Complication-specific pir gene upregulation.

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 characterised 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. The RNA of the parasite isolated from 23 patients (uncomplicated group = 6, hepatic dysfunction group = 12, and cerebral malaria group = 5) was subjected to microarray hybridisation, and the data obtained showed a wide range of pir subfamilies to have been differentially expressed. We report the upregulation of 24 pir genes in the cerebral malaria group (n = 5) and 28 pir genes in the hepatic dysfunction group (n = 12), which belong to different subfamilies in at least 50% of the severe malaria patients’ group. Out of the upregulated pir genes in the cerebral malaria group, members of vir subfamily E (n = 8 genes) and the pvpir subfamily H (n = 6 genes) are expressed in a higher proportion compared to the hepatic dysfunction group, where members of vir subfamily E (n = 9) and C (n = 6) are expressed in a major proportion.