Generation and amplification of temperature-sensitive mutants during serial undiluted passages of vesicular stomatitis virus

Youngner, Julius S.; Jones, Elaine V.; Kelly, Marion E.; Frielle, Debra W.

doi:10.1016/0042-6822(81)90529-8

Cited by 32 publications

(16 citation statements)

References 16 publications

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“…The establishment of baculovirns persistent infections apparently independent of DI particles in the inoculum distinguishes them from many vertebrate persistent infections (11,29). A long term study of reovirus in Mouse L cells (1) and Sindbis virus in B H K -2 t cells (20) revealed a situation similar to that described in this paper.…”

Section: Mechanism Of Cell Resistancesupporting

confidence: 64%

Persistent baculovirus infections:Spodoptera frugiperda NPV andAutographa californica NPV inSpodoptera frugiperda cells

Crawford¹,

Sheehan²

1983

Archives of Virology

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Establishment of a persistent infection of Spodoptera frugiperda nuclear polyhedrosis virus (NPV) in Spodoptera frugiperda (S.f.) cells occurred in three phases: the first phase was characterised by high levels of cell infection and death, the second phase by decreasing cell infection levels leading to the final phase where less than one per cent of the cells were infected during any subculture. The virus persisted at this level of infection provided the cells were maintained by regular subculturing and incubated at the optimum growth temperature of 27 degrees C. Because of the low proportion of cells infected, cultures of virus-free cells could be selected ('cured') by dilution of the persistent infection without the use of viral antiserum. Unlike the parent S.f. cells, cultures of cured cells were partially resistant to infection with S. frugiperda NPV or infection with an unrelated baculovirus Autographa californica NPV. A. californica NPV, which is cytolytic for the parent S.f. cell line, established a persistent infection in the cured cells. The establishment pattern was similar to that previously found for S. frugiperda NPV and only one to five per cent of the cells were infected at equilibrium. Cured cells from the A. californica NPV persistent infection were highly resistant to infection with both S. frugiperda NPV and A. californica NPV. All attempts to find a viral interference phenomenon to explain the resistance of the cured cells were unsuccessful. All cell types adsorbed virus equally well. Slower growth of S.f. cells cured from the persistent A. californica NPV infection is the only difference so far observed between any of the S.f. cell types.

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Section: Mechanism Of Cell Resistancesupporting

confidence: 64%

Persistent baculovirus infections:Spodoptera frugiperda NPV andAutographa californica NPV inSpodoptera frugiperda cells

Crawford¹,

Sheehan²

1983

Archives of Virology

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“…However, the particulate nature of the interfering activity for RS virus described here suggests that if IFN is present, it is not active under the conditions of either the colorimetric or the RIY assay. Recent studies indicate that some ts viruses can interfere with standard virus replication (Youngner & Quagliana, 1976;Ahmed et al, 1980) and that ts viruses can be generated on undiluted passage (Youngner et al, 1981). However, no evidence of ts virus was found in the DI particle preparation used in this study.…”

Section: Discussioncontrasting

confidence: 46%

A Colorimetric Assay for Quantification of Defective Interfering Particles of Respiratory Syncytial Virus

Treuhaft

1983

Journal of General Virology

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SUMMARYA colorimetric assay for defective interfering (DI) particles of respiratory syncytial (RS) virus was developed. This quantitative biological assay is based on neutral red dye uptake by DI particle-protected cells that survive standard virus challenge. This assay was more sensitive than the reduction of infectious yield (RIY) assay and was capable of detecting 1 x 104 to 2 x 104 DI particles/ml. The coefficient of variation for parallel, simultaneous replicates (n = 10) was 23%. Cell-protecting activity in the colorimetric assay appeared simultaneously with activity in the RIY assay on undiluted passage of plaque-purified virus. Both activities were particulate, were inactivated by RS virus antiserum and exhibited similar ultraviolet-inactivation kinetics. The absolute values of the slopes of dilution curves for both assays were similar, and using regression analysis both assays enabled estimation of similar numbers of active particles. These results suggest that both activities are mediated by the same DI particle. The mechanism of cell protection does not appear to involve extracellular interferon because the inclusion of interferon antibody in the assay did not diminish DI particle cell protection. Finally, the colorimetric assay was used to reveal alternating cycles of infectious and DI virus production on serial undiluted passage.

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“…In HeLa cells, detectable DI particles are not generated (Holland et al, 1976). Bovine kidney cells fail to produce DI particles through 10 serial undiluted passages, while BHK-21 cells are efficient producers of DI particles (Youngner et al, 1981). Importantly, in vivo DI particles can also play a role in viral pathogenesis by modulating the host immune response (Cave et al, 1985; Plakhov et al, 1995a).…”

Section: Replicationmentioning

confidence: 99%

Understanding and altering cell tropism of vesicular stomatitis virus

Hastie¹,

Cataldi²,

Marriott³

et al. 2013

Virus Research

115

116

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Vesicular stomatitis virus (VSV) is a prototypic nonsegmented negative-strand RNA virus. VSV’s broad cell tropism makes it a popular model virus for many basic research applications. In addition, a lack of preexisting human immunity against VSV, inherent oncotropism and other features make VSV a widely used platform for vaccine and oncolytic vectors. However, VSV’s neurotropism that can result in viral encephalitis in experimental animals needs to be addressed for the use of the virus as a safe vector. Therefore, it is very important to understand the determinants of VSV tropism and develop strategies to alter it. VSV glycoprotein (G) and matrix (M) protein play major roles in its cell tropism. VSV G protein is responsible for VSV broad cell tropism and is often used for pseudotyping other viruses. VSV M affects cell tropism via evasion of antiviral responses, and M mutants can be used to limit cell tropism to cell types defective in interferon signaling. In addition, other VSV proteins and host proteins may function as determinants of VSV cell tropism. Various approaches have been successfully used to alter VSV tropism to benefit basic research and clinically relevant applications.

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Generation and amplification of temperature-sensitive mutants during serial undiluted passages of vesicular stomatitis virus

Cited by 32 publications

References 16 publications

Persistent baculovirus infections:Spodoptera frugiperda NPV andAutographa californica NPV inSpodoptera frugiperda cells

Persistent baculovirus infections:Spodoptera frugiperda NPV andAutographa californica NPV inSpodoptera frugiperda cells

A Colorimetric Assay for Quantification of Defective Interfering Particles of Respiratory Syncytial Virus

Understanding and altering cell tropism of vesicular stomatitis virus

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