Simple method for rapid and highly sensitive detection of antiviral-antibodies in serum and cerebrospinal fluid of small laboratory animals

Sigmund, Martin; Einberger, Helmut; Neubert, Wolfgang J.

doi:10.1016/0166-0934(88)90105-x

Cited by 6 publications

(4 citation statements)

References 8 publications

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“…Virus and Cells-Sendai virus (strain Fushimi) and for immunofluorescence studies a recombinant SeV coding for the reporter protein "green fluorescent protein" by an insertion between the two viral genes for P and M in the wild-type genome were grown in 9-day-old embryonated chicken eggs as described previously (29,30). CV-1 cells (African green monkey kidney cells) were obtained from the American Type Culture Collection (ATCC, Manassas, VA), and MCF7 cells (human breast carcinoma) from the European Collection of Animal Cell Cultures (ETACC, Salisbury, United Kingdom).…”

Section: Methodsmentioning

confidence: 99%

Caspase-8 and Apaf-1-independent Caspase-9 Activation in Sendai Virus-infected Cells

Bitzer¹,

Armeanu²,

Prinz³

et al. 2002

Journal of Biological Chemistry

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Apoptotic cell death is of central importance in the pathogenesis of viral infections. Activation of a cascade of cysteine proteases, i.e. caspases, plays a key role in the effector phase of virus-induced apoptosis. However, little is known about pathways leading to the activation of initiator caspases in virus-infected host cells. Recently, we have shown that Sendai virus (SeV) infection triggers apoptotic cell death by activation of the effector caspase-3 and initiator caspase-8. We now investigated mechanisms leading to the activation of another initiator caspase, caspase-9. Unexpectedly we found that caspase-9 cleavage is not dependent on the presence of active caspases-3 or -8. Furthermore, the presence of caspase-9 in mouse embryonic fibroblast (MEF) cells was a prerequisite for Sendai virus-induced apoptotic cell death. Caspase-9 activation occurred without the release of cytochrome c from mitochondria and was not dependent on the presence of Apaf-1 or reactive oxygen intermediates. Our results therefore suggest an alternative mechanism for caspase-9 activation in virally infected cells beside the well characterized pathways via death receptors or mitochondrial cytochrome c release.

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Section: Methodsmentioning

confidence: 99%

Caspase-8 and Apaf-1-independent Caspase-9 Activation in Sendai Virus-infected Cells

Bitzer¹,

Armeanu²,

Prinz³

et al. 2002

Journal of Biological Chemistry

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“…Virus and cells. SV (strain Fushimi) was grown in 9-day-old embryonated chicken eggs as described previously (43). CV-1 (African green monkey kidney) cells were obtained from the American Type Culture Collection (Rockville, Md.…”

Section: Methodsmentioning

confidence: 99%

Sendai Virus Infection Induces Apoptosis through Activation of Caspase-8 (FLICE) and Caspase-3 (CPP32)

Bitzer

Prinz

Bauer

et al. 1999

J Virol

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Sendai virus (SV) infection and replication lead to a strong cytopathic effect with subsequent death of host cells. We now show that SV infection triggers an apoptotic program in target cells. Incubation of infected cells with the peptide inhibitor z-VAD-fmk abrogated SV-induced apoptosis, indicating that proteases of the caspase family were involved. Moreover, proteolytic activation of two distinct caspases, CPP32/caspase-3 and, as shown for the first time in virus-infected cells, FLICE/caspase-8, could be detected. So far, activation of FLICE/caspase-8 has been described in apoptosis triggered by death receptors, including CD95 and tumor necrosis factor (TNF)-R1. In contrast, we could show that SV-induced apoptosis did not require TNF or CD95 ligand. We further found that apoptosis of infected cells did not influence the maturation and budding of SV progeny. In conclusion, SV-induced cell injury is mediated by CD95- and TNF-R1-independent activation of caspases, leading to the death of host cells without impairment of the viral life cycle.

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“…A recombinant SeV coding for the reporter gene gfp by an insertion between the leader sequence and the start of the viral n gene in the wild-type genome was grown in 9-day-old embryonated chicken eggs as described previously (23,24). The generation and amplification of single gene-deleted SeV particles SeV-⌬M-GFP, SeV-⌬F-GFP, and SeV-⌬HN-GFP was performed as described recently (25).…”

Section: Virus Recovery and Propagationmentioning

confidence: 99%

Severe Impairment of Dendritic Cell Allostimulatory Activity by Sendai Virus Vectors Is Overcome by Matrix Protein Gene Deletion

Armeanu¹,

Bitzer²,

Smirnow³

et al. 2005

The Journal of Immunology

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Delivery of Ags to dendritic cells (DCs) plays a pivotal role in the induction of efficient immune responses ranging from immunity to tolerance. The observation that certain viral pathogens are able to infect DCs has led to a concept in which applications of recombinant viruses are used for Ag delivery with the potential benefit of inducing potent Ag-specific T cell responses directed against multiple epitopes. As a prerequisite for such an application, the infection of DCs by recombinant viruses should not interfere with their stimulatory capacity. In this context, we could show that an emerging negative-strand RNA viral vector system based on the Sendai virus (SeV) is able to efficiently infect monocyte-derived human DCs (moDCs). However, after infection with SeV wild type, both the response of DCs to bacterial LPS as a powerful mediator of DC maturation and the allostimulatory activity were severely impaired. Interestingly, using various recombinant SeV vectors that were devoid of single viral genes, we were able to identify the SeV matrix (M) protein as a key component in moDC functional impairment after viral infection. Consequently, use of M-deficient SeV vectors preserved the allostimulatory activity in infected moDCs despite an efficient expression of all other virally encoded genes, thereby identifying M-deficient vectors as a highly potent tool for the genetic manipulation of DCs.

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Simple method for rapid and highly sensitive detection of antiviral-antibodies in serum and cerebrospinal fluid of small laboratory animals

Cited by 6 publications

References 8 publications

Caspase-8 and Apaf-1-independent Caspase-9 Activation in Sendai Virus-infected Cells

Caspase-8 and Apaf-1-independent Caspase-9 Activation in Sendai Virus-infected Cells

Sendai Virus Infection Induces Apoptosis through Activation of Caspase-8 (FLICE) and Caspase-3 (CPP32)

Severe Impairment of Dendritic Cell Allostimulatory Activity by Sendai Virus Vectors Is Overcome by Matrix Protein Gene Deletion

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