Journal: Journal of Neurovirology

Article Title: Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells

doi: 10.1007/s13365-019-00800-8

Figure Lengend Snippet: VP1 increased BBB permeability in vivo. a Western blotting showed the increased albumin in the brain tissues from the mice treated with VP1. b Immunohistochemistry staining revealed evident albumin in the brain tissues from the mice treated with VP1. c , d Fluorescence intensity of Evans blue dye (EBD) or FD4 was significantly elevated in the brain tissues from the mice treated with VP1. e Expression levels of tight junction proteins in the brain tissues. ZO-1 was comparable in the mice treated with normal saline or VP1. Claudin-5 was significantly reduced in the brain tissues treated with VP1. * p < 0.05

Article Snippet: EV-A71 VP1 neutralizing antibody (Cat.No.40013-H136) was purchased from Sino Biological (Beijing, China).

Techniques: Permeability, In Vivo, Western Blot, Immunohistochemistry, Staining, Fluorescence, Expressing

Journal: Journal of Neurovirology

Article Title: Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells

doi: 10.1007/s13365-019-00800-8

Figure Lengend Snippet: VP1 reduced claudin-5 and disrupted BBB in vitro. a VP1 significantly decreased the trans-endothelial electrical resistance (TEER). b VP1 damaged the tight junctions between endothelia cells observed with transmission electron microscope. c , d VP1 directly decreased claudin-5 in the brain endothelial cells; in contrast, ZO-1 was comparable in different groups. ** p < 0.01

Article Snippet: EV-A71 VP1 neutralizing antibody (Cat.No.40013-H136) was purchased from Sino Biological (Beijing, China).

Techniques: In Vitro, Transmission Assay, Microscopy

Journal: Journal of Neurovirology

Article Title: Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells

doi: 10.1007/s13365-019-00800-8

Figure Lengend Snippet: VP1 promoted the expression of vimentin in the brain tissues. a qRT-PCR showed the vimentin mRNA was significantly increased in the brain tissues from the mice treated with VP1. b Western blotting further showed the vimentin protein was significantly increased in the brain tissues from the mice treated with VP1. c In the immunohistochemistry analysis, vimentin was widely distributed in brain tissues and significantly increased upon VP1 challenge. ** p < 0.01. d EV-A71 receptors SCARB2 and HSP-70 were almost unchanged on the brain endothelia cells treated with VP1. e EV-A71 receptor Annexin II was slightly decreased on the brain endothelia cells treated with VP1. Expression of PSGL-1 was comparable in the different groups

Article Snippet: EV-A71 VP1 neutralizing antibody (Cat.No.40013-H136) was purchased from Sino Biological (Beijing, China).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Immunohistochemistry

Journal: Journal of Neurovirology

Article Title: Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells

doi: 10.1007/s13365-019-00800-8

Figure Lengend Snippet: VP1 increased the expression of vimentin on the brain endothelial cells. a A dose-dependent increase of vimentin on the endothelial cells treated with VP1 for 24 h. VP1 with 0.1 μg/ml was enough to stimulate the expression of vimentin. b A time-dependent increase of vimentin on the endothelial cells treated with 0.1 μg/ml VP1. c Immunofluorescence analysis showed the enhanced expression of vimentin on endothelial cells treated with VP1 for 24 h. d VP1 neutralization antibody competitively inhibited the roles of VP1 in the upregulation of vimentin. Ctrl-Ab control antibody, Anti-VP1 VP1 neutralization antibody. e , f Expression of EV-A71 receptors SCARB2, HSP-70, and Annexin II was similar in the different groups. PSGL-1 was decreased in the endothelia cells treated with VP1

Article Snippet: EV-A71 VP1 neutralizing antibody (Cat.No.40013-H136) was purchased from Sino Biological (Beijing, China).

