Scientists from Singapore's Nanyang Technological University (NTU) have discovered a key process during the invasion of the blood
cell by the Malaria parasite, and more importantly, found a way to block this invasion.
The newly invented technique utilises a high - throughput fluorescence scanning approach — if antibodies or drugs fail to prevent the invasion of the red blood
cell by the malaria parasites, the sample will light up.
Not exact matches
By contrast, women who carry a sickle -
cell allele, which protects against
malaria, have only about 50 percent more surviving children in
malaria - infested regions than women lacking the variant.
Researchers at Harvard T. H. Chan School of Public Health and the Broad Institute have identified a protein on the surface of human red blood
cells that serves as an essential entry point for invasion
by the
malaria parasite.
Scientists have identified a protein on the surface of human red blood
cells that serves as an essential entry point for invasion
by the
malaria parasite.
The risk of developing severe
malaria turns out to be strongly linked to the process
by which the
malaria parasite gains entry to the human red blood
cell.
First, after a person is bitten
by a parasite - carrying mosquito there is an initial infection in the liver, followed
by the long - lasting red blood
cell stage where the clinical symptoms of the
malaria disease occur, and finally the mosquito stage, which is required to transmit the parasites to other people.
But now University of Pennsylvania biochemist Doron Greenbaum has found a way to lock
malaria inside the
cells by blocking the action of a key host protein, called calpain, that allows its escape.
The gene codes for an immune receptor on red blood
cells; lack of that receptor prevents infection
by Plasmodium vivax, a species of the
malaria parasite.
Apparently, antibodies to this protein protected against
malaria by trapping the schizont inside the red blood
cell — not
by preventing it from infecting new ones.
Snell is particularly encouraged
by the possibility of controlling
malaria, which is caused
by the single -
celled protozoan Plasmodium falciparum.
Microbes that cause diseases like HIV,
malaria, and hepatitis C exploit and often activate the same checkpoint pathways —
cell surface receptors such as CTLA4 and PD - 1 — to slow immune
cells and prevent their elimination
by the host.
«Our study shows that the ability of
malaria parasites to engage red blood
cells is driven
by an ancient mechanism for cellular attachment,» said lead author Aditya Paul, a postdoctoral researcher at the Harvard Chan School.
Malaria is caused
by a single -
celled parasite called Plasmodium that spreads from person to person through mosquito bites.
In 2008, researchers led
by YongKeun Park and Monica Diez - Silva of the Massachusetts Institute of Technology found that red blood
cells vibrated less when they were infected with the
malaria parasite, apparently because the infection made the
cells stiffer than normal (Proceedings of the National Academy of Sciences, DOI: 10.1073 / pnas.0806100105).
A new study shows that a 70 - year - old
malaria drug can block immune
cells in the liver so nanoparticles can arrive at their intended tumor site, overcoming a significant hurdle of targeted drug delivery, according to a team of researchers led
by Houston Methodist.
It built on previous ground - breaking work on
malaria published in 2011
by author Monash Professor Christian Doerig, and others, who found that if host
cell protein kinases were prevented from working it would kill
malaria parasites.
Malaria is a life - threatening disease caused
by a parasite that invades one red blood
cell after another.
«Many researchers are trying to find ways to develop a
malaria vaccine
by preventing the parasite from entering the red blood
cell, and here we found a way to block it from leaving the
cell once it has entered.
Avian
malaria is mainly caused
by the parasite Plasmodium relictum, which reproduces in red blood
cells.
Dr. Jonathan Kurtis, professor of pathology and laboratory medicine at Brown, made global headlines last year when he and colleagues revealed a promising protein that combats
malaria by preventing the parasite from exiting red blood
cells to spread.
The
malaria parasite survives in its host
by remodeling the red blood
cells in which it dwells.
Malaria results from infection of human red blood
cells (RBC)
by the plasmodium parasite.
By teasing apart the structure of an enzyme vital to the parasites that cause toxoplasmosis and
malaria, Whitehead Institute scientists have identified a potentially «drugable» target that could prevent parasites from entering and exiting host
cells.
Her newest project, funded
by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health, will look at the crucial time when
malaria is transmitted — when reproductive
cell precursors known as gametocytes develop.
Peter Agre, MD, professor and director of the Johns Hopkins
Malaria Research Institute, was among the scientists and policymakers attending the March 9 signing of the Stem
Cell Executive Order and Presidential Memorandum on Scientific Integrity
by President Barack Obama.
Malaria is caused
by species of single -
celled parasites in the genus Plasmodium, vectored
by mosquitoes primarily in the genera Aedes and Anopheles between many vertebrate hosts, including humans.
«Most vaccine candidates for
malaria have worked
by trying to prevent parasites from entering red blood
cells,» said Dr Jonathan Kurtis of Rhode Island Hospital, the team's spokesman.