Porcine epidemic diarrhoea virus (PEDV) infection causes watery diarrhoea, vomiting, anorexia, and weight loss, especially among neonatal piglets, inflicting on them morbidity and mortality potentially reaching 90%–100%. Despite it being known that certain mammalian cell phases are arrested by PEDV, the mechanisms have not been elucidated, and PEDV pathogenesis is poorly understood. This study determined the effect of an epidemic PEDV strain on cell cycle progression. We observed the effect of the PEDV SHpd/2012 strain on an infected Vero cell cycle through flow cytometry and Western blot, investigating the interrelationships of cell-cycle arrest, the DNA damage–signalling pathway caused by PEDV and the phosphorylation levels of the key molecules Chk.2 and H2A.X involved upstream and downstream in this pathway. PEDV induced Vero cell-cycle arrest at the G1/G0 phase. The phosphorylation levels of Chk.2 and H2A.X increased with the prolongation of PEDV infection, and no significant cell-cycle arrest was observed after treatment with ATM or Chk.2 inhibitors. The proliferation of PEDV was also inhibited by treatment with ATM or Chk.2 inhibitors. PEDV-induced cell-cycle arrest is associated with activation of DNA damage–signalling pathways. Our findings elucidate the molecular basis of PEDV replication and provide evidence to support further evaluation of PEDV pathogenesis.

This research illustrates the development of a new sliver nanoparticle (Ag-NPs) formulation. Its shape, size, solubility, and stability were characterized using Scanning Electron Microscope (SEM 3D), Transmission Electron Microscope (TEM 2D), Atomic Force Microscope (AFM), and Zeta size and Zeta potential. Exposure of Trichinella spiralis adult worms to 3, 6, 9 and 12 ppm of Ag-NPs each for 3,6,12 and 24 h. In vitro revealed a direct relation between mortalities and the tested drug concentration and exposure time. Anti- T. spiralis effect of Ag-NPs was evaluated by assessing mortality rate and damage in DNA by comet assay and by SEM analysis. Mean mortalities increased from 6.66% after exposure to 3.0 ppm/1 h to 100% after exposure to 12.0 ppm/12 h. The calculated LC50 was 3.0 ppm/10 h, 6 ppm/6 h, 9.0 ppm/4 h and 12.0 ppm/ 3.30 h, while LC100 was 9.0 ppm/24 h and 12.0 ppm/12 h. DNA genotoxic damage of dead worms was directly related to Ag-NPs concentrations for 12h using comet assay as expressed by variations in the percentage of DNA in the tail segment, tail length (μm), tail moment (μm), and olive tail moment. No significant difference (p ≤ .05) between the recorded mortalities and DNA damage between that obtained using the Ag-NPs LC100 and that recorded using Albendazole (50 mg/kg B.W.) for 12 h. SEM images on dead worms revealed clear morphological alteration, multiple vesicles, and blebs, detachment of the epidermis and the sub-epidermal layer with partial sloughing of the cuticle, and loss of normal creases, ridges, and annulations. These morphological alterations were directly related to the concentration of the tested Ag-NPs. The tested new formulation of Ag-NPs appears to be effective in the control of Trichinellosis as an alternative to other resistant drugs.