When a mosquito bites someone with malaria, the tiny parasites inside their blood have one job: figure out how to jump into the mosquito and keep the infection going. But scientists in Barcelona have discovered something surprising — when that person has a high fever, the parasites lose their ability to make that jump. The parasites become temporarily trapped, unable to spread the disease further.
Researchers at the Barcelona Institute for Global Health, a research center supported by the "la Caixa" Foundation, made this discovery while studying how malaria parasites survive heat stress. Malaria affects roughly 260 million people every year and causes about 600,000 deaths, most of them children in Africa. Finding new ways to stop its spread could save many lives.
The study, published in the journal PLOS Pathogens, focused on a specific stage of the parasite called gametocytes — the only form capable of infecting mosquitoes. When a mosquito bites an infected person, it picks up these gametocytes and becomes a carrier.
The researchers found that when a patient runs a fever, temperatures inside their blood can reach 41°C (about 106°F). This heat triggers what scientists call the Heat Shock Response, a protective mechanism that helps the parasite's proteins survive. Normally, this protection works well for most stages of the parasite. But here's the catch: gametocytes at later stages of development lose this ability.
"Our findings suggest that fever could temporarily reduce the ability of a person with malaria to transmit the infection," said Neus Ràfols, a researcher at ISGlobal and first author of the study. The team discovered that even just 10 minutes of heat exposure is enough to activate this protective response. More surprisingly, they found the parasites use this protection in a preventive way — turning it on before serious damage occurs, rather than waiting until they're already harmed.
The researchers also found that dihydroartemisinin, the main drug used in malaria treatment, triggers the same protective response. This suggests the Heat Shock Response helps parasites survive multiple types of stress, not just fever.
The team developed a new testing method using a water bath instead of an incubator, which let them control temperatures more precisely and study very short heat exposures. They identified a protein called AP2-HS that acts like a switch, turning on the genes that protect the parasite from heat damage. Parasites with incomplete versions of this protein were more vulnerable to heat stress.
Understanding how malaria transmission works could eventually help health workers interrupt the cycle of infection — one mosquito bite at a time.