Research published last week in PNAS shows that malaria succeeds thanks to a surprising trick. It creates a signaling molecule called a cytokine that disrupts the normal immune system response. This insight could be crucial to developing a cure, and it explains why it often takes a second infection to overwhelm the immune system.
A healthy immune system produces both short-lived and long-lived immune cells. The latter, called memory T cells, sustain an attack after the initial immune response and protect a person when reinfection occurs.
A team lead by researchers at Yale University found that the parasite responsible for malaria creates a signaling molecule that converts long-term memory T cells into short-term immune cells, thereby tipping the balance in favor of the parasite.
The parasite, called plasmodium, is transmitted from one person to another by mosquitoes and lives in the liver before multiplying and circulating in the bloodstream. Malaria infects at least 150 million people per year and kills over half a million people, according to the WHO, and the CDC estimates that half the world’s population is susceptible to the disease.
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