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Journal of Virology, August 2000, p. 7619-7627, Vol. 74, No. 16
Department of Microbiology and Center for
Salmon Disease Research, Oregon State University, Corvallis, Oregon
97331-3804
Received 6 January 2000/Accepted 24 April 2000
Infectious hematopoietic necrosis virus (IHNV) infection in tissue
culture cells has previously been shown to result in the shutdown of
host protein synthesis, cell rounding, and cell death. We report here
an investigation of the cytopathogenicity of the viral phosphoprotein
(P or M1), matrix (M or M2), and nonvirion (NV) proteins in cultured
fish cells. The expression of M alone potently inhibited reporter gene
expression from a viral and an interferon (IFN)-inducible promoter,
whereas P and NV did not produce a similar effect. Northern blot
analysis further revealed a reduction in the steady-state level of
reporter mRNA when the M gene was cotransfected into cells; conversely,
M mRNA was not drastically reduced in the same cells. By
immunofluorescence confocal microscopy, fragmented nuclei were found in
some cells expressing M protein but not in cells expressing P, NV, or
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Infectious Hematopoietic Necrosis Virus Matrix
Protein Inhibits Host-Directed Gene Expression and Induces
Morphological Changes of Apoptosis in Cell Cultures

-galactosidase protein. Electron microscopy revealed the
morphological changes associated with apoptosis in the M-transfected
cells. Furthermore, IHNV infection was shown to produce DNA
"laddering" in cultured cells. Taken together, these data suggested
at least two functions for M protein in an IHNV infection: down
regulation of host transcription and the induction of programmed cell
death. In the course of these experiments, we also discovered that NV
expression was associated with cell rounding, the first biological
effect on cells to be attributed to the NV gene.
*
Corresponding author. Mailing address: Department of
Microbiology, North Hall 220, Oregon State University, Corvallis, OR 97331-3804. Phone: (541) 737-1834. Fax: (541) 737-0496. E-mail: leongj{at}orst.edu.
Oregon Agricultural Experiment Station technical paper 11,687.
Present address: Biotechnology Center, University of Connecticut,
Storrs, CT 06269-3149.
§
Present address: Department of Biochemistry, Microbiology, and
Molecular Biology, University of Maine, Orono, ME 04469.
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