Korean J Vet Res.
2013 Mar;53(1):11-17.
Sequential hepatic ultrastructural changes and apoptosis in rabbits experimentally infected with Korean strain of rabbit hemorrhagic disease virus (RHDVa)
- Affiliations
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- 1Animal, Plant and Fisheries Quarantine and Inspection Agency, Anyang 430-757, Korea.
- 2Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul 120-749, Korea.
- 3Department of Animal Science, College of Life Science and Natural Resources, Sangji University, Wonju 220-702, Korea.
- 4College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju 690-756, Korea.
- 5College of Veterinary Medicine, Konkuk University, Seoul 143-701, Korea.
- 6Department of Clinical Laboratory Science, Semyung University, Jecheon 390-711, Korea. ghwoo@naver.com
Abstract
- 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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