The persistence of the human malaria parasite during blood stage proliferation in its host depends on the successive expression of variant molecules at the surface of infected erythrocytes. This variation is mediated by the differential control of a family of surface molecules termed PfEMP1 encoded by approximately 60 genes. Each individual parasite expresses a single gene at a time, maintaining all other members of the family in a transcriptionally silent state. PfEMP1/ enables parasitized erythrocytes to adhere within the microvasculature, resulting in severe disease. This review highlights key regulatory mechanisms thought to be critical for monoallelic expression of genes. Antigenic variation is orchestrated by epigenetic factors including monoallelic transcription at separate spatial domains at the nuclear periphery, differential histone marks on otherwise identical genes, and silencing mediated by telomeric heterochromatin. In addition, controversies surrounding genetic elements in antigenic variation are discussed.


Article metrics loading...

Loading full text...

Full text loading...


Data & Media loading...

  • Article Type: Review Article
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error