Comparative clinical transcriptome of pir genes in severe Plasmodium vivax malaria

Vir genes, a multigene family in Plasmodium vivax that are a part of a larger superfamily of genes called the pir (Plasmodium interspersed repeat) genes have been reported earlier to be potentially involved in cyto-adherence and evasion of splenic clearance. Plasmodium vivax, historically characterized as a "benign" malaria parasite, has been associated with clinical outcomes including hepatic dysfunction, renal failure, and cerebral malaria in India and several global regions. It constitutes an economic burden and presents a public health challenge alongside other Plasmodium species. Here, we present a part of global transcriptomic studies using custom designed microarrays, that compare the transcriptome of the parasite responsible for severe Plasmodium vivax manifestations, specifically hepatic dysfunction and cerebral malaria from India, with an emphasis on the pir genes, some of which are reported to play a role in cyto-adherence. 23 patients with Plasmodium vivax malaria (Uncomplicated=6, Hepatic dysfunction=12 and Cerebral malaria=5) were subjected to microarray hybridization and the data so obtained showed a wide range of pir subfamilies have been differentially expressed. Upregulation has been seen in 24 pir genes in cerebral malaria samples (n=5) and 28 genes in hepatic dysfunction samples (n=12) belonging to different subfamily in at least 50% of the patient samples. Out of the upregulated pir genes in cerebral malaria manifestation, members of vir subfamily E and pvpir H are maximum in number whereas in hepatic dysfunction manifestation, members of vir subfamily E and C comprise a significant proportion.