Duck Tembusu virus (DTMUV) (DTMUV)

Duck Tembusu virus (DTMUV) is an emerging avian-pathogenic mosquito-borne flavivirus that primarily affects ducks, causing significant economic losses in the poultry industry across Southeast Asia and China [3, 6]. First identified in 2010, the virus is the causative agent of duck Tembusu virus disease, characterized by acute egg drop syndrome in laying ducks and severe neurological disorders in ducklings [6, 7, 14]. The DTMUV genome is a single-stranded positive-sense RNA that encodes a polyprotein cleaved into structural proteins (C, prM, E) and non-structural proteins (NS1 to NS5) [10, 12]. The envelope (E) protein is the primary surface protein responsible for host cell receptor binding and membrane fusion, making it a key target for neutralizing antibodies and entry inhibitors [4, 10, 13]. Non-structural proteins such as NS3 and NS5 are essential for viral replication and have been shown to modulate host processes like autophagy and innate immune signaling to facilitate infection [1, 6, 12]. Experimental antiviral strategies have explored the use of compounds like curcumin and epigallocatechin-3-gallate (EGCG) to inhibit viral entry and replication [4, 8]. Additionally, modulating host pathways such as the interferon response and autophagy has shown potential in reducing viral load in vivo [1, 4]. While primarily an avian pathogen, the detection of neutralizing antibodies in humans suggests a potential for zoonotic transmission [15]. The rapid spread and high morbidity of DTMUV necessitate the development of specific vaccines and effective therapeutic interventions [6, 16]. Overall, DTMUV represents a significant veterinary challenge with potential public health implications [3, 15].

Other names

Tembusu virusDTMUVBYD virusBaiyangdian virusSitiawan virusDuck egg drop syndrome virus

Inhibition of viral entry and adsorption; inhibition of post-adsorption viral replication; modulation of host autophagy pathways; upregulation of type I interferon signaling.