Abortive infection of a rabbit cornea cell line by vesicular stomatitis virus: conversion to productive infection by superinfection with vaccinia virus.

1975 ◽  
Vol 16 (2) ◽  
pp. 322-329 ◽  
Author(s):  
H R Thacore ◽  
J S Youngner
Keyword(s):  
Vaccinia Virus ◽  
Cell Line ◽  
Vesicular Stomatitis Virus ◽  
Productive Infection ◽  
Abortive Infection ◽  
Rabbit Cornea ◽  
Vesicular Stomatitis

scholarly journals Neutralizing activity of Sputnik V vaccine sera against SARS-CoV-2 variants

2021 ◽  
Author(s):  
Satoshi Ikegame ◽  
Mohammed Siddiquey ◽  
Chuan-Tien Hung ◽  
Griffin Haas ◽  
Luca Brambilla ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Cell Line ◽  
Vesicular Stomatitis Virus ◽  
Neutralizing Antibodies ◽  
Vaccine Development ◽  
The Novel ◽  
Serum Samples ◽  
Egfp Reporter ◽  
Vesicular Stomatitis ◽  
Reduced Activity

Abstract The novel pandemic betacoronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected at least 120 million people since its identification as the cause of a December 2019 viral pneumonia outbreak in Wuhan, China1,2. Despite the unprecedented pace of vaccine development, with six vaccines already in use worldwide, the emergence of SARS-CoV-2 ‘variants of concern’ (VOC) across diverse geographic locales have prompted re-evaluation of strategies to achieve universal vaccination3. All three officially designated VOC carry Spike (S) polymorphisms thought to enable escape from neutralizing antibodies elicited during initial waves of the pandemic4–8. Here, we characterize the biological consequences of the ensemble of S mutations present in VOC lineages B.1.1.7 (501Y.V1) and B.1.351 (501Y.V2). Using a replication-competent EGFP-reporter vesicular stomatitis virus (VSV) system, rcVSV-CoV2-S, which encodes S from SARS coronavirus 2 in place of VSV-G, and coupled with a clonal HEK-293T ACE2 TMPRSS2 cell line optimized for highly efficient S-mediated infection, we determined that only 1 out of 12 serum samples from a cohort of recipients of the Gamaleya Sputnik V Ad26 / Ad5 vaccine showed effective neutralization (IC90) of rcVSV-CoV2-S: B.1.351 at full serum strength. The same set of sera efficiently neutralized S from B.1.1.7 and showed only moderately reduced activity against S carrying the E484K substitution alone. Taken together, our data suggest that control of some emergent SARS-CoV-2 variants may benefit from updated vaccines.

scholarly journals Ruxolitinib and Polycation Combination Treatment Overcomes Multiple Mechanisms of Resistance of Pancreatic Cancer Cells to Oncolytic Vesicular Stomatitis Virus

2017 ◽  
Vol 91 (16) ◽  
Author(s):  
Sébastien A. Felt ◽  
Gaith N. Droby ◽  
Valery Z. Grdzelishvili
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Vesicular Stomatitis Virus ◽  
Oncolytic Virus ◽  
Ductal Adenocarcinoma ◽  
Mechanisms Of Resistance ◽  
Pdac Cell ◽  
Ldl Uptake ◽  
Vesicular Stomatitis ◽  
Pdac Cell Line

