Basis for key parasite function in malaria found
Focus on NIAID
- About NIAID
- HIV/AIDS: 30 years of hard-won victories
- Q & A with Tony Fauci
- NTDs and the skewed burden of disease
- Research targets new diagnostics, drugs and vaccines for TB
- NIAID-funded centers seek to enhance malaria control
- ICER program fosters research collaborations in developing countries
- Centers expand global reach of influenza research
- Funding and training for foreign scientists
- Giant steps in the battle against HIV/AIDS: opinion by Fogarty Director Dr. Roger I. Glass
Plasmodium gallinaceum causes
malaria in poultry.
Inside a human red blood cell, the malaria parasite both hides from the immune system and fuels its own growth by digesting hemoglobin, the cell’s main protein. The parasite, however, must obtain additional nutrients from the bloodstream via tiny pores in the cell membrane. Investigators at the National Institute of Allergy and Infectious Diseases (NIAID) - who previously discovered the main feeding pore on parasite-infected red blood cells - recently found the genes that malaria parasites use to create these feeding pores.
The discovery of parasite genes required for feeding pore activity opens up several new research directions. For example, development of antimalarial drugs that target these channels could be accelerated. The NIAID team has already found channel inhibitors that kill malaria parasites. They also are exploring how the feeding channel protein is transported from the parasite to the red blood cell membrane, as preventing this transport may be another way to kill malaria parasites.
In addition to funding from NIAID’s Division of Intramural Research, this study was supported by Medicines for Malaria Venture, a not-for-profit public-private partnership headquartered in Switzerland.
This article was adapted from NIAID Global Research: Improving Health in a Changing World [PDF 7M, 24 pages] .
-
ghmjul-aug2011.pdf (2.18 MB)
To view Adobe PDF files, download current, free accessible plug-ins from Adobe's website .