Research Team

The RIFINs are one of the adhesive proteins expressed by P. falciparum and localized to the surface of the parasite-infected RBCs. Emerging reports have shown its role in the development of severe malaria in humans. The mechanisms of RIFINs mediated development of severe malaria are largely unknown. Here, we investigate the mechanisms of RIFINs contributions to the development of severe malaria.

The Plasmodium falciparum Erythrocyte Membrane Protein 1 (PfEMP1) is the key antigenic variation protein expressed by a parasite and exported to the surface of infected RBCs. The PfEMP1 is encoded by a multigene family called var genes. The P. falciparum contains 60 var genes and expresses one var gene at the time of infection. The parasite switches the expression of var genes in response to host immunity. Here, we investigate how various epigenetic players contribute to the differential expression of var genes in response to host immunity.

The epigenetic players significantly contribute to the differential gene expression in the human malaria parasite Plasmodium falciparum. However, the stage-specific regulator in P. falciparum remains unknown. We aim to investigate the function of various unique epigenetic modifications from the malaria parasite P. falciparum.

The antigenic variation, virulence, and parasite invasion are largely controlled by epigenetic reader domain proteins in the malaria parasites. Our current work focuses on the investigation of various Epigenetic reader domain proteins from the human malaria parasite P. falciparum and its functions in malaria virulence.

Artemisinin-based combination therapies are the most effective treatment for controlling malaria to date. Artemisinin resistance is posing a major threat to curbing this disease. K13 is recognized as the molecular marker for artemisinin resistance. So, we mainly focus on the role of K13 mutations in mediating artemisinin resistance in Plasmodium falciparum. 

Translational plasticity is the key mechanism the malaria parasite adopts during its development in RBC and liver. Earlier studies from our lab have identified that the YTH domain protein regulates the mRNA fate and translations. We aim to investigate mechanisms of YTH - m6A  axis in regulation of translational plasticity of human malaria parasite.

Plasmodium spp harbors unique epigenetic modifications in the chromatin of parasites, and the functions of these epigenetic marks remain unknown. We aim to identify and characterize the various epigenetic marks from Plasmodium species.