Credit: Cellular host and microbe (2023). DOI: 10.1016/j.chom.2023.10.019
Researchers who have studied malaria for decades, hoping to find a cure, long thought they had identified a blood type that seemed to defend against the disease.
But a new study published in Cellular host and microbe concludes that even some people belonging to the protective blood group were infected. The question now is: how?
“This could mean that the specific genetic mutation linked to this blood type does not completely stop malaria, or that the malaria virus could have found another way to enter blood cells,” said Peter Zimmerman, professor of pathology. at Case Western Reserve University. School of Medicine and lead author of the study. “This is a big deal because it could change the way we try to get rid of this type of malaria parasite.”
“This malaria parasite, called Plasmodium vivax — or P. vivax — was common in northeast Ohio,” said Christopher King, study co-investigator and professor of pathology. “And it was transmitted to the United States – in Florida and Texas – this summer for the first time in 20 years.
“We know,” King said, “that the United States is at risk of reintroducing malaria due to climate change, increasing immigration and travel from areas where malaria is endemic.”
Study collaborators include French researchers (Célia Dechavanne and Benoit Gamain, from the National Institute of Blood Transfusion, INSERM/Université Paris Diderot); and Madagascar (Arsène Ratsimbasoa, from the University of Fianarantsoa).
The study
“Malaria researchers have been trying for more than 100 years to better understand the resistance and susceptibility of Africans to P. vivax infection,” Zimmerman said. “More than 2.5 billion people may live in Africa and Southeast Asia, where the parasite is present. Hundreds of thousands of people die each year from malaria. In general, malaria is one of three major global infectious diseases: malaria, tuberculosis and HIV/AIDS.”
The team is studying a specific blood type (Fy-negative) found in the blood of most Africans and people of African descent, called “the silent Duffy blood type.” Duffy negative people have a mutation in the DNA code (GATA-1) that causes the protein to not be expressed on the surface of red blood cells.
Researchers conducted experiments using lab-grown blood cells and cells taken from bone marrow to study the Duffy-silent blood type.
“Surprisingly, we found that even when people are missing the GATA-1 DNA code, the Duffy protein sometimes appears in their red blood cells,” Zimmerman said. “Our results suggest that bone marrow and other places where blood cells are first made are important for the malaria parasite to find red blood cells containing the Duffy protein, grow and cause disease.”
In other laboratory experiments, they examined the blood of people with the silent Duffy blood type. They noticed that P. vivax malaria infection was often detected using a special test rather than the usual microscopic test.
This means that people with the Duffy-silent blood type can still be infected, but it’s not always easy to detect during regular blood tests. In other words, they found that P. vivax can invade the red blood cells of people with the Duffy-silent trait. Additionally, if they have an infection in the bone marrow, they produce the transmissible form of the parasite. Mosquitoes can acquire it and cause infections in other people.
“This finding raises questions about how malaria parasites cause infection and disease, particularly because some infected people don’t show many signs in their blood,” Zimmerman said. “We need to look at the blood more closely to better understand how widespread and severe this type of malaria is in people with the Duffy-silent trait.”
More information:
Celia Dechavanne et al, The Duffy antigen is expressed during erythropoiesis in Duffy negative individuals, Cellular host and microbe (2023). DOI: 10.1016/j.chom.2023.10.019
Provided by Case Western Reserve University
Quote: New study concludes that finding a cure for malaria could be even more difficult than previously thought (December 6, 2023) retrieved December 7, 2023 from
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