Please use this identifier to cite or link to this item: https://doi.org/10.1038/emi.2016.56
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dc.titleCooperative effect of the VP1 amino acids 98E, 145A and 169F in the productive infection of mouse cell lines by enterovirus 71 (BS strain)
dc.contributor.authorVictorio, C.B
dc.contributor.authorXu, Y
dc.contributor.authorNg, Q
dc.contributor.authorMeng, T
dc.contributor.authorChow, V.T
dc.contributor.authorChua, K.B
dc.date.accessioned2020-09-23T01:43:46Z
dc.date.available2020-09-23T01:43:46Z
dc.date.issued2016
dc.identifier.citationVictorio, C.B, Xu, Y, Ng, Q, Meng, T, Chow, V.T, Chua, K.B (2016). Cooperative effect of the VP1 amino acids 98E, 145A and 169F in the productive infection of mouse cell lines by enterovirus 71 (BS strain). Emerging microbes & infections 5 : e60. ScholarBank@NUS Repository. https://doi.org/10.1038/emi.2016.56
dc.identifier.issn2222-1751
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/176522
dc.description.abstractEnterovirus 71 (EV71) is a neurotrophic virus that causes hand, foot and mouth disease (HFMD) and occasional neurological infection among children. It infects primate cells but not rodent cells, primarily due to the incompatibility between the virus and the expressed form of its receptor, scavenger receptor class B member 2 (SCARB2) protein, on rodent cells (mSCARB2). We previously generated adapted strains (EV71:TLLm and EV71:TLLmv) that were shown to productively infect primate and rodent cell lines and whose genomes exhibited a multitude of non-synonymous mutations compared with the EV71:BS parental virus. In this study, we aimed to identify mutations that are necessary for productive infection of murine cells by EV71:BS. Using reverse genetics and site-directed mutagenesis, we constructed EV71 infectious clones with specific mutations that generated amino acid substitutions in the capsid VP1 and VP2 proteins. We subsequently assessed the infection induced by clone-derived viruses (CDVs) in mouse embryonic fibroblast NIH/3T3 and murine neuroblastoma Neuro-2a cell lines. We found that the CDV:BS-VP1(K98E,E145A,L169F) with three substitutions in the VP1 protein-K98E, E145A and L169F-productively infected both mouse cell lines for at least three passages of the virus in murine cells. Moreover, the virus gained the ability to utilize the mSCARB2 protein to infect murine cell lines. These results demonstrate that the three VP1 residues cooperate to effectively interact with the mSCARB2 protein on murine cells and permit the virus to infect murine cells. Gain-of-function studies similar to the present work provide valuable insight into the mutational trajectory required for EV71 to infect new host cells previously non-susceptible to infection.
dc.sourceUnpaywall 20200831
dc.subjectamino acid
dc.subjectcapsid protein
dc.subjectCD36 antigen
dc.subjectlysosome associated membrane protein
dc.subjectScarb2 protein, mouse
dc.subjectVP1 protein, Foot-and-mouth disease virus
dc.subjectVP2 protein, Foot-and-mouth disease virus
dc.subjectamino acid sequence
dc.subjectamino acid substitution
dc.subjectanimal
dc.subjectcell line
dc.subjectchemistry
dc.subjectChlorocebus aethiops
dc.subjectEnterovirus A
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectmouse
dc.subjectmutation
dc.subjectNIH 3T3 cell line
dc.subjectphysiology
dc.subjectreverse genetics
dc.subjectsite directed mutagenesis
dc.subjecttumor cell line
dc.subjectVero cell line
dc.subjectAmino Acid Sequence
dc.subjectAmino Acid Substitution
dc.subjectAmino Acids
dc.subjectAnimals
dc.subjectAntigens, CD36
dc.subjectCapsid Proteins
dc.subjectCell Line
dc.subjectCell Line, Tumor
dc.subjectCercopithecus aethiops
dc.subjectEnterovirus A, Human
dc.subjectLysosome-Associated Membrane Glycoproteins
dc.subjectMice
dc.subjectMutagenesis, Site-Directed
dc.subjectMutation
dc.subjectNIH 3T3 Cells
dc.subjectReverse Genetics
dc.subjectVero Cells
dc.typeArticle
dc.contributor.departmentMICROBIOLOGY AND IMMUNOLOGY
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1038/emi.2016.56
dc.description.sourcetitleEmerging microbes & infections
dc.description.volume5
dc.description.pagee60
dc.published.statePublished
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