Adaptive mutations in the genomes of enterovirus 71 strains following infection of mouse cells expressing human P-selectin glycoprotein ligand-1

• Published in: Journal of general virology Vol. 92; no. Pt 2; pp. 287 - 291
• Main Authors: MIYAMURA, Kohei, NISHIMURA, Yorihiro, ABO, Masahiro, WAKITA, Takaji, SHIMIZU, Hiroyuki
• Format: Journal Article
• Language: English
• Published: Reading Society for General Microbiology 01.02.2011
• Subjects: Adaptation, Physiological; Animal; Animals; Biological and medical sciences; Cell Line; Enterovirus; Enterovirus A, Human - genetics; Enterovirus A, Human - physiology; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation; Genome, Viral; Humans; Membrane Glycoproteins - genetics; Membrane Glycoproteins - metabolism; Mice; Microbiology; Miscellaneous; Molecular Sequence Data; Mutation; Virology; Virus Replication - genetics; Virus Replication - physiology; Human; Enterovirus 71; Picornaviridae; Rodentia; P Glycoprotein; Enterovirus; Strain; Virus; P Selectin; Vertebrata; Mammalia; Mouse; Mutation; Genome
• ISSN: 0022-1317; 1465-2099; 1465-2099
• DOI: 10.1099/vir.0.022418-0

We recently identified human P-selectin glycoprotein ligand-1 (PSGL-1) as a functional enterovirus 71 (EV71) receptor and demonstrated PSGL-1-dependent replication for some EV71 strains in human leukocytes. Here, we report that four out of five PSGL-1-binding strains of EV71 replicated poorly in mouse L929 cells stably expressing human PSGL-1 (L-PSGL-1 cells). Therefore, we compared the replication kinetics and entire genomic sequence of five original EV71 strains and the corresponding EV71 variants (EV71-LPS), which were propagated once in L-PSGL-1 cells. Direct sequence comparison of the entire genome of the original EV71 strains and EV71-LPS variants identified several possible adaptive mutations during the course of replication in L-PSGL-1 cells, including a putative determinant of the adaptive phenotype in L-PSGL-1 cells at VP2-149. The results suggest that an adaptive mutation, along with a PSGL-1-binding phenotype, may facilitate efficient PSGL-1-dependent replication of the EV71 strains in L-PSGL-1 cells.