CorrectionWhile reviewing the proof of our article [1] after it waspublished on-line in its provisional form, we noticedtwo incidences where sentences in our article share ahigh level of similarity with two previously publishedpapers. The first incidence is in the first paragraph ofthe results section where four sentences in our articleshare similarity to sentences in the results section of apreviously published article [2]:“In order to determine the optimal conditions to ana-lyze secreted proteins during JEV infection, it was impor-tant to choose a period of secretion that allowed formaximal protein accumulation in the medium combinedwith minimal cell lysis or death. To this end, we devisedan assay to search for JEV induced secreted proteins asshowninFigureoneA.UponinfectionwithJEV,theBHK-21 cells were cultured for two days in the presenceof serum. The cells were then washed extensively toremove the proteins from fetal bovine serum present inthe growth medium and cells were grown in serum-freemedia for an additional day before being harvested(Figure one A).”“The secretion media was concentrated by ultrafiltra-tion with a 10-kDa molecular weight cut-off, and theprotein profile was analyzed by SDS-PAGE.”The second incidence was in the second and thirdparagraph of the discussion section where six sentencesin our article share similarity to sentences in the intro-duction of a previously published article [3]:“While GRP78 itself is protective against cell death,prolonged and extensive UPR and ER stress leads toapoptosis.Induction of the UPR accompanied by GRP78 up-reg-ulation and cell death has been described for a numberof viruses, including bovine viral diarrhea virus, Tulavirus, West Nile virus, Japanese encephalitis virus, andDengue virus, the last four of which are in the flavivirusfamily. Infection by the hepatitis C virus (HCV), also amember of the family Flaviviridae and related to JEV,induces the GRP78 promoter and GRP78 mRNA levelsare induced in cells expressing the HCV subgenomicreplicon or the HCV envelope. Additionally, expressionof the HCV structural proteins can induce GRP78protein, ER stress, and CHOP-mediated apoptosis.Recently, GRP78 has been shown to be up-regulated inDENV-infected cells and is necessary for DENV antigenproduction and/or accumulation. A similar report hasalso shown that GRP78 was up-regulated in the HCV-infected cells in an in vivo mouse model of HCV infec-tion in association with ER stress and hepatocyteapoptosis.”Upon making this discovery, we immediately con-tacted the Editor-in-Chief to make the journal aware ofthe issue. Subsequently, we conducted our own investi-gation and provided a full report to the publisher, whoperformed an independent investigation.We would like to sincerely apologize to our colleaguesin the field for this mistake, whose work was both inappro-priately utilized and not properly referenced. We wouldalso like to apologize to the reviewers of our manuscriptand the journal Editors. We are grateful for the opportu-nity to acknowledge and correct this mistake.