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© Research
Publication : Cell reports

KDEL Receptors Assist Dengue Virus Exit from the Endoplasmic Reticulum

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell reports - 05 Mar 2015

Li MY, Grandadam M, Kwok K, Lagache T, Siu YL, Zhang JS, Sayteng K, Kudelko M, Qin CF, Olivo-Marin JC, Bruzzone R, Wang PG

Link to Pubmed [PMID] – 25753416

Cell Rep 2015 Mar;10(9):1496-1507

Membrane receptors at the surface of target cells are key host factors for virion entry; however, it is unknown whether trafficking and secretion of progeny virus requires host intracellular receptors. In this study, we demonstrate that dengue virus (DENV) interacts with KDEL receptors (KDELR), which cycle between the ER and Golgi apparatus, for vesicular transport from ER to Golgi. Depletion of KDELR by siRNA reduced egress of both DENV progeny and recombinant subviral particles (RSPs). Coimmunoprecipitation of KDELR with dengue structural protein prM required three positively charged residues at the N terminus, whose mutation disrupted protein interaction and inhibited RSP transport from the ER to the Golgi. Finally, siRNA depletion of class II Arfs, which results in KDELR accumulation in the Golgi, phenocopied results obtained with mutagenized prME and KDELR knockdown. Our results have uncovered a function for KDELR as an internal receptor involved in DENV trafficking.

https://www.ncbi.nlm.nih.gov/pubmed/25753416