RK-13

Characterization and Pathogenicity of Equine Herpesvirus Type 8 Using Rabbit Kidney (RK-13) Cells

Equine herpesvirus type 8 (EHV-8) is predominantly isolated from donkeys, but its biological properties and pathogenic potential remain underexplored. Ji’s team investigated the biological characteristics and pathogenicity of the EHV-8 LCDC01 isolate by examining its effects in rabbit kidney (RK-13) cells and BALB/c mice.

Figure 1 shows the infection of EHV-8 and the effect of EHV-8 on RK-13 cells. Figure 1A shows the results of immunofluorescence. EHV-8-specific fluorescence was abundant in the infected cells (Fig. 1(Ab)), and the control group had no signal (Fig. 1(Aa)). These results showed that EHV-8 could efficiently infect and replicate in RK-13 cells. Figure 1B shows apoptosis after infection. The number of green fluorescence (white arrows) positive cells in the early apoptosis group in the infected group (Fig. 1(Bc)) was significantly increased compared to the control group (Fig. 1(Ba)). The number of red fluorescence (yellow arrows) positive cells in the late apoptosis/necrosis group in the infected group (Fig. 1 (Bd)) was significantly increased compared to the control group (Fig. 1(Bb)). These data showed that EHV-8 infection could effectively induce apoptosis of RK-13 cells.

Inactivation of Equine Arteritis Virus by Indolicidin Peptide

Equine viral arteritis is an economically important contagious disease caused by equine arteritis virus (EAV). Metz et al. evaluated the antiviral activity of indolicidin and K-indolicidin peptides against EAV.

Cytotoxicity of Indolicidin and K-indolicidin was first screened on EAV-susceptible RK-13 and Vero CCL-81 cells. Within 24 h, 50 µM detached all cells; 25 and 12 µM were severely toxic, whereas 6 µM only altered morphology without loss of viability (confirmed by Trypan Blue; Fig. 2a). No effect was seen at 3 µM. Therefore, 5 µM (sub-toxic) was selected for antiviral tests. At this concentration, Indolicidin completely prevented EAV CPE and plaque formation in RK-13 cells at MOI = 1, indicating full inhibition of replication. K-indolicidin lacked activity, presumably because the extra N-terminal lysine changes net charge and target interaction. Antiviral efficacy of Indolicidin remained consistent in Vero cells but declined as viral inoculum increased (Fig. 3).