Autophagy promoted infectious kidney and spleen necrosis virus replication and decreased infectious virus yields in CPB cell line

2017 ◽  
Vol 60 ◽  
pp. 25-32 ◽  
Author(s):  
Chen Li ◽  
Xiaozhe Fu ◽  
Qiang Lin ◽  
Lihui Liu ◽  
Hongru Liang ◽  
...  
Keyword(s):  
Cell Line ◽  
Virus Replication ◽  
Infectious Virus ◽  
Necrosis Virus ◽  
Spleen Necrosis Virus ◽  
Spleen Necrosis

scholarly journals Avian Reticuloendotheliosis Virus Strain A and Spleen Necrosis Virus Do Not Infect Human Cells

2000 ◽  
Vol 74 (1) ◽  
pp. 518-522 ◽  
Author(s):  
R. Gautier ◽  
A. Jiang ◽  
V. Rousseau ◽  
R. Dornburg ◽  
T. Jaffredo
Keyword(s):  
Cell Line ◽  
Retroviral Vectors ◽  
Human Cells ◽  
Published Data ◽  
Reticuloendotheliosis Virus ◽  
Necrosis Virus ◽  
Packaging Cell Line ◽  
Packaging Cell ◽  
Spleen Necrosis Virus ◽  
Spleen Necrosis

ABSTRACT Spleen necrosis virus (SNV) andReticuloendotheliosis virus strain A (REV-A) belong to the family of reticuloendotheliosis viruses and are 90% sequence related. SNV-derived retroviral vectors produced by the REV-A-based D17.2G packaging cell line were shown to infect human cells (H.-M. Koo, A. M. C. Brown, Y. Ron, and J. P. Dougherty, J. Virol. 65:4769–4776, 1991), while similar vectors produced by another SNV-based packaging cell line, DSH134G, are not infectious in human cells (reviewed by R. Dornburg, Gene Ther. 2:301–310, 1995). Here we describe a careful reevaluation of the infectivity of vectors produced from the most commonly used REV-A- or SNV-based packaging cells obtained from various sources with, among them, one batch of D17.2G packaging cells obtained from the American Type Culture Collection. None of these packaging cells produced vectors able to infect human cells. Thus, contrary to previously published data, we conclude that REV-based vectors are not infectious in human cells.

scholarly journals Spliced Spleen Necrosis Virus Vector RNA Is Not Encapsidated: Implications for Retroviral Replication and Vector Design

2004 ◽  
Vol 9 (4) ◽  
pp. 557-565 ◽  
Author(s):  
Adrienne Goodrich ◽  
Zahida Parveen ◽  
Ralph Dornburg ◽  
Matthias J Schnell ◽  
Roger J Pomerantz
Keyword(s):  
Virus Vector ◽  
Necrosis Virus ◽  
Spleen Necrosis Virus ◽  
Retroviral Replication ◽  
Spleen Necrosis

scholarly journals The Nucleocapsid Domain Is Responsible for the Ability of Spleen Necrosis Virus (SNV) Gag Polyprotein To Package both SNV and Murine Leukemia Virus RNA

1999 ◽  
Vol 73 (11) ◽  
pp. 9170-9177 ◽  
Author(s):  
Jeanine L. Certo ◽  
Timur O. Kabdulov ◽  
Michelle L. Paulson ◽  
Jeffrey A. Anderson ◽  
Wei-Shau Hu
Keyword(s):  
Murine Leukemia Virus ◽  
Viral Vector ◽  
Leukemia Virus ◽  
Gene Products ◽  
Rna Packaging ◽  
Packaging Signal ◽  
Necrosis Virus ◽  
Spleen Necrosis Virus ◽  
Spleen Necrosis ◽  
Murine Leukemia

ABSTRACT Murine leukemia virus (MLV)-based vector RNA can be packaged and propagated by the proteins of spleen necrosis virus (SNV). We recently demonstrated that MLV proteins cannot support the replication of an SNV-based vector; RNA analysis revealed that MLV proteins cannot efficiently package SNV-based vector RNA. The domain in Gag responsible for the specificity of RNA packaging was identified using chimericgag-pol expression constructs. A competitive packaging system was established by generating a cell line that expresses one viral vector RNA containing the MLV packaging signal (Ψ) and another viral vector RNA containing the SNV packaging signal (E). The chimericgag-pol expression constructs were introduced into the cells, and vector titers as well as the efficiency of RNA packaging were examined. Our data confirm that Gag is solely responsible for the selection of viral RNAs. Furthermore, the nucleocapsid (NC) domain in the SNV Gag is responsible for its ability to interact with both SNV E and MLV Ψ. Replacement of the SNV NC with the MLV NC generated a chimeric Gag that could not package SNV RNA but retained its ability to package MLV RNA. A construct expressing SNV gag-MLVpol supported the replication of both MLV and SNV vectors, indicating that the gag and pol gene products from two different viruses can functionally cooperate to perform one cycle of retroviral replication. Viral titer data indicated that SNVcis-acting elements are not ideal substrates for MLVpol gene products since infectious viruses were generated at a lower efficiency. These results indicate that the nonreciprocal recognition between SNV and MLV extends beyond the Gag-RNA interaction and also includes interactions between Pol and othercis-acting elements.

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