XML Feed for RxPG News   Add RxPG News Headlines to My Yahoo!   Javascript Syndication for RxPG News

Research Health World General
 
  Home
 
 Latest Research
 Cancer
 Psychiatry
 Genetics
 Surgery
 Aging
 Ophthalmology
 Gynaecology
 Neurosciences
 Pharmacology
 Cardiology
 Obstetrics
 Infectious Diseases
  AIDS
  Influenza
  MRSA
  Tuberculosis
  Shigella
  HCV
  SARS
  Ebola
  Dengue
  Malaria
   Plasmodium
  Pertussis
  Mumps
  Prion Diseases
  Small Pox
  Anthrax
  Leishmaniasis
 Respiratory Medicine
 Pathology
 Endocrinology
 Immunology
 Nephrology
 Gastroenterology
 Biotechnology
 Radiology
 Dermatology
 Microbiology
 Haematology
 Dental
 ENT
 Environment
 Embryology
 Orthopedics
 Metabolism
 Anaethesia
 Paediatrics
 Public Health
 Urology
 Musculoskeletal
 Clinical Trials
 Physiology
 Biochemistry
 Cytology
 Traumatology
 Rheumatology
 
 Medical News
 Health
 Opinion
 Healthcare
 Professionals
 Launch
 Awards & Prizes
 
 Careers
 Medical
 Nursing
 Dental
 
 Special Topics
 Euthanasia
 Ethics
 Evolution
 Odd Medical News
 Feature
 
 World News
 Tsunami
 Epidemics
 Climate
 Business
 
 India
Search

Last Updated: Nov 18, 2006 - 12:32:53 PM

Plasmodium Channel
subscribe to Plasmodium newsletter

Latest Research : Infectious Diseases : Malaria : Plasmodium

   DISCUSS   |   EMAIL   |   PRINT
How Plasmodium breaks in to blood cells
Aug 30, 2005 - 1:17:00 AM, Reviewed by: Dr. Priya Saxena

In effect, if the gene finds all the doors locked, then it will try all the windows until it finds one it can force open.

 
Plasmodium falciparum, the most lethal malaria parasite, is a housebreaking villain of the red blood cell world. Like a burglar searching for a way in to his targeted premises, the parasite explores a variety of potential entry points to invade the red blood cells of its human victims. When a weak point is found, the intrusion proceeds.

Scientists have known about the parasite's housebreaking habit for a decade, but just how it breaks in to blood cells has been unknown.

Now, an international team of scientists, led by WEHI's Professor Alan Cowman, has discovered the gene - known as PfRh4 - that the parasite uses as a tool to switch between potential invasion points. More specifically, the gene provides the parasite with the ability to switch from receptors on red blood cells that contain sialic acid to those that do not.

In effect, if the gene finds all the doors locked, then it will try all the windows until it finds one it can force open.

The team who performed the research work consisted of Janine Stubbs, Ken Simpson, Tony Triglia, David Plouffe, Christopher J. Tonkin, Manoj T. Duraisingh, Alexander G. Maier and Elizabeth Winzeler. Professor Cowman and his team at WEHI worked with researchers from the Scripps Research Institute (TSRI) in La Jolla, California and the Genomics Institute of the Novartis Research Foundation in San Diego, California.

This discovery made by the group will have a profound impact upon the design of new anti-malarial vaccines, since the inactivation of this single protein could block multiple entry points currently open to the parasite.
 

- The results of the new study are published in the 26 August 2005 issue of the prestigious journal, Science.
 

Walter & Eliza Hall Institute

 
Subscribe to Plasmodium Newsletter
E-mail Address:

 

This discovery made by the group will have a profound impact upon the design of new anti-malarial vaccines, since the inactivation of this single protein could block multiple entry points currently open to the parasite.

Related Plasmodium News

AgDscam gene Holds the Key to Broad-Based Pathogen Recognition
Genes responsible for malaria parasite's survival pin pointed
Malaria parasite plasmodium impairs key immune system cells
How Plasmodium falciparum sneaks past the human immune system
How Plasmodium breaks in to blood cells


For any corrections of factual information, to contact the editors or to send any medical news or health news press releases, use feedback form

Top of Page

 

© Copyright 2004 onwards by RxPG Medical Solutions Private Limited
Contact Us