A VP24-truncated isolate of white spot syndrome virus is inefficient in per os infection

AbstractWhite spot syndrome virus (WSSV) is a major pathogen of penaeid shrimp. Here we identified a new WSSV strain, WSSV-CN04, from naturally infectedMarsupenaeus japonicus. Whole genomic sequencing results indicate that the WSSV-CN04 genome was 281  054 bp in length, and encoded 157 hypothetic proteins. The genome sequence of WSSV-CN04 was most closely related to the low-virulent strain WSSV-CN03, sharing 97.5% sequence identity. Notably, in WSSV-CN04, the major envelop protein VP24 was not only truncated but also absent in the virions. Sinc e VP24 was previously reported to be essential for WSSVper os infection by mediating WSSV-chitin interaction, we further analyzed the peroral infection of WSSV-CN03 and -CN04 inLitopenaeus vannamei, and show that the infectivity of WSSV-CN04 was significantly lower than that of WSSV-CN03. When compared with WSSV-CN03-infected shrimp, fewer virions were detected in the digestive tract tissues of WSSV-CN04-infected shrimp at 4 hours post-infection (hpi), and the viral titers in the animals at 24 hpi were much lower. Moreover, a peptide corresponding to VP24 chitin-binding domain reduced the amount of WSSV-CN03 in the midgut to a level similar to that of WSSV-CN04 at 4 hpi. These findings indicate that the truncation of VP24 may attenuate the peroral infectivity of WSSV-CN04, and therefore verify the important role of VP24 in WSSVper os infection.
Source: Veterinary Research - Category: Veterinary Research Source Type: research