Preliminary Study On The Function Of Non-structural Proteins P16,P23in Rabbit Hemorrhagic Disease Virus(RHDV)

The rabbit hemorrhagic disease is one of the highly contagious and pathogenic Rabbit illness. This disease mortality rate is up to100%, and it is caused by the rabbit hemorrhagic disease virus. After infecting with the virus, the main symptoms are respiratory bleeding, liver necrosis, edema, congestion and hemorrhage of organs and other symptoms. The disease was reported in China in1984for the first time, and then spread to Europe, Africa, Australia, New Zealand and the United States through the animal husbandry business. Infection of breeding rabbits and hares can lead to its death, these have not only caused huge economic losses, but also posed a significant and huge threat to the survival rabbits. Thus the rabbit hemorrhagic disease virus has gotten widespread attention.The rabbit hemorrhagic disease virus belongs to the genus Lagovirus, family Calciviridae. It contains a single-stranded and positive-sense RNA genome which is7.4kb long. The virions have no capsule membrane structure, and the capsid is20sides symmetrical structure and consisting of VP60. At present, the study on fuction of the2c-like protease, Vpg,3c-like protease, RdRp, VP60, and VP2proteins has made some progress.After the rabbits infected with the rabbit hemorrhagic disease virus, it showed significantly apoptosis phenomenon in liver and kidney. This phenomenon demonstrated that the RHDV could induce apoptosis. Some researches presented that the deletion of the VP2could weaken the effects of apoptosis induced by RHDV. This indicate that the VP2is not the main cause of apotosis. We can conduct a preliminary speculation that the main reason of apoptosis is possibly resulted of another protein, the interaction of several proteins, or the reproduction process of RHDV.This research is studying on the localization of non-structral protiens p16and p23, and the connection with the apoptosis induced by RHDV in RK13via building eukaryotic vector. The experiment results display:p16is located in the nuclear of RK13, and its expression can result in the disruption and death of RK13. The studying of this phenomenon by the laboratory techniques of DNA Ladder, caspase activity assay, and Flow Cytometry etc, the consequences indicate that the pathway of the death in RK13induced by p16is non-apoptosis and independent of caspases. And this indicates that the apoptosis induced by RHDV has no direct connection to the death caused by p16protien which may be connected with the result that the existence of the p16protein can lead to the stagnation of the cell cycle in S phase. In addition, the research on Hela, one cell line which is sensitive to apoptosis, indicates p16can induce the very obvious pathological changes in Hela, and eventually death. But the result of caspase activity assay shows:the death is also irrelevant with apoptosis.Meanwhile, the study results of another important non-strucral protein p23display, p23is located in the plasma of RK13, and its expression has no obvious effect on RK13. These consquences indicate the protien p23is irrelevant with the apoptosis induced by RHDV.