Malaria parasites avoid destruction by their host's immune response through systematic and coordinated expression switching between members of a network of variant antigen-encoding genes, a process that is mediated by a uniquely conserved gene called var2csa.

The first comprehensive analysis of antigenic switching in the malaria-causing parasite Plasmodium falciparum provides new insights into the process that prevents individuals from acquiring immunity to the disease.

Mapping DNA replication timing, allied to genetic analysis of a RecQ repair helicase, reveals that antigenic variation in the African trypanosome may be initiated by locus-specific, replication-derived sequence instability.

Nuclear phosphoinositide signaling controls telomeric gene repression and activation essential for switching expression of surface antigen genes and thus antigenic variation.

The VSG gene controls its monoallelic expression, and expression site activity determines developmental progression.

Single-cell RNA-sequencing resolves the transcriptional landscape of asexual development in Toxoplasma gondii, revealing concerted genetic programs to Plasmodiumfalciparum and a novel transcriptional factor that controls antigen switching.

Combined antigenic and genetic analysis shows that different strains of the human influenza virus display dramatically different rates of antigenic drift, and that these differences have a significant impact on the number of new infections in each flu season.

Each dengue serotype contains moderate antigenic diversity, and population immunity drives clade turnover in a hyperendemic population.

A robust procedure to purify mRNAs and their associated proteins identify CFB2 as the critical protein that binds and influences the fate of the main virulence factor in Trypanosoma brucei.

Parasite variants associated with severe malaria do not have an intrinsic growth or survival advantage in vivo, which indicates that a change in host environment is required for their selection.