Taura syndrome virus loads in Litopenaeus vannamei hemolymph following infection are related to differential mortality

被引:8
作者
Cao, Zhiming [1 ]
Wang, Shiao Y. [1 ]
Breeland, Verlee [2 ]
Moore, Anne-Marie [2 ]
Lotz, Jeffrey M. [2 ]
机构
[1] Univ So Mississippi, Dept Biol Sci, Hattiesburg, MS 39406 USA
[2] Univ So Mississippi, Gulf Coast Res Lab, Dept Coastal Sci, Ocean Springs, MS 39566 USA
基金
美国农业部;
关键词
Taura syndrome virus; Litopenaeus vannamei; Shrimp; Virus; SHRIMP PENAEUS-VANNAMEI; TSV; RESISTANCE; OUTBREAKS; TAIWAN; MODEL;
D O I
10.3354/dao02258
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
Taura syndrome is an economically important disease that can cause catastrophic losses of farmed shrimp. Without effective treatments for Taura syndrome virus (TSV), one approach to managing the problem is to selectively breed shrimp populations with increased disease resistance. To better understand why some shrimp can survive exposure to TSV, information is needed on how viral loads progress and persist following infection. Data reported here show that mortalities occurring mostly within 1 wk of infection are associated with high viral titers, and titers as high as 10(8.7) genome copies per mu l hemolymph can persist for up to 3 wk in survivors. Thereafter, and up to similar to 9 wk post-exposure, most surviving shrimp remain chronically infected with TSV loads ranging from 10(4) to 10(8) genome copies per mu l hemolymph. Challenging shrimp from families with varying TSV resistance showed that in shrimp from less resistant families, the TSV load in hemolymph increased earlier and reached higher peaks than in shrimp from more resistant families. Although TSV loads in moribund shrimp from families differing in resistance did not differ significantly, infection loads among survivors were lower in shrimp from more resistant families. Taken together, the data suggest that lethal infection loads can occur in both more and less susceptible shrimp and that survivors represent shrimp in which viral expansion is better contained.
引用
收藏
页码:97 / 103
页数:7
相关论文
共 22 条
[1]   Selective breeding of Pacific white shrimp (Litopenaeus vannamei) for growth and resistance to Taura Syndrome Virus [J].
Argue, BJ ;
Arce, SM ;
Lotz, JM ;
Moss, SM .
AQUACULTURE, 2002, 204 (3-4) :447-460
[2]   Taura syndrome of marine penaeid shrimp: Characterization of the viral agent [J].
Bonami, JR ;
Hasson, KW ;
Mari, J ;
Poulos, BT ;
Lightner, DV .
JOURNAL OF GENERAL VIROLOGY, 1997, 78 :313-319
[3]  
Brock JA, 1995, SWIMMING THROUGH TROUBLED WATER, P84
[4]   Update on viral accommodation, a model for host-viral interaction in shrimp and other arthropods [J].
Flegel, T. W. .
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY, 2007, 31 (03) :217-231
[5]   Taura syndrome virus (TSV) lesion development and the disease cycle in the Pacific white shrimp Penaeus vannamei [J].
Hasson, KW ;
Lightner, DV ;
Mohney, LL ;
Redman, RM ;
Poulos, BT ;
White, BM .
DISEASES OF AQUATIC ORGANISMS, 1999, 36 (02) :81-93
[6]   TAURA SYNDROME IN PENAEUS-VANNAMEI - DEMONSTRATION OF A VIRAL ETIOLOGY [J].
HASSON, KW ;
LIGHTNER, DV ;
POULOS, BT ;
REDMAN, RM ;
WHITE, BL ;
BROCK, JA ;
BONAMI, JR .
DISEASES OF AQUATIC ORGANISMS, 1995, 23 (02) :115-126
[7]   The geographic distribution of Taura Syndrome Virus (TSV) in the Americas: determination by histopathology and in situ hybridization using TSV-specific cDNA probes [J].
Hasson, KW ;
Lightner, DV ;
Mari, J ;
Bonami, JR ;
Poulos, BT ;
Mohney, LL ;
Redman, RM ;
Brock, JA .
AQUACULTURE, 1999, 171 (1-2) :13-26
[8]   Role of lymphoid organ spheroids in chronic Taura syndrome virus (TSV) infections in Penaeus vannamei [J].
Hasson, KW ;
Lightner, DV ;
Mohney, LL ;
Redman, RM ;
White, BM .
DISEASES OF AQUATIC ORGANISMS, 1999, 38 (02) :93-105
[9]  
Jimenez R, 1992, Aquacultura del Ecuador, P1
[10]   Picornavirales, a proposed order of positive-sense single-stranded RNA viruses with a pseudo-T=3 virion architecture [J].
Le Gall, Olivier ;
Christian, Peter ;
Fauquet, Claude M. ;
King, Andrew M. Q. ;
Knowles, Nick J. ;
Nakashima, Nobuhiko ;
Stanway, Glyn ;
Gorbalenya, Alexander E. .
ARCHIVES OF VIROLOGY, 2008, 153 (04) :715-727