User login
Photo by Sakurai Midori
The parasite responsible for a form of malaria now spreading from macaques to humans in South Asia could evolve to infect humans more efficiently, according to a study published in Nature Communications.
Researchers identified a sugar variant on the surface of human red blood cells (RBCs) that currently limits the ability of the parasite Plasmodium knowlesi to invade.
But the team also found the parasite can evolve to get around this barrier and pass into the human population in a more virulent form.
“With increasing concern about the spread of P knowlesi into human populations, it is great to be able to gain insight into what the molecular stumbling blocks are for P knowlesi infection of humans and how the parasite can potentially overcome them,” said study author Selasi Dankwa, PhD, of Harvard T.H. Chan School of Public Health in Boston, Massachusetts.
The macaque malaria parasite P knowlesi has emerged as a major source of human infections in Southeast Asia. While most human infections are mild, increasing numbers of severe infections are being reported, leading to concerns that the parasite is adapting to infect humans more efficiently.
With this in mind, Dr Dankwa and her colleagues decided to explore the parasite’s ability to invade and adapt.
The team introduced the macaque sugar variant onto the human RBC surface and demonstrated that the parasite normally dependent on the macaque variant for invasion was unable to use the human version.
Specifically, macaques synthesize the sialic acid variant N-glycolylneuraminic acid (Neu5Gc), but humans lack Neu5Gc because of an Alu-mediated exon deletion in the gene encoding CMAH, which converts N-acetylneuraminic acid (Neu5Ac) to Neu5Gc.
So the absence of Neu5Gc on human RBCs limits P knowlesi invasion, but the researchers found that parasites can evolve to invade human RBCs via sialic acid-independent pathways.
Following prolonged adaptation to growth on human RBCs, P knowlesi invaded human RBCs independently of Neu5Gc. This occurred via duplication of the region containing the sialic acid-independent gene PkDBPα and complete deletion of the sialic acid-dependent gene PkDBPγ.
Based on these findings, the researchers are calling for continued monitoring of the P knowlesi parasite to ensure that it has not switched to using a sialic acid-independent pathway to invade human RBCs. 
Photo by Sakurai Midori
The parasite responsible for a form of malaria now spreading from macaques to humans in South Asia could evolve to infect humans more efficiently, according to a study published in Nature Communications.
Researchers identified a sugar variant on the surface of human red blood cells (RBCs) that currently limits the ability of the parasite Plasmodium knowlesi to invade.
But the team also found the parasite can evolve to get around this barrier and pass into the human population in a more virulent form.
“With increasing concern about the spread of P knowlesi into human populations, it is great to be able to gain insight into what the molecular stumbling blocks are for P knowlesi infection of humans and how the parasite can potentially overcome them,” said study author Selasi Dankwa, PhD, of Harvard T.H. Chan School of Public Health in Boston, Massachusetts.
The macaque malaria parasite P knowlesi has emerged as a major source of human infections in Southeast Asia. While most human infections are mild, increasing numbers of severe infections are being reported, leading to concerns that the parasite is adapting to infect humans more efficiently.
With this in mind, Dr Dankwa and her colleagues decided to explore the parasite’s ability to invade and adapt.
The team introduced the macaque sugar variant onto the human RBC surface and demonstrated that the parasite normally dependent on the macaque variant for invasion was unable to use the human version.
Specifically, macaques synthesize the sialic acid variant N-glycolylneuraminic acid (Neu5Gc), but humans lack Neu5Gc because of an Alu-mediated exon deletion in the gene encoding CMAH, which converts N-acetylneuraminic acid (Neu5Ac) to Neu5Gc.
So the absence of Neu5Gc on human RBCs limits P knowlesi invasion, but the researchers found that parasites can evolve to invade human RBCs via sialic acid-independent pathways.
Following prolonged adaptation to growth on human RBCs, P knowlesi invaded human RBCs independently of Neu5Gc. This occurred via duplication of the region containing the sialic acid-independent gene PkDBPα and complete deletion of the sialic acid-dependent gene PkDBPγ.
Based on these findings, the researchers are calling for continued monitoring of the P knowlesi parasite to ensure that it has not switched to using a sialic acid-independent pathway to invade human RBCs.
Photo by Sakurai Midori
The parasite responsible for a form of malaria now spreading from macaques to humans in South Asia could evolve to infect humans more efficiently, according to a study published in Nature Communications.
Researchers identified a sugar variant on the surface of human red blood cells (RBCs) that currently limits the ability of the parasite Plasmodium knowlesi to invade.
But the team also found the parasite can evolve to get around this barrier and pass into the human population in a more virulent form.
“With increasing concern about the spread of P knowlesi into human populations, it is great to be able to gain insight into what the molecular stumbling blocks are for P knowlesi infection of humans and how the parasite can potentially overcome them,” said study author Selasi Dankwa, PhD, of Harvard T.H. Chan School of Public Health in Boston, Massachusetts.
The macaque malaria parasite P knowlesi has emerged as a major source of human infections in Southeast Asia. While most human infections are mild, increasing numbers of severe infections are being reported, leading to concerns that the parasite is adapting to infect humans more efficiently.
With this in mind, Dr Dankwa and her colleagues decided to explore the parasite’s ability to invade and adapt.
The team introduced the macaque sugar variant onto the human RBC surface and demonstrated that the parasite normally dependent on the macaque variant for invasion was unable to use the human version.
Specifically, macaques synthesize the sialic acid variant N-glycolylneuraminic acid (Neu5Gc), but humans lack Neu5Gc because of an Alu-mediated exon deletion in the gene encoding CMAH, which converts N-acetylneuraminic acid (Neu5Ac) to Neu5Gc.
So the absence of Neu5Gc on human RBCs limits P knowlesi invasion, but the researchers found that parasites can evolve to invade human RBCs via sialic acid-independent pathways.
Following prolonged adaptation to growth on human RBCs, P knowlesi invaded human RBCs independently of Neu5Gc. This occurred via duplication of the region containing the sialic acid-independent gene PkDBPα and complete deletion of the sialic acid-dependent gene PkDBPγ.
Based on these findings, the researchers are calling for continued monitoring of the P knowlesi parasite to ensure that it has not switched to using a sialic acid-independent pathway to invade human RBCs.