Arrested spread of vesicular stomatitis virus infections in vitro depends on interferon-mediated antiviral activity

2005 ◽  
Vol 90 (7) ◽  
pp. 793-804 ◽  
Author(s):  
Vy Lam ◽  
Karen A. Duca ◽  
John Yin
Keyword(s):  
Antiviral Activity ◽  
Vesicular Stomatitis Virus ◽  
Virus Infections ◽  
Vesicular Stomatitis

In vitro antiviral activity of dehydroepiandrosterone and its synthetic derivatives against vesicular stomatitis virus

2009 ◽  
Vol 182 (2) ◽  
pp. 327-335 ◽  
Author(s):  
Carina Romanutti ◽  
Andrea C. Bruttomesso ◽  
Viviana Castilla ◽  
Juan A. Bisceglia ◽  
Lydia R. Galagovsky ◽  
...  
Keyword(s):  
Antiviral Activity ◽  
Vesicular Stomatitis Virus ◽  
Vesicular Stomatitis ◽  
Synthetic Derivatives

Curcumin and Boswellia serrata gum resin extract inhibit chikungunya and vesicular stomatitis virus infections in vitro

2016 ◽  
Vol 125 ◽  
pp. 51-57 ◽  
Author(s):  
Christine von Rhein ◽  
Tatjana Weidner ◽  
Lisa Henß ◽  
Judith Martin ◽  
Christopher Weber ◽  
...  
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Virus Infections ◽  
Boswellia Serrata ◽  
Vesicular Stomatitis ◽  
Resin Extract

Further studies on the relative antiviral efficacies of interferons induced by polyI:C and Mengo virus

1976 ◽  
Vol 22 (5) ◽  
pp. 712-718 ◽  
Author(s):  
J. B. Campbell
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Reduction Method ◽  
Mouse Serum ◽  
Antiviral Action ◽  
Virus Infections ◽  
Lethal Infection ◽  
Vesicular Stomatitis ◽  
Mengo Virus

Mouse serum interferons induced by polyI:C, vesicular stomatitis virus (VSV), reovirus, and Mengo virus were assayed in monolayers of mouse L-929 cells by the plaque-reduction method using both VSV and Mengo as challenge viruses. Titers obtained with Mengo virus as challenge were all lower than with VSV. With the interferons induced by VSV, reovirus, and polyI:C, the reductions were of the order of two- to three-fold. With Mengo virus-induced interferon the reduction was much greater (about 17-fold). This offers an explanation for the observation that, unit for unit (measured by the plaque reduction of VSV), Mengo virus-induced interferon is only about [Formula: see text] as effective as polyI:C-induced interferon in protecting mice against lethal infection with Mengo virus. The data are consistent with the hypothesis that an interferon antagonist is produced in the serum of mice infected with Mengo virus. This antagonist, which is not produced in mice inoculated with polyI:C, or reovirus, effectively blocks the antiviral action of interferon during Mengo virus infections, both in vivo and in vitro.

scholarly journals Tamoxifen Protects from Vesicular Stomatitis Virus Infection

2019 ◽  
Vol 12 (4) ◽  
pp. 142 ◽  
Author(s):  
Lamin B. Cham ◽  
Sarah-Kim Friedrich ◽  
Tom Adomati ◽  
Hilal Bhat ◽  
Maximilian Schiller ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Vesicular Stomatitis Virus ◽  
Early Stage ◽  
Vero Cells ◽  
Inhibitory Effect ◽  
Virus Infections ◽  
Biological Targets ◽  
Vesicular Stomatitis

Background: Tamoxifen (TAM) is an estrogen-receptor antagonist, widely used in the adjuvant treatment of early stage estrogen-sensitive breast cancer. Several studies have revealed new biological targets of TAM that mediate the estrogen receptor independent activities of the drug. Recently, the antiviral activity of TAM on replication of human immunodeficiency virus (HIV), hepatitis C virus (HCV) and Herpes simplex virus (HSV-1) in vitro was described. In the current study, we aimed to investigate the effect of TAM on infection with vesicular stomatitis virus (VSV). Methods: Vero cells were treated with different concentrations of TAM for 24 h and then infected with VSV. Additionally, C57BL/6 mice were pretreated with 4 mg TAM, one day and three days before infection with VSV. Results: Treatment of Vero cells with TAM suppressed the viral replication of VSV in vitro and in vivo. The inhibitory effect of TAM on VSV replication correlated with an enhanced interferon-I response and stimulation of macrophages. Conclusions: TAM was identified as being capable to protect from VSV infection in vitro and in vivo. Consequently, this antiviral function (as an advantageous side-effect of TAM) might give rise to new clinical applications, such as treatment of resistant virus infections, or serve as an add-on to standard antiviral therapy.

scholarly journals Study of Glutoxim antiviral activity in the fibroblast cell line infected with vesicular stomatitis virus

