Fig. 2

MAP2K7 exhibits antiviral effects both in vivo and in vitro. (A) Survival (Kaplan-Meier Curve) of wide-type (WT) and map2k7+/? zebrafish (n = 10 per group) at various days after injected i.p. with SVCV (5 × 108 TCID50/mL, 5 ?L/individual). (B to D) qPCR analysis of SVCV p, n, g, and l mRNA in the spleen, liver, and kidney of WT and map2k7+/? zebrafish (n = 5 per group) given an injection i.p. of SVCV (5 × 108 TCID50/mL, 5 ?L/individual) for 48 h. Each dot point represents one independent biological replicate. (E to H) Microscopy of H&E-stained heart (E), liver (F), spleen (G), and kidney (H) sections from WT and map2k7+/? zebrafish treated with SVCV (5 × 108 TCID50/mL, 5 ?L/individual) for 72 h. (I and J) EPC cells were transfected with 250 ng of MAP2K7-Myc or empty vector. At 24 hours posttreatment (hpt), cells were infected with SVCV (MOI, 1) for 48 h. Then, cells were fixed with 4% PFA and stained with 1% crystal violet (I). Culture supernatants from the cells infected with SVCV were collected, and the viral titer was measured according to the method of Reed and Muench (J). (K and M) EPC cells were transfected with 2 ?g MAP2K7-Myc(sh-MAP2K7) or empty vector. At 24 hpt, cells were infected with SVCV (MOI, 1). After 24 h of infection, total RNA was extracted to examine the mRNA levels of cellular p, n, g, l, and m. (L) EPC cells were transfected with 2 ?g sh-MAP2K7 or empty vector. At 24 hpt, cells were infected with SVCV (MOI, 1). After 24 h of infection, total RNA was extracted to examine the mRNA levels of cellular map2k7. The relative mRNA levels were normalized to the transcription of ?-actin and represented as fold induction relative to the mRNA level in control cells, which was set to 1. Data were expressed as mean ± SEM (n = 3). *, P < 0.05 (compared with the control group).