Abstract
Why does Plasmodium falciparum cause severe illness in some but not all infections? How is clinical immunity acquired? These questions have intrigued investigators since the clinical epidemiology of malaria was first described. The search for answers to both questions has highlighted the changes that take place at the surface of infected red blood cells during the last half of the erythrocytic cycle. These changes specify the antigenic and adhesive or cytoadherence phenotypes for the infected cell. Now the antigenic and adhesive phenotypes appear to be linked and together undergo clonal variation. In this article David Roberts, Beverley-Ann Biggs, Graham Brown and Christopher Newbold explain how clonal phenotypic variation and the linkage between adhesive and antigenic types contribute to our understanding of naturally acquired immunity and of pathogenesis of severe malaria.
| Original language | English |
|---|---|
| Pages (from-to) | 281-286 |
| Number of pages | 6 |
| Journal | Parasitology Today |
| Volume | 9 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - Aug 1993 |
| Externally published | Yes |
Bibliographical note
Funding Information:The authors would like to acknowledge their discussions with Tony Berendt, Kevin Harsh, Robin Anders and Ross Coppel and thank David Ferguson for providing electron micrographs. DJR is a Medical Research Council Training Fellow. BB is a Keir Fellow of the Royal Melbourne Hospital. This work was supported by the Medical Research Council, the Weltcome Trust, The National Health and Medical Research Council of Australia and the John D. and Catherine T. MacArthur Foundation.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
Fingerprint
Dive into the research topics of 'Protection, pathogenesis and phenotypic plasticity in Plasmodium falciparum malaria'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver