Sequential hepatic ultrastructural changes and apoptosis in rabbits experimentally infected with Korean strain of rabbit hemorrhagic disease virus (RHDVa)
2013
Park, J.W., Plant and Fisheries Quarantine and Inspection Agency, Anyang, Republic of Korea | Chun, J.E., Plant and Fisheries Quarantine and Inspection Agency, Anyang, Republic of Korea | Bak, E.J., Yonsei University, Seoul, Republic of Korea | Kim, H., Plant and Fisheries Quarantine and Inspection Agency, Anyang, Republic of Korea | Lee, M.H., Plant and Fisheries Quarantine and Inspection Agency, Anyang, Republic of Korea | Hwang, E.K., Sangji University, Wonju, Republic of Korea | Kim, J.H., Jeju National University, Jeju, Republic of Korea | Lee, C.B., Konkuk University, Seoul, Republic of Korea | Woo, G.H., Semyung University, Jecheon, Republic of Korea
In this study, to understand the pathogenesis of new rabbit hemorrhagic disease virus (RHDVa) serotype, we carried out to administrate RHDVa to rabbits, and to examine sequential electron microscopic changes and relationship between pathogenesis and apoptosis. TUNEL-positive cells began to be observed from 24 hours after inoculation (HAI) and the number of positive cells was slightly increased with the course of time. Whereas marked increase of positive cells was seen in the liver from the rabbits died acutely. Typical viral particles with cup-like projections and a diameter of 30~40 nm were detected in homogenized liver samples and tissues at 36 and 48, and 48 HAI, respectively. Ultrastructurally, glycogen deposition was observed from the first stage of hepatocellular degeneration by RHDVa infection and then, swelling and disruption of cristae of mitochondria by viral particles, swelling of smooth endoplasmic reticulum, vacuoles and vesicles were detected. Condensation, margination and fragmentation of chromatin were observed in degenerative hepatocytes at 36 and 48 HAI, indicating apoptotic bodies. These data offer that hepatocytic apoptosis by RHDV infection could be closely related with mitochondrial impairment in the hepatocytes.
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