Our laboratory is investigating role of actin-cytoskeleton/ microfilament system in Leishmania donovani. This protozoan parasite causes a disease commonly called as "Kala-Azar" (black-fever), the “Leishmaniasis”. Following a digenetic life cycle these parasites exist in a highly motile promastigote form (in the insect vector) and non motile amastigote form (in human). Transmitted through the bite of an insect vector ‘sand-fly’, they invade macrophages and other tissues, grow inside the parasitophorous vacuoles and initiate a cascade of events that ultimately results in fatal visceral-leishmaniasis. Current treatment regimens for visceral-leishmaniasis are costly, highly toxic and often suffer from complications of drug-resistance. Therefore, studies are required to understand fundamentals of the cell and molecular biology of Leishmania and other related parasites, to facilitate the development of effective treatment for this disease.

During the transformation from spindle-shaped flagellated form to oval-aflagellated form, Leishmania parasites undertake a rigorous cytoskeletal rearrangement. Several cellular processes are dependent on the cytoskeletal functioning of the cells which are central for parasite survival. Our major objectives of research consolidate characterizing actin-cytoskeleton based cellular processes in these parasites. At present we are focusing on functional aspects of actin-network proteins accommodating actin, coronin, ADF/cofilin and myosin in Leishmania donovani (dd8).