AAEL002524) was significantly upregulated by JEV infection and facilitated infection <i>in vivo</i> and <i>in vitro</i> mosGCTL-7 bound to the N-glycan at N154 on the JEV envelope protein.
Envelope protein gene based molecular characterization of Japanese encephalitis virus clinical isolates from West Bengal, India: a comparative approach with respect to SA14-14-2 live attenuated vaccine strain.
Changes in the envelope protein's hinge region, or its putative receptor-binding domain, are associated with changes in neurovirulence in animal models of JE.
Immunization with plasmid DNA encoding the envelope glycoprotein of Japanese Encephalitis virus confers significant protection against intracerebral viral challenge without inducing detectable antiviral antibodies.
As the initial step to produce a second-generation vaccine, recombinant DNA technology was utilized to express the JE virus envelope glycoprotein V3 (E) gene in yeast cells.This report describes the construction of a yeast expression vector in which a cDNA clone covering the V3 gene was connected to the acid-phosphatase promoter of a yeast vector plasmid.
AAEL002524) was significantly upregulated by JEV infection and facilitated infection <i>in vivo</i> and <i>in vitro</i> mosGCTL-7 bound to the N-glycan at N154 on the JEV envelope protein.
Envelope protein gene based molecular characterization of Japanese encephalitis virus clinical isolates from West Bengal, India: a comparative approach with respect to SA14-14-2 live attenuated vaccine strain.
Changes in the envelope protein's hinge region, or its putative receptor-binding domain, are associated with changes in neurovirulence in animal models of JE.
Exogenous expression of duKPNA4 significantly elevated the expression of IFN-α and IFN-β induced by JEV infection and inhibited JEV replication in DEFs.
TNFA rs1800629 A and CCR5 rs1799987 A alleles were associated with susceptibility while combination lacking TNFA rs1800629 A, CCR5 rs333 Δ32, and rs1799987 A alleles and CCL2rs1024611 G/G genotype was associated with protection to JE.
Although the CCR2-CCL2 axis is important for monocytes trafficking during JEV infection, little is known about its role in CNS trafficking of CD8<sup>+</sup> T cells.
ICAM-1 (K469E) and MCP-1-2518 A > G polymorphisms lead to increased level of ICAM-1 and MCP-1 in Japanese Encephalitis which may be associated with severity as well as an adverse outcome of the disease.