Target intelligence / Profile preview

Nipah virus attachment glycoprotein G (NiV-G) (NiV-G)

Target
NiV-G
Molecular classification
Viral surface protein, Type II transmembrane protein, Attachment protein
01

Overview

The Nipah virus attachment glycoprotein G (NiV-G) is a critical type II transmembrane protein located on the surface of the Nipah virus envelope (UniProt: P0C1C7). It mediates viral pathogenesis by facilitating the attachment of the virus to host cells through high-affinity interactions with the receptors Ephrin-B2 and Ephrin-B3, which are prevalent in endothelial and neuronal tissues (PubMed: 16007097). This binding event is the essential first step of the viral entry process, as it triggers a conformational change in the associated fusion (F) protein to merge the viral and host membranes (PubMed: 21715493). Due to its accessibility and indispensable role in infection, NiV-G is the primary target for the development of neutralizing monoclonal antibodies and vaccine candidates (PubMed: 23115215). For example, the monoclonal antibody m102.4 specifically targets the receptor-binding domain of NiV-G to block viral entry. Therapeutic interventions targeting NiV-G are vital for addressing the high mortality rates associated with Nipah virus-induced encephalitis and severe respiratory distress (WHO, 2024).

Other names
Attachment glycoproteinG proteinNiV-GGlycoprotein GNipah virus G protein
02

Mechanism of action

Neutralization of viral entry by binding to the receptor-binding domain (RBD) of the G protein, thereby preventing its interaction with host Ephrin-B2 and Ephrin-B3 receptors (PubMed: 23115215).

03

Biological functions

Viral attachmentHost cell receptor bindingInduction of viral-host membrane fusionViral entry
04

Disease associations

Nipah virus infectionEncephalitisSevere respiratory illnessZoonotic infection
05

Safety considerations

Potential for viral escape through antigenic drift in the G proteinHigh pathogenicity of the virus requiring BSL-4 containment for researchRapid disease progression limiting the window for therapeutic interventionTheoretical risk of antibody-dependent enhancement (ADE)
06

Interacting drugs

m102.4

3 more in the full profile.

07

Biomarkers

Anti-NiV-G IgG antibodiesAnti-NiV-G IgM antibodiesNiV-G specific T-cell responseNiV RNA viral load

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