ABSTRACT Vesicular stomatitis virus (VSV) is a promising oncolytic virus (OV). Although VSV is effective against a majority of pancreatic ductal adenocarcinoma cell (PDAC) cell lines, some PDAC cell lines are highly resistant to VSV, and the mechanisms of resistance are still unclear. JAK1/2 inhibitors (such as ruxolitinib and JAK inhibitor I) strongly stimulate VSV replication and oncolysis in all resistant cell lines but only partially improve the susceptibility of resistant PDACs to VSV. VSV tumor tropism is generally dependent on the permissiveness of malignant cells to viral replication rather than on receptor specificity, with several ubiquitously expressed cell surface molecules playing a role in VSV attachment to host cells. However, as VSV attachment to PDAC cells has never been tested before, here we examined if it was possibly inhibited in resistant PDAC cells. Our data show a dramatically weaker attachment of VSV to HPAF-II cells, the most resistant human PDAC cell line. Although sequence analysis of low-density lipoprotein (LDL) receptor (LDLR) mRNA did not reveal any amino acid substitutions in this cell line, HPAF-II cells displayed the lowest level of LDLR expression and dramatically lower LDL uptake. Treatment of cells with various statins strongly increased LDLR expression levels but did not improve VSV attachment or LDL uptake in HPAF-II cells. However, LDLR-independent attachment of VSV to HPAF-II cells was dramatically improved by treating cells with Polybrene or DEAE-dextran. Moreover, combining VSV with ruxolitinib and Polybrene or DEAE-dextran successfully broke the resistance of HPAF-II cells to VSV by simultaneously improving VSV attachment and replication. IMPORTANCE Oncolytic virus (OV) therapy is an anticancer approach that uses viruses that selectively infect and kill cancer cells. This study focuses on oncolytic vesicular stomatitis virus (VSV) against pancreatic ductal adenocarcinoma (PDAC) cells. Although VSV is effective against most PDAC cells, some are highly resistant to VSV, and the mechanisms are still unclear. Here we examined if VSV attachment to cells was inhibited in resistant PDAC cells. Our data show very inefficient attachment of VSV to the most resistant human PDAC cell line, HPAF-II. However, VSV attachment to HPAF-II cells was dramatically improved by treating cells with polycations. Moreover, combining VSV with polycations and ruxolitinib (which inhibits antiviral signaling) successfully broke the resistance of HPAF-II cells to VSV by simultaneously improving VSV attachment and replication. We envision that this novel triple-combination approach could be used in the future to treat PDAC tumors that are highly resistant to OV therapy.

Inducible Vesicular Stomatitis Virus (VSV) L Cell Line for Packaging of Recombinant VSV

Virus Genes ◽  
2005 ◽  
Vol 31 (2) ◽  
pp. 195-201 ◽  
Author(s):  
Seong-Karp Hong ◽  
Yong-Tae Jung ◽  
Seung-Won Park ◽  
Soon-Young Paik
Keyword(s):  
Cell Line ◽  
Vesicular Stomatitis Virus ◽  
L Cell ◽  
Vesicular Stomatitis

Enhanced adaptation of vesicular stomatitis virus in cells infected with vaccinia virus

2008 ◽  
Vol 8 (5) ◽  
pp. 614-620 ◽  
Author(s):  
Francy Y.E. Carrillo ◽  
Rafael Sanjuán ◽  
Andrés Moya ◽  
José M. Cuevas
Keyword(s):  
Vaccinia Virus ◽  
Vesicular Stomatitis Virus ◽  
Vesicular Stomatitis ◽  
In Cells

scholarly journals A GP64-Null Baculovirus Pseudotyped with Vesicular Stomatitis Virus G Protein

2001 ◽  
Vol 75 (6) ◽  
pp. 2544-2556 ◽  
Author(s):  
J. T. Mangor ◽  
S. A. Monsma ◽  
M. C. Johnson ◽  
G. W. Blissard
Keyword(s):  
G Protein ◽  
Vesicular Stomatitis Virus ◽  
Viral Entry ◽  
Viral Envelope ◽  
Productive Infection ◽  
Pseudotyped Virus ◽  
Sf9 Cells ◽  
Viral Envelope Protein ◽  
Virion Protein ◽  
Vesicular Stomatitis

