DAO 38:93-105 (1999) - doi:10.3354/dao038093
Role of lymphoid organ spheroids in chronic Taura syndrome virus (TSV) infections in Penaeus vannamei
Kenneth W. Hasson1,*, Donald V. Lightner2, Leone L. Mohney2, Rita M. Redman2, Brenda M. White2
ABSTRACT: Lesion development was documented in Penaeus vannamei juveniles with experimentally induced, chronic phase Taura syndrome virus (TSV) infections, by both routine histology and in situ hybridization, during a 48 wk time course study. Histologically, the defining characteristics of TSV chronicity in P. vannamei include the absence of acute phase histological lesions, a low prevalence of ectopic spheroid development, and rapid successive lymphoid organ spheroid (LOS) formation and morphogenesis. Three distinct LOS morphotypes (Types A, B, and C) were identified by light microscopy. The earliest detectable LOS, Type A, appeared to evolve from activated LO tubule phagocytes that had sequestered TSV. The succeeding LOS, Type B, contained necrotic cells that were consistently TSV-positive by in situ hybridization for up to 32 wk following an acute phase infection. These persistent, long-term infections suggested that TSV replication occurred within Type B LOS, and this satisfied the definition of a chronic infection. The terminal Type C LOS were consistently found to be TSV-negative and characterized by cells with condensed basophilic nuclei, a reduction in overall cell size, and progressive atrophy leading to degradation without an inflammatory response. These cellular changes are characteristic of apoptotic cells, suggesting that TSV-infected LOS cells self-destruct, resulting in TSV elimination. TSV infections appear to have 3 potential outcomes: (1) the virus may continue to replicate within LOS cells unchecked, (2) it may be eliminated by LOS cells, or (3) viral replication and elimination may occur concurrently, resulting in persistent infections. Ectopic spheroids were TSV-induced and observed in sites normally occupied by tegmental glands within appendages, suggesting that they developed from either hemolymph-borne phagocytes or fixed phagocytes associated with the gland. We suggest that these cellular masses arise from migrating and/or resident phagocytes transformed in response to chronic viral infections or non-self substances too small for hemocyte encapsulation. The possibility that spheroid development represents an unexplored and significant branch of the cell-mediated immune response of penaeid shrimp is discussed.
KEY WORDS: Taura syndrome virus (TSV) · Penaeid shrimp · Lymphoid organ · In situ hybridization · Apoptosis · Picornaviridae · Immune response
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