Host–Virus Interactions in Japanese Encephalitis Virus

Abstract

Japanese encephalitis (JE) is a mosquito-borne zoonotic disease that causes severe brain inflammation. The JE virus envelope protein domain III (JEV-ED3) plays a critical role in activating receptor binding and membrane fusion. This communication briefly describes, in a computational approach, how structural changes within the JEV-ED3 mutant epitopes suppress their antibody neutralization function. The simulated results demonstrate that mutant Ser40Lys acts as an antibody neutralization escape while Asp41Arg may play the role of an escape mutant. Additionally, an examination of the double mutants on JEV-ED3 suggests that these mutants may qualify as stronger neutralizing escape agents than their single variants. The structural analysis of this work helps to identify the proper antiviral target sequences and specific monoclonal antibodies for the JEV-ED3 escape mutants.