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

• Main Authors: Yali Han, Fang Li, Limei Xu, Feng Yang
• Format: Article
• Language: English
• Published: BMC 2017-12-01
• Series: Veterinary Research
• Online Access: http://link.springer.com/article/10.1186/s13567-017-0492-8

Abstract White spot syndrome virus (WSSV) is a major pathogen of penaeid shrimp. Here we identified a new WSSV strain, WSSV-CN04, from naturally infected Marsupenaeus 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. Since VP24 was previously reported to be essential for WSSV per os infection by mediating WSSV-chitin interaction, we further analyzed the peroral infection of WSSV-CN03 and -CN04 in Litopenaeus 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 WSSV per os infection.