WASHINGTON — A form of malaria largely absent in sub-Saharan Africa has begun to make inroads there. Ominous signals are emerging simultaneously in population studies and under the microscope that Plasmodium vivax, a malaria parasite well known in Asia and Latin America, may have found a way to infect Africans. Researchers presented the results November 15 at the annual meeting of the American Society of Tropical Medicine and Hygiene.
Most Africans and many African Americans carry a genetic trait that makes it hard for the vivax protozoan to infect their red blood cells. These people lack a receptor protein on their red blood cells called the Duffy protein. Missing this protein doesn’t seem to cause health problems. Rather, it’s a plus because P. vivax hijacks the Duffy protein to gain entry into red blood cells and commandeer them.
Didier Ménard of the Pasteur Institute in Phnom Penh, Cambodia, presented data from Madagascar revealing that vivax malaria that evades people’s genetic protection is showing up in the island country. Ménard and his colleagues found that, among blood samples from 183 people in Madagascar who had vivax malaria, 9.3 percent lacked the Duffy protein, suggesting the people had no business getting a vivax infection.
The finding follows recent reports of vivax cropping up in Duffy-negative people in Angola, Mauritania, Kenya, Equatorial Guinea and most recently Ethiopia, said Peter Zimmerman, a molecular biologist at Case Western Reserve University in Cleveland.
Meanwhile, lab work has shown that some P. vivax parasites have developed a duplicate version of the gene encoding the protein that the parasite normally uses to bind to the Duffy protein. Geneticist David Serre of the Cleveland Clinic and others obtained 189 samples of vivax malaria parasites that had infected people in Madagascar and found that 100 had the duplication of the gene.
Zimmerman hypothesized that a parasite armed with a duplicate gene encoding the Duffy binding protein might be able to infect Duffy-negative people. Perhaps the duplicated gene can generate so much of the binding protein that it can somehow get into a red blood cell.
Serre and others plan to investigate that possibility. The key will be to screen Duffy-negative individuals who are in the throes of a vivax infection, Serre said, and examine red blood cells to see if there are a lot of these binding proteins resulting from the duplication. In essence, the researchers hope to catch the unusual parasite in the act.
“It’s the same story over and over again in evolution,” said David Walker, a physician at the University of Texas Medical Branch in Galveston and president of the American Society of Tropical Medicine and Hygiene. “Something is finding a way to expand its population.” In this case, he said, the parasite may have found a new strategy.
If an altered vivax were to spread widely in Africa, the consequences could be worrisome, the researchers said. The most common and severe malaria in Africa is caused by the Plasmodium falciparum parasite. While vivax is not as dangerous, it can still be lethal. What’s more, it has a dormant stage that makes it hard to treat. “When infected with P. falciparum, you’re in bed, you’re sick and not going anywhere,” Serre said. “With vivax, you’re sick but you get treated and feel better and you travel.” This could worsen spread of the altered parasite.