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Antigenic variation in  Plasmodium falciparum  is regulated by transcriptional switches among members of the  var  gene family, each expressed in a mutually exclusive manner and encoding a different variant of the surface antigens collectively named PfEMP1. Antigenic switching starts when the first merozoites egress from the liver and begin their asexual proliferation within red blood cells. By erasing the epigenetic memory we created parasites with no  var  background, similar to merozoites that egress from the liver where no  var  gene is expressed. Creating a null- var  background enabled us to investigate the onset of antigenic switches at the early phase of infection. At the onset of switching,  var  transcription pattern is heterogeneous with numerous genes transcribed at low levels including upsA  vars , a subtype that was implicated in severe malaria, which are rarely activated in growing cultures. Analysis of subsequent  in vitro  switches shows that the probability of a gene to turn on or off is not associated with its chromosomal position or promoter type  per se  but on intrinsic properties of each gene. We concluded that  var  switching is determined by gene specific associated switch rates rather than general promoter type or locus associated switch rates. In addition, we show that fine tuned reduction in  var  transcription increases their switch rate, indicating that transcriptional perturbation can alter antigenic switching.

Erasing the Epigenetic Memory and Beginning to Switch—The Onset of Antigenic Switching of var Genes in Plasmodium falciparum