ABSTRACT The Autographa californica multiple nucleopolyhedrovirus (AcMNPV) GP64 protein is an essential virion protein that is involved in both receptor binding and membrane fusion during viral entry. Genetic studies have shown that GP64-null viruses are unable to move from cell to cell and this results from a defect in the assembly and production of budded virions (BV). To further examine requirements for virion budding, we asked whether a GP64-null baculovirus, vAc64−, could be pseudotyped by introducing a heterologous viral envelope protein (vesicular stomatitis virus G protein [VSV-G]) into its membrane and whether the resulting virus was infectious. To address this question, we generated a stably transfected insect Sf9 cell line (Sf9VSV-G) that inducibly expresses the VSV-G protein upon infection with AcMNPV Sf9VSV-G and Sf9 cells were infected with vAc64−, and cells were monitored for infection and for movement of infection from cell to cell. vAc64− formed plaques on Sf9VSV-G cells but not on Sf9 cells, and plaques formed on Sf9VSV-G cells were observed only after prolonged intervals. Passage and amplification of vAc64− on Sf9VSV-G cells resulted in pseudotyped virus particles that contained the VSV-G protein. Cell-to-cell propagation of vAc64− in the G-expressing cells was delayed in comparison to wild-type (wt) AcMNPV, and growth curves showed that pseudotyped vAc64− was generated at titers of approximately 106 to 107 infectious units (IU)/ml, compared with titers of approximately 108 IU/ml for wt AcMNPV. Propagation and amplification of pseudotyped vAc64− virions in Sf9VSV-G cells suggests that the VSV-G protein may either possess the signals necessary for baculovirus BV assembly and budding at the cell surface or may otherwise facilitate production of infectious baculovirus virions. The functional complementation of GP64-null viruses by VSV-G protein was further demonstrated by identification of a vAc64−-derived virus that had acquired the G gene through recombination with Sf9VSV-G cellular DNA. GP64-null viruses expressing the VSV-G gene were capable of productive infection, replication, and propagation in Sf9 cells.

scholarly journals Response of Three Different Viruses to Interferon Priming and Dithiothreitol Treatment of Avian Cells

2016 ◽  
Vol 90 (18) ◽  
pp. 8328-8340 ◽  
Author(s):  
Irene Lostalé-Seijo ◽  
José Martínez-Costas ◽  
Javier Benavente
Keyword(s):  
Protein Kinase ◽  
Vaccinia Virus ◽  
Vesicular Stomatitis Virus ◽  
Rna Binding ◽  
Initiation Factor ◽  
Type I ◽  
Avian Reovirus ◽  
Double Stranded Rna ◽  
Vesicular Stomatitis ◽  
Eif2 Phosphorylation

ABSTRACTWe have previously shown that the replication of avian reovirus (ARV) in chicken cells is much more resistant to interferon (IFN) than the replication of vesicular stomatitis virus (VSV) or vaccinia virus (VV). In this study, we have investigated the role that the double-stranded RNA (dsRNA)-activated protein kinase (PKR) plays in the sensitivity of these three viruses toward the antiviral action of chicken interferon. Our data suggest that while interferon priming of avian cells blocks vaccinia virus replication by promoting PKR activation, the replication of vesicular stomatitis virus appears to be blocked at a pretranslational step. Our data further suggest that the replication of avian reovirus in chicken cells is quite resistant to interferon priming because this virus uses strategies to downregulate PKR activation and also because translation of avian reovirus mRNAs is more resistant to phosphorylation of the alpha subunit of initiation factor eIF2 than translation of their cellular counterparts. Our results further reveal that the avian reovirus protein sigmaA is able to prevent PKR activation and that this function is dependent on its double-stranded RNA-binding activity. Finally, this study demonstrates that vaccinia virus and avian reovirus, but not vesicular stomatitis virus, express/induce factors that counteract the ability of dithiothreitol to promote eIF2 phosphorylation. Our data demonstrate that each of the three different viruses used in this study elicits distinct responses to interferon and to dithiothreitol-induced eIF2 phosphorylation when infecting avian cells.IMPORTANCEType I interferons constitute the first barrier of defense against viral infections, and one of the best characterized antiviral strategies is mediated by the double-stranded RNA-activated protein kinase R (PKR). The results of this study revealed that IFN priming of avian cells has little effect on avian reovirus (ARV) replication but drastically diminishes the replication of vaccinia virus (VV) and vesicular stomatitis virus (VSV) by PKR-dependent and -independent mechanisms, respectively. Our data also demonstrate that the dsRNA-binding ability of ARV protein sigmaA plays a key role in the resistance of ARV toward IFN by preventing PKR activation. Our findings will contribute to improve the current understanding of the interaction of viruses with the host's innate immune system. Finally, it would be of interest to uncover the mechanisms that allow avian reovirus transcripts to be efficiently translated under conditions (moderate eIF2 phosphorylation) that block the synthesis of cellular proteins.

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