9,060 research outputs found
LL-18 binds directly to virus particles.
No full text(A) 1H NMR data showing the chemical shifts. Spectra of LL-37 (left panel) or LL-18 (right panel) peptide in the absence or presence of EV71 virus (green line) or CVB5 virus (red line). (B-C) 293T cells cotransfected with GFP or GFP-tagged LL-18 (B) or LL-37 (C) and HA-tagged VP1, VP2, or VP3 plasmids were immunoprecipitated with anti-HA antibody, and interactions between LL-18 and viral structural proteins were detected by anti-GFP antibody.</p
LL-18 interferes with virus-SCARB2 interaction.
No full text(A) Molecular docking model of LL-18 with EV71 virion. EV71 capsid proteins VP1 (green), VP2 (pink), and VP3(blue), all interact with LL-18 displayed in red sticks (left panel). The amino acid residues of capsid protein interacting with both LL-18 and SCARB2 are indicated (right panel). (B) 293T cells expressing SCARB2-Flag were lysed and cell lysates were incubated with EV71 virus in the absence or presence of the indicated amount of LL-18. Cell lysates were then immunoprecipitated with anti-Flag antibody and the precipitated virus was determined with anti-VP1 antibody. (C) 293T cells expressing Annexin 2-Flag were lysed and cell lysates were incubated with EV71 virus in the absence or presence of LL-18. Cell lysates were then immunoprecipitated with anti-Flag antibody and the precipitated virus was determined with anti-VP1 antibody.</p
LL-18 inhibits mEV71 infection <i>in vivo</i>.
No full text(A) mEV71 was pre-treated with PBS or LL-18 and used to infect 6-day old ICR mice. The survival rate of mice infected with the mEV71 virus with or without LL-18 was recorded. (B) Mice infected with the mEV71 virus with or without LL-18 pre-treatment were sacrificed 1 day post infection (d.p.i.) and viral titers from brain and muscle tissues were determined. ***, P<0.001. (C) H&E staining of muscle tissue from mice infected with the mEV71 virus with or without LL-18. Blue arrows indicate infiltrated neutrophils. Bar, 20μm.</p
LL-18 binds directly to virus particles.
No full text(A) RD cells were pre-incubated with indicated amounts of LL-18, FF-18, DL-37, or LL-37 for 2 hrs before they were washed extensively to remove unbound peptides. Cells were then infected with the EV71 virus (MOI = 1) and cell viability was determined 24 h.p.i. Values were normalized to uninfected RD cells. ***, P1H NMR spectra of FF-18 peptide in the absence or presence of EV71 virus (green line) or CVB5 virus (red line). (TIF)</p
LL-18 did not induce virus resistance.
No full text(A) Diagram of resistance induction assay. (B) RD cells infected with parental EV71 or P30 with or without 1.5 μM LL-18 pre-incubation were tested for cell viability 24 h.p.i. ns, not significant; ***, P<0.001.</p
LL-18 and FF-18 effectively inhibit EV71 infection.
No full text(A-D) Cell viability of RD cells treated with the indicated amount of DL-37 (A), LL-37 (B), LL-18 (C), or FF-18 (D) was plotted against peptide concentration, and the cytotoxicity was determined. (E) EV71 virus pre-incubated with indicated amounts of DL-37, and the cell viability was determined 24 h.p.i. ***, P (TIF)</p
LL-18 stabilizes the viral particles by inhibiting uncoating.
No full text(A) EV71 virus (MOI = 10) was pre-incubated with PBS, indicated amount of LL-18 or NaCl for 1 hr and then mixed with SYBR green dyes II before they were heated to indicated temperatures. The fluorescent signals were measured and plotted against temperature. PBS was used as a negative control. (B) EV71 virus (MOI = 10) was pre-incubated with PBS, LL-18, or 12s for 2 hrs. Half of the samples were then treated with 1.5 μg SCARB2 protein and incubated at 37°C for 2 hrs at pH 5.5. Samples were then subjected to ultracentrifugation as detailed in materials and methods. The numbers above represent the fractions collected from top to bottom.</p
LL-18 and FF-18 inhibit viral attachment and internalization.
No full text(A) EV71 virus (MOI = 10) was pre-incubated with 3 μM LL-18 or FF-18 before they were used to incubate with RD cells at 4°C for 1 hr. Cells were then washed extensively and kept cultured for 24 hrs before viral VP1 expression was determined with immunoblotting. (B) EV71 virus (MOI = 10) was pre-incubated with 3 μM LL-18 or FF-18 before they were used to incubate with RD cells at 4°C for 1 hr followed by 37°C incubation for 1 hr. Cells were then washed extensively and kept cultured for 24 hrs before viral VP1 expression was determined with immunoblotting. (TIF)</p
LL-18 inhibits mEV71 infection <i>in vivo</i>.
No full text(A) 6-day-old ICR mice were infected with parental EV71 or mouse-adapted virus (mEV71) and the mice survival rate was determined. (B) RD cells infected with mEV71 pre-incubated with PBS or LL-18 for 1 hr were determined for virus titer 24 h.p.i. ***, P (TIF)</p
LL-18 and FF-18 inhibit viral attachment and internalization.
No full text(A) EV71 virus (MOI = 1) was pre-incubated with 1.5 μM LL-18, FF-18 or 12 μM 12s before they were used to incubate with RD cells at 4°C for 1 hr. Viral RNA was then determined with q-RT-PCR. Values are normalized to vehicle treated cells. ***, PRenilla luciferase reporter gene. (D) RD cells transfected with EV71 SGR RNA were treated with 1.5 μM LL-18 or FF-18 for 3 hrs (left panel) or 6 hrs (right panel) before luciferase activity was measured. ns, not significant.</p
- …
