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Replication and pathogenesis of white sturgeon iridovirus (WSIV) in experimentally infected white sturgeon Acipenser transmontanus juveniles and sturgeon cell lines.

Identifieur interne : 001829 ( Main/Merge ); précédent : 001828; suivant : 001830

Replication and pathogenesis of white sturgeon iridovirus (WSIV) in experimentally infected white sturgeon Acipenser transmontanus juveniles and sturgeon cell lines.

Auteurs : L R Watson [États-Unis] ; J M Groff ; R P Hedrick

Source :

RBID : pubmed:9676244

English descriptors

Abstract

Characteristics of the in vitro propagation of the white sturgeon iridovirus (WSIV) were examined in 6 sturgeon cell lines. One new cell line originating from gonadal tissues (WSGO) produced up to 12-fold more WSIV [approximately 22 TCID50 (50% tissue culture infective dose) cell-1], than that of a previously established reference spleen cell line (WSS-2). Infected WSGO cell cultures were examined using phase microscopy, viral infectivity assay and transmission electron microscopy (TEM). At 15 degrees C, both mature virions and infectious virus were first detected after 7 d post-infection. Capsids acquired envelopes in the cytoplasm and virions remained primarily cell-associated during the 35 d replication cycle. Cellular changes including hyper-refractility and cytoplasmic swelling with dense cytoplasmic inclusions correlated to extensive proliferation of cytoplasmic vesicles and viral assembly sites. These cytological characteristics corresponded to changes in target cells of WSIV-infected juvenile white sturgeon following bath challenge. Microscopic changes in stained tissue sections of the host epithelium were detected 4 d post-challenge, approximately 8 d prior to the onset of clinical signs. Hypertrophied Malpighian cells surrounded by a prominent pericellular cisternum characterized epithelial lesions in the skin. Similar changes to epithelial cells of the barbels, olfactory organs and esophagus were also observed. Destruction of the sensory epithelium is suggested as a cause for cessation of feeding which occurs early in the infection of white sturgeon juveniles with WSIV.

DOI: 10.3354/dao032173
PubMed: 9676244

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pubmed:9676244

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<name sortKey="Watson, L R" sort="Watson, L R" uniqKey="Watson L" first="L R" last="Watson">L R Watson</name>
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<nlm:affiliation>Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis 95616, USA.</nlm:affiliation>
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<name sortKey="Groff, J M" sort="Groff, J M" uniqKey="Groff J" first="J M" last="Groff">J M Groff</name>
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<term>DNA Virus Infections (virology)</term>
<term>Esophagus (pathology)</term>
<term>Esophagus (virology)</term>
<term>Fish Diseases (virology)</term>
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<term>Sense Organs (virology)</term>
<term>Skin (pathology)</term>
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<term>Virus Replication</term>
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<term>Esophagus</term>
<term>Gills</term>
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<div type="abstract" xml:lang="en">Characteristics of the in vitro propagation of the white sturgeon iridovirus (WSIV) were examined in 6 sturgeon cell lines. One new cell line originating from gonadal tissues (WSGO) produced up to 12-fold more WSIV [approximately 22 TCID50 (50% tissue culture infective dose) cell-1], than that of a previously established reference spleen cell line (WSS-2). Infected WSGO cell cultures were examined using phase microscopy, viral infectivity assay and transmission electron microscopy (TEM). At 15 degrees C, both mature virions and infectious virus were first detected after 7 d post-infection. Capsids acquired envelopes in the cytoplasm and virions remained primarily cell-associated during the 35 d replication cycle. Cellular changes including hyper-refractility and cytoplasmic swelling with dense cytoplasmic inclusions correlated to extensive proliferation of cytoplasmic vesicles and viral assembly sites. These cytological characteristics corresponded to changes in target cells of WSIV-infected juvenile white sturgeon following bath challenge. Microscopic changes in stained tissue sections of the host epithelium were detected 4 d post-challenge, approximately 8 d prior to the onset of clinical signs. Hypertrophied Malpighian cells surrounded by a prominent pericellular cisternum characterized epithelial lesions in the skin. Similar changes to epithelial cells of the barbels, olfactory organs and esophagus were also observed. Destruction of the sensory epithelium is suggested as a cause for cessation of feeding which occurs early in the infection of white sturgeon juveniles with WSIV.</div>
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