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Dengue fever is an endemic virus-borne disease that causes many severe ailments, including dengue hemorrhagic fever and dengue shock syndrome. NS2B-NS3 protease is present in all four strains of the dengue virus. NS2B-NS3 is a non-structural protein that performs three distinct functions: protease activity, helicase activity, and nucleoside triphosphatase activity. NS2B-NS3 pro-complex plays a crucial role in viral replication, and NS2B interacts with NS3 protease at a flat active site with an amino acid of the  N - terminal  region. NS2B acts as a cofactor for NS3 protease. In the current study, the conserved residues of NS2B were identified. Dengue virus-2 NS2B was mutated at the identified conserved amino acid region to investigate the role of NS2B on activation of NS3 pro. Molecular dynamics simulations were performed to investigate the mutated complex’s changes in stability, conformation, and free energy. The EAG mutant complex exhibited more unstable conformation, less hydrogen bond formation, and high binding energy than wild type. This result suggests a vital role of E63, A65, G69 mutation in NS2B for the interruption of activation of the NS3. Communicated by Ramaswamy H. Sarma

Effect of mutation of NS2B cofactor residues on Dengue 2 NS2B-NS3 protease complex – an insight to viral replication