Covid face masks should be sufficient to keep them at bay. For the time being, that and your body heat. “Fungal diseases are on the rise, owing largely to an increase in the number of people with weakened immune systems or underlying health conditions,” Gusa explained. Pathogenic fungi, on the other hand, may be adapting to warmer temperatures as well.
Gusa led research in Professor Sue Jinks-lab Robertson’s that focused on three transposable elements that were particularly active in C. deneoformans under heat stress. However, she believes that there are at least another 25 transposable elements in that species that could be mobilized.
Gusa explained that the team used ‘long-read’ DNA sequencing to detect changes that would otherwise have gone undetected. They were able to map transposons using computational analysis and then see how they moved. “We now have better tools to detect these movements that were previously hidden in our blind spots.”
Heat stress accelerated the mutations. Following 800 generations of growth in laboratory medium, the rate of transposon mutations in fungi raised at body temperature (37 Celsius) was five times higher than in fungi raised at 30C.
One of the transposable elements, called T1, had a tendency to insert itself between coding genes, which could lead to changes in the way genes are controlled. An element called Tcn12 often landed within the sequence of a gene, potentially disrupting that gene’s function and possibly leading to drug resistance. And a third kind, Cnl1, tended to land near or in the telomere sequences at the ends of chromosomes, an effect which Gusa said isn’t fully understood.
The mobilization of transposable elements also appeared to increase more in fungi living in mice than in lab culture. “We saw evidence of all three transposable elements mobilizing in the fungus genome within just ten days of infecting the mouse,” Gusa said. The researchers suspect that the added challenges of surviving in an animal with immune responses and other stressors may drive the transposons to be even more active.
“This is an intriguing study that shows how rising global temperatures can affect fungal evolution in unexpected ways,” said Arturo Casadevall, MD, PhD, chair of molecular microbiology and immunology at Johns Hopkins University. “Transposons in soil fungi like Cryptococcus neoformans may become more mobile as the world warms, increasing genomic changes that could enhance virulence and drug resistance. Another reason to be concerned about global warming!”
