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Abstract

Grouper iridovirus of Taiwan (TGIV) is one of the most devastating infectious pathogens of grouper fry in Taiwan. As environmental temperature often plays an important role in the outbreak of diseases, we assayed the impact of different temperatures (18, 25 and 32℃) on TGIV infection both in vitro and in vivo. Cytopathic effect (CPE) characterized as cell rounding and lysis were observed in TGIV-infected grouper SB (swim bladder) cells at 25℃ and 32℃, but was absent at 18℃. With temperature rising to 32℃, the presence of pycnotic nuclei and chromatin margination became prominent in the infected cells, indicating an apoptotic death. The morphological feature of apoptotic cell was further supported by the observation under electron microscope. In addition, the apoptosis of TGIV-infected cells promoted by hyperthermia (32℃) was confirmed by the assays of DNA laddering, DNA content and annexin V staining. To measure the temperature impact on the defense in TGIV-infected host, grouper fry was experimentally infected with the virus at 25℃ and 32℃, respectively. Cumulative mortalities reached 100% in the fish held at 25℃ on day 10 post-infection, whereas only 37.5% at 32℃ at 2-week post-infection. In addition, the mortality in the infected fish of the 32-to-25℃ group skyrocketed to 97.5% by day 8. All together, the data suggest different impacts of temperatures on the pathogenicity of TGIV in grouper: while the lower temperature (18℃) adversely affects the propagation of TGIV, the hyperthermic temperature (32℃) promotes apoptosis to prevent the spreading of virus, resulting in higher resistance of the host against the virus.

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