Abstract
White Spot Syndrome Virus (WSSV) infects several economically important aquacultural species, causing significant losses to the industry. This virus belongs to the Nimaviridae family, and has a dsDNA genome ranging from 257 to 309 kb (more than 20 isolate genomes fully sequenced and published to date). Multiple routes of infection could be the cause of the high virulence and mortality rates detected in shrimp species. In particular, Penaeus vannamei, differences in isolate virulence have been observed, along with controversy over whether deletions or insertions are associated with gain or loss of virulence.The pathogenicity of three isolates from three locations in Mexico (two from Sinaloa: 'CIAD', and 'Angostura', and one from Sonora: 'Sonora') was evaluated in vivo in white shrimp (P. vannamei) infection assays. Differences were observed in the mortality rate of shrimp among the three isolates, with the Sonora isolate being the most virulent. Subsequently, the complete WSSV genomes were sequenced in depth from the tissues of infected shrimp, and assembled in reference to the genome of isolate CN01 (KT995472), identifying genome sizes for Angostura and Sonora of 289,350 bp and 288,995 bp, respectively. Where three deletion zones were identified compared to CN01 comprising 15 genes, including three envelope proteins VP41A, VP52A and VP41B, one non-structural protein ICP35 and 11 others encoding proteins whose function is currently unknown. In addition, five genes (wsv129, wsv178, wsv204, wsv249 and wsv497) show a modified number of repeat motifs. The main implications and possible effects on viral infection of these modifications are discussed.
Efficacy of double-stranded RNA against white spot syndrome virus (WSSV) non-structural (orf89, wsv191) and structural (vp28, vp26) genes in the Pacific white shrimp Litopenaeus vannamei
