prM and E proteins from flaviviruses, such as yellow fever virus [11] , Japanese encephalitis virus (JEV) [12, 13] , West Nile virus (WNV) [14] and tick-bone encephalitis virus (TBEV) [15, 16] , are able to assemble into subviral particles in the absence of any other viral component. Subviral particles and infectious virions are coproduced in infected cells, assemble in an immature form, and subsequently undergo the same maturation process and display similar fusion activity as infectious viruses [17, 18] . Therefore, subviral particles could be a precious tool for research on cell biology of DVs. Although there have been attempts by several groups to obtain DV RSPs, either their production was inefficient or the sequence of DVs structural proteins had to be substantially modified [19] before they could efficiently generate RSPs. For example, the furin cleavage site on prM had to be mutated to establish the DV2 RSPs producing CHO cell line because it was found that the DV2 RSPs cause cell-cell fusion [20, 21] . Others replaced a portion of the carboxy-terminal region of DV1 and DV2 E genes with the corresponding sequence of JEV to observe significant RSP secretion [22, 23] . In either case, these modifications may interfere with the interactions with cytosolic proteins and, possibly, with the maturation and folding of the structural proteins.