title: Exploitation of cellular pathways by Dengue virus.
abstract: Dengue virus (DENV) is the causative agent of the most prevalent arthropod-borne viral disease, thus representing a significant global health burden. Because of its limited coding capacity, DENV exploits components and pathways of the host cell to assure productive replication. In the past few years, important insights into this intimate interaction between DENV and the host cell have been gained. These include the identification of the ER-associated degradation pathway, autophagy, the unfolded protein response or lipid droplets that all play a crucial role for efficient DENV replication. In addition, strategies used by the virus to combat innate antiviral responses have been unraveled. Improving our understanding of the DENV-host cell relation will facilitate our attempts to develop efficient antiviral strategies.
authors.affiliation: Department of Infectious Diseases, Molecular Virology, Heidelberg University, Im Neuenheimer Feld 345, 69120 Heidelberg, Germany.
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Fischl
authors.forename: Ralf
authors.initials: R
authors.lastname: Bartenschlager
mesh_terms: D000818:Animals; D001343:Autophagy; D036022:Capsid Proteins / Q000378:metabolism; D003715:Dengue / Q000276:immunology / Q000821:virology; D003716:Dengue Virus / Q000276:immunology / Q000378:metabolism / Q000472:pathogenicity* / Q000502:physiology; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D050356:Lipid Metabolism; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D025801:Ubiquitin / Q000378:metabolism; D056811:Unfolded Protein Response; D014779:Virus Replication
chemical_list: D036022:Capsid Proteins; D025801:Ubiquitin; D046988:Proteasome Endopeptidase Complex