Successful
invasion by the parasite can cause flulike illness, and in severe cases, death.
The association of the Duffy blood group (FY) with P. vivax human malaria has been well - documented, where Duffy - negative individuals are naturally resistant to
invasion by this parasite [2].
Not exact matches
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 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.
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 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.
Now, the Laboratory of Malaria Immunology Team at the Immunology Frontier Research Center (IFReC), Osaka University, headed
by Professor Cevayir COBAN, have used mouse malaria models to show that robust immune activation and
invasion of
parasite by - products into the bone marrow during and after malaria infection leads to an adverse balance in bone homeostasis - a process usually tightly controlled -
by bone forming osteoblasts and bone resorbing osteoclasts.
That effort has been helped
by extra funding from the Australian government (Department of the Environment, Water, Heritage and the Arts) to look at pheromones and spawning - site choice in toads; from the Invasive Animals Co-Operative Research Centre to explore effects of
parasites on toads in Queensland; and from the Western Australians Department of Environment & Conservation, to understand frog and toad
parasites at the toad
invasion front.
Conversely, down - regulation of PKAc1 or stabilisation of a dominant - negative PKAr isoform that does not bind cAMP triggers premature
parasite egress from infected cells followed
by serial
invasion attempts leading to host cell lysis.