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

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

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Abstract White spot syndrome virus (WSSV) is a major pathogen of penaeid shrimp.Here we identified a new WSSV johnny cash style clothing 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 bostik universal primer pro 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.