Deletion of 55 open reading frames from the termini of vaccinia virus

Perkus, Marion E.; Goebel, Scott J.; Davis, Stephen W.; Johnson, Gerard P.; Norton, Elizabeth; Paoletti, Enzo

doi:10.1016/0042-6822(91)90047-f

Cited by 98 publications

(65 citation statements)

References 22 publications

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“…A virus deletion mutant (vKL4) lacking the majority of the K2L ORF was produced. The construetion of this virus demonstrated that K2L is non-essential for vaccinia virus (strain WR) replication in vitro (seven different cell lines were tested), and is consistent with the data of Perkus et aL (1986Perkus et aL ( , 1989Perkus et aL ( , 1991 which show this region of the genome to be non-essential in both the WR and Copenhagen strains of vaccinia virus.…”

Section: Discussionsupporting

confidence: 76%

“…Hybridization with the deleted fragment failed to detect either the wildtype 4.5 kb or the mutant 3.8 kb fragment, thus confirming the absence of these sequences from the deletion mutant (data not shown). In agreement with the previous findings that the K2L O R F is non-essential for the in vitro replication of the W R (Perkus et al, 1986(Perkus et al, , 1989 and Copenhagen (Perkus et al, 1991) strains of vaccinia virus, vKL4 was able to replicate in each of the seven cell lines tested (CV-1, BS-C-1, TK-143, BHK-21, RK13, D980R and Vero).…”

Section: Construction Of a Deletion Mutant Lacking The K2l Genesupporting

confidence: 79%

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A vaccinia serine protease inhibitor which prevents virus-induced cell fusion

Law

Smith

1992

Journal of General Virology

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A deletion mutant lacking the non-essential vaccinia virus gene K2L, a member of the serine protease inhibitor superfamily, was constructed. This virus replicates in vitro in all cell types tested and its virulence and immunogenicity in vivo are comparable to those of the parent virus in intranasally inoculated mice. However, in a variety of cell lines the cytopathic effect of the deletion mutant (vKL4) is markedly different from that caused by the parent virus: the absence of K2L in infected cells results in extensive polykaryocytosis. Reinsertion of the K2L gene into vKL4 abolishes this fusion activity, thus confirming that the polykaryocytosis is the result of the deletion of K2L rather than of spontaneous mutations elsewhere in the genome, and that in cells infected with the WR strain of vaccinia virus the K2L gene product prevents fusion. The cell type-specific polykaryocytosis induced by vKL4 is apparent at late times post-infection, occurs from within and requires the synthesis of at least one late virus protein. Other vaccinia virus proteins known to be involved in fusion of infected cells are a 14K membrane protein which is required for fusion, and the haemagglutinin which prevents fusion. The haemadsorption properties of cells infected with the parent virus and the deletion mutant were indistinguishable: both haemadsorbed chicken erythrocytes. A monoclonal antibody against the 14K protein inhibited fusion of vKL4-infected cells, thus demonstrating that in addition to the absence of the K2L gene product, the 14K protein is required for fusion to occur.

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Section: Discussionsupporting

confidence: 76%

Section: Construction Of a Deletion Mutant Lacking The K2l Genesupporting

confidence: 79%

A vaccinia serine protease inhibitor which prevents virus-induced cell fusion

Law

Smith

1992

Journal of General Virology

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“…Recombinant vaccinia virus strain Copenhagen expressing ␤-galactosidase, VV65, was provided by G. McFadden (Robarts Research Institute, London, ON, Canada) (14). The deletion viruses VV811 and VV759 were a generous gift from Enzo Paoletti (Virogenetics, Troy, NY) (15).…”

Section: Methodsmentioning

confidence: 99%

Vaccinia virus encodes a previously uncharacterized mitochondrial-associated inhibitor of apoptosis

Wasilenko

Stewart²,

Meyers³

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

142

171

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To circumvent apoptotic death, many viruses encode Bcl-2 homologous proteins that function at the mitochondria. Vaccinia virus, the prototypic member of the Poxviridae family, does not encode a Bcl-2 homolog but inhibits the mitochondrial arm of the apoptotic cascade by an unknown mechanism. We now report that F1L, a previously unidentified protein in vaccinia virus, is responsible for the inhibition of apoptosis. Cells infected with vaccinia virus are resistant to staurosporine-mediated cleavage of poly(ADP-ribose) polymerase, caspases 3 and 9, and release of cytochrome c. In contrast, a vaccinia virus deletion mutant, VV811, was unable to inhibit apoptosis; however, the antiapoptotic function was restored by expression of the F1L ORF, which is absent in VV811. Although F1L displays no homology to members of the Bcl-2 family, it localizes to the mitochondria through a C-terminal hydrophobic domain. We show that expression of F1L interferes with apoptosis by inhibiting the loss of the inner mitochondrial membrane potential and the release of cytochrome c.

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“…One mutant isolated in our laboratory from the Copenhagen strain, designated VV hr, has 18 kbp deleted near the left end of the genome (Drillien et al, 1981). Similar mutants have been isolated by multiple passages of the CVA strain on chick embryo fibroblasts (Mayr et al, 1975;Altenburger et al, 1989;Meyer et al, 1991) or by directed deletion of VV sequences using recombinant plasmids (Perkus et al, 1991). The VV hr mutant we "~ Present address: Laboratorio de Gen&ica, Instituto Butantan, Av.…”

mentioning

confidence: 99%

Detection of a protein encoded by the vaccinia virus C7L open reading frame and study of its effect on virus multiplication in different cell lines

Oguiura

Spehner

Drillien

1993

Journal of General Virology

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Vaccinia virus encodes several proteins, the activity of which is essential for multiplication in different cell types. Both the C7L and K1L open reading frames (ORFs) have been characterized as viral determinants for multiplication in human cells. To confirm and extend these findings we inserted the C7L ORF into the genome of a mutant virus unable to multiply in human cells and showed that this virus recovered its ability to replicate. Deletion of C7L from a wild-type viral genome did not adversely affect virus multiplication in human cells but it did reduce replication in hamster Dede ceils. When both C7L and K1L were deleted from the vaccinia virus genome only poor or no viral yields were obtained from various human cell lines. Recombinant viruses were also constructed to facilitate the study of C7L protein synthesis during infection. One virus in which the lacZ ORF was fused downstream and in-frame with the C7L ORF enabled us to characterize the C7L protein as an early gene product. Another recombinant virus was constructed so that the carboxy terminus of the C7L ORF product contained an additional 28 amino acids from the carboxy terminus of K1L. Tagging of C7L in this way allowed us to detect the fusion protein by immunoprecipitation with antibodies against the K1L protein. Furthermore, the hybrid protein retained its biological properties. The recombinant viruses constructed in this work should be useful for studies of the molecular basis of the activity of viral host range proteins.

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Deletion of 55 open reading frames from the termini of vaccinia virus

Cited by 98 publications

References 22 publications

A vaccinia serine protease inhibitor which prevents virus-induced cell fusion

A vaccinia serine protease inhibitor which prevents virus-induced cell fusion

Vaccinia virus encodes a previously uncharacterized mitochondrial-associated inhibitor of apoptosis

Detection of a protein encoded by the vaccinia virus C7L open reading frame and study of its effect on virus multiplication in different cell lines

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