HYDERABAD: Reserchers from the School of Life Sciences in University of Hyderabad (UoH) have discovered the mechanism behind the reduction of platelets in dengue patients. The study can help with better management of the vectorborne disease for which there is no specific drug. Loss of platelets leads to internal haemorrhage and even death if not treated on time. The study suggests that mitochondrial dysfunction might be one of the reasons for the decrease in the number of platelets that results in thrombocytopenia - a condition manifested in dengue patients.
The study provided novel insights on the import of nonstructural protein-3 (NS3) into host mitochondria. More importantly, under its interaction with the NS3 of the dengue virus, the protein coding gene could be a potential target to develop antidengue drugs. Using in-silico analysis, a group of researchers led by Dr M Venkata Ramana and Professor Naresh Babu Sepuri showed that the NS3 enters the host mitochondrial matrix and cleaves a very important protein coding gene - GrpEL1 - that is essential for major functions of the mitochondria.
The Ribonucleic acid (RNA) genome of this dengue virus encodes three structural and seven non-structural (NS) proteins along with two un-translated regions, one each on both ends. Amongst them, dengue protease (NS3), the NS protein, plays a pivotal role in polyprotein processing and virus multiplication. Mitochondria are essential organelles in the cell, consisting of an extensive membrane network and matrix fluid besides their genome. The interaction between viral proteins and the mitochondrial membrane proteins that interfere with mitochondrial functions is known, however the association of a virus-coded protein with the mitochondrial matrix still remains unknown.