Journal of Virology, May 2001, p. 4068-4079, Vol. 75, No. 9
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.9.4068-4079.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Howard Hughes Medical Institute1 and Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, Illinois 60208-3500,2 and Children's Research Institute, Children's Hospital, and Division of Pathology, Department of Pediatrics, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 432053
Received 7 November 2000/Accepted 5 February 2001
In some cell types the paramyxovirus simian virus 5 (SV5) causes
little cytopathic effect (CPE) and infection continues productively for
long periods of time; e.g., SV5 can be produced from MDBK cells for up
to 40 days with little CPE. SV5 differs from most paramyxoviruses in
that it encodes a small (44-amino-acid) hydrophobic integral membrane
protein (SH). When MDBK cells were infected with a recombinant SV5
containing a deletion of the SH gene (rSV5
SH), the MDBK cells
exhibited an increase in CPE compared to cells infected with wild-type
SV5 (recovered from cDNA; rSV5). The increased CPE correlated with an
increase in apoptosis in rSV5
SH-infected cells over mock-infected
and rSV5-infected cells when assayed for annexin V binding, DNA content
(propidium iodide staining), and DNA fragmentation (terminal
deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling
assay). In rSV5
SH-infected MDBK cells an increase in caspase-2 and
caspase-3 activities was observed. By using peptide inhibitors of
individual caspases it was found that caspase-2 and caspase-3 were
activated separately in rSV5
SH-infected cells. Expression of
caspase-2 and -3 in rSV5
SH-infected MDBK cells appeared not to
require STAT1 protein, as STAT1 protein could not be detected in
SV5-infected MDBK cells. When mutant mice homologous for a targeted
disruption of STAT1 were used as a model animal system
and infected with the viruses it was found that rSV5
SH caused less
mortality than wild-type rSV5, consistent with the notion of clearance
of apoptotic cells in a host species.
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