Techniques: Expressing, Immunofluorescence, Neutralization

Journal: Journal of Neurovirology

Article Title: Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells

doi: 10.1007/s13365-019-00800-8

Figure Lengend Snippet: TGF-/Smad3 and NF-κB-dependent expression of vimentin on brain endothelial cells treated with VP1. a In the VP1-treated endothelial cells, TGF-β and Smad-3 was increased and activated. b NF-κB p65 was activated; and STAT3 was not changed. c NF-κB inhibitor BAY or Smad-3 inhibitor SIS3 suppressed the elevation of vimentin on the VP1-treated endothelial cells

Article Snippet: EV-A71 VP1 neutralizing antibody (Cat.No.40013-H136) was purchased from Sino Biological (Beijing, China).

Techniques: Expressing

Journal: Nature Communications

Article Title: A rationally designed 2C inhibitor prevents enterovirus D68-infected mice from developing paralysis

doi: 10.1038/s41467-025-61083-8

Figure Lengend Snippet: a Antiviral EC 50 values were determined in the CPE assay with EV-D68 US/MO/14-18947 in RD cells. Cytotoxicity CC 50 values were determined using the neutral red uptake method in RD cells. The results are the mean ± standard deviation (SD) of two independent experiments with three repeats in each experiment. *The antiviral activity EC 50 values of Jun5532 and Jun5253 were reported earlier . SI selectivity index. b Antiviral activity of selected 2C inhibitors against EV-A71 Tainan strain in plaque assay. c Antiviral activity of selected 2C inhibitors against CVB3 Nancy strain in plaque assay. The EC 50 values in the plaque assay are the mean ± SD of two biological replicates. Source data are provided as a Source Data file.

Article Snippet: Enterovirus D68 (EV-D68) strains US/MO/14-18947, US/KY/14-18953, US/MO/14-18949, US/IL/14-18952, and US/IL/14-18956 (ATCC); Coxsackievirus B3 (CVB3) Nancy strain (VR-30); Enterovirus A71 (EV-A71) Tainan/4643/1998 (BEI Resources, NR-471); Coxsackievirus A6 (CVA6, VR-1801); and human rhinovirus 16 (RV16, VR-283) were sourced from ATCC or BEI Resources.

Techniques: Standard Deviation, Activity Assay, Plaque Assay

Journal: Nature Communications

Article Title: A rationally designed 2C inhibitor prevents enterovirus D68-infected mice from developing paralysis

doi: 10.1038/s41467-025-61083-8

Figure Lengend Snippet: a Antiviral activity of Jun6504 against five contemporary EV-D68 strains in RD cells. EC 50 values against EV-D68 strains were determined using the cytopathic effect (CPE) assay in RD cells after 60 h of compound incubation. The EC 50 values are the mean ± SD of three biological replicates. b Antiviral activity of Jun6504 against poliovirus, CVA16, CVA6, and CVB3 in CPE assay. The EC 50 values are the mean ± SD of two biological replicates. c Antiviral activity of Jun6504 against EV-A71 and EV-D68 in plaque assay. The EC 50 values are the mean ± SD of two biological replicates. d Cytotoxicity of Jun6504 in HeLa, RD, and Vero cells. The results are from two biological replicates. e DSF assay of Jun6504 with EV-A71, EV-D68, and CVB3 2 C proteins. The results are from two biological replicates. f Jun6504 time-of-addition experiment in a single cycle of EV-D68 replication. g Viral titers in the time-of-addition experiment. EC 50 and CC 50 curve fittings using log 10 (concentration of Jun6504 ) vs. percentage of positive control with variable slopes were performed in Prism 8. Error bars denote mean ± SD of two biological replicates. Source data are provided as a Source Data file.

Article Snippet: Enterovirus D68 (EV-D68) strains US/MO/14-18947, US/KY/14-18953, US/MO/14-18949, US/IL/14-18952, and US/IL/14-18956 (ATCC); Coxsackievirus B3 (CVB3) Nancy strain (VR-30); Enterovirus A71 (EV-A71) Tainan/4643/1998 (BEI Resources, NR-471); Coxsackievirus A6 (CVA6, VR-1801); and human rhinovirus 16 (RV16, VR-283) were sourced from ATCC or BEI Resources.

Techniques: Activity Assay, Incubation, Plaque Assay, Concentration Assay, Positive Control