The effect of water temperature on the pathogenicity of decapod iridescent virus 1 (DIV1) in Litopenaeus vannamei

Abstract

Decapod iridescent virus 1 (DIV1) has caused huge losses to the shrimp breeding industry in recent years as a new shrimp virus. In this study, white leg shrimp, Litopenaeus vannamei, were cultured at different temperatures (26 ± 1 °C and 32 ± 1 °C) and the same salinity, then infected with DIV1 by intramuscular injection to determine the effects of water temperature on viral infection. The DIV1 copy counts in the gills, hepatopancreas, pleopods, intestines, and muscles of L. vannamei were measured in samples collected at 6, 12, and 24 h post-infection (hpi), and the survival rate of L. vannamei was assessed every 6 h after infection. At 96 hpi, the survival rates of L. vannamei in the high (32 ± 1 ℃) and standard (26 ± 1 ℃) water temperature groups were 2.22% and 4.44%, respectively. The peak time of mortality in the high-water temperature group was 6 h earlier than in the standard water temperature group. After 24 hours of DIV1 infection, the DIV1 copy counts in the standard water temperature treatment group were significantly higher than those in the high-water temperature treatment group. The tissues with the highest virus copy counts in the standard and high-temperature groups were the intestines (2.9×1011 copies/g) and muscles (7.0×108 copies/g). The effect of temperature on the pathogenicity of DIV1 differs from that of other previously studied viruses, such as white spot syndrome virus, Taura syndrome virus, and infectious hypodermal and hematopoietic necrosis virus, because the high-water temperature did not mitigate the damage caused by DIV1 infection.