Scientists have discovered an unexpected vulnerability in the parasite that causes malaria: high body temperatures during fever episodes may temporarily prevent the parasite from being transmitted to mosquitoes.

The findings were published in the journal PLOS Pathogens.

Researchers from the Barcelona Institute for Global Health (ISGlobal) found that Plasmodium falciparum—the parasite responsible for the deadliest form of malaria—loses its ability to activate its heat-stress defense mechanism during the gametocyte stage. This stage of the parasite's life cycle is responsible for transmitting the infection from humans to mosquitoes.

During malaria attacks, a patient's body temperature can rise to as high as 41°C (105.8°F). Under normal circumstances, such temperatures trigger a cellular heat-stress response that protects proteins from damage. In P. falciparum, this protective system is controlled by a protein known as AP2-HS.

The researchers developed a new experimental method that allowed them to precisely control heat exposure. They found that just 10 minutes of elevated temperature was sufficient to activate the parasite's heat-defense response. Remarkably, the mechanism was triggered even at moderate temperature increases, before the cells experienced significant damage.

However, this protective response was not active throughout all stages of the parasite's development. Mature gametocytes—the forms required for infecting mosquitoes—were largely unable to activate the heat-stress defense, making them particularly vulnerable during episodes of high fever.

According to the researchers, if a mosquito bites an infected person during this period, it may fail to acquire viable parasites and therefore be unable to transmit malaria to other people.

The team also discovered that the same protective mechanism is activated after exposure to dihydroartemisinin, the active metabolite of modern artemisinin-based antimalarial drugs. This suggests that the heat-stress response helps the parasite cope not only with elevated temperatures but also with other forms of cellular stress.

The findings have so far been confirmed only in laboratory experiments. The next step will be to determine whether the same phenomenon occurs during natural malaria infections and whether there is a fever threshold above which infected individuals temporarily become unable to transmit the parasite to mosquitoes.