2018 ◽  
Vol 2018 (6) ◽  
pp. 25-29 ◽  
Author(s):  
Сергей Ожерелков ◽  
Sergey Ozherelkov ◽  
Татьяна Кожевникова ◽  
Tat'yana Kozhevnikova ◽  
Александр Санин ◽  
...  
Keyword(s):  
Antiviral Activity ◽  
Cell Lines ◽  
Vesicular Stomatitis Virus ◽  
Fibroblast Cell ◽  
Antiviral Effect ◽  
Low Doses ◽  
Vesicular Stomatitis ◽  
Cytopathic Action ◽  
Fibroblast Cell Lines

New strategy for the treatment of animal infectious diseases is based upon the modulation of the host immune response in order to enhance the clearance of infectious agents and reduce the damaging effects of inflammation in the tissues. The modern approach to the use of immunomodulators (IMD) in veterinary practice consists in the usage of such drugs, which are not only immunomodulating, but also have antiviral, antioxidant, anti-inflammatory, hemostimulating and/or other important properties. The aim of the study was to identify possible antiviral activity of known IMD Glutoxim (GLT) during infection of diploid fibroblast cell lines M-8 and M-22 with vesicular stomatitis virus (VSV). Materials and methods: VSV, strain Indiana, was used. Antiviral activity of GLT investigated: 1) at doses recommended for experiments in vitro: 1, 4 and 8 µg/ml; 2) at low doses: 0,1; 0,25 and 0,5 µg/ml. GLT was added to the cell monolayer according to preventive (for 24 hours prior to VSV infection of cells) and treatment (unanimous with VSV infection) protocols. The antiviral activity of GLT was assessed by the following criteria: ability of the drug to prevent the development of virus cytopathic action, to inhibit the reproduction of VSV, and by expessing virucidal action. Results: GLT in doses recommended for in vitro experiments (1, 4, 8 µg/ml) did not delay the development of a specific virus-induced cytopathic action. The VSV titers in infected cells in the presence of GLT did not differ from those in the control cell lines infected with VSV without the addition of GLT. The latter had no virucidal effect against the VSV. Inoculation of GLT into the cell culture at low doses of 0.1, 0.25 and 0.5 mg/ml led to a significant (more than 100-fold) inhibition of VSV replication 24 hours after infection of cells. At later stages, 40 and 48 hours following infection, the antiviral effect of GLT was not detected. Thus, we established that GLT possesses antiviral effect in vitro, which is manifested 24 hours following infection of diploid fibroblast cell lines with VSV.

scholarly journals Natural killer T cell immunotherapy combined with oncolytic vesicular stomatitis virus or reovirus treatments differentially increases survival in mouse models of ovarian and breast cancer metastasis

2021 ◽  
Vol 9 (3) ◽  
pp. e002096
Author(s):  
Simon Gebremeskel ◽  
Adam Nelson ◽  
Brynn Walker ◽  
Tora Oliphant ◽  
Lynnea Lobert ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vesicular Stomatitis Virus ◽  
Cell Activation ◽  
Tumor Burden ◽  
Oncolytic Viruses ◽  
Nkt Cell ◽  
Cell Immunotherapy ◽  
Vesicular Stomatitis ◽  
Better Than

BackgroundOncolytic viruses reduce tumor burden in animal models and have generated promising results in clinical trials. However, it is likely that oncolytic viruses will be more effective when used in combination with other therapies. Current therapeutic approaches, including chemotherapeutics, come with dose-limiting toxicities. Another option is to combine oncolytic viruses with immunotherapeutic approaches.MethodsUsing experimental models of metastatic 4T1 breast cancer and ID8 ovarian peritoneal carcinomatosis, we examined natural killer T (NKT) cell-based immunotherapy in combination with recombinant oncolytic vesicular stomatitis virus (VSV) or reovirus. 4T1 mammary carcinoma cells or ID8 ovarian cancer cells were injected into syngeneic mice. Tumor-bearing mice were treated with VSV or reovirus followed by activation of NKT cells via the intravenous administration of autologous dendritic cells loaded with the glycolipid antigen α-galactosylceramide. The effects of VSV and reovirus on immunogenic cell death (ICD), cell viability and immunogenicity were tested in vitro.ResultsVSV or reovirus treatments followed by NKT cell activation mediated greater survival in the ID8 model than individual therapies. The regimen was less effective when the treatment order was reversed, delivering virus treatments after NKT cell activation. In the 4T1 model, VSV combined with NKT cell activation increased overall survival and decreased metastatic burden better than individual treatments. In contrast, reovirus was not effective on its own or in combination with NKT cell activation. In vitro, VSV killed a panel of tumor lines better than reovirus. VSV infection also elicited greater increases in mRNA transcripts for proinflammatory cytokines, chemokines, and antigen presentation machinery compared with reovirus. Oncolytic VSV also induced the key hallmarks of ICD (calreticulin mobilization, plus release of ATP and HMGB1), while reovirus only mobilized calreticulin.ConclusionTaken together, these results demonstrate that oncolytic VSV and NKT cell immunotherapy can be effectively combined to decrease tumor burden in models of metastatic breast and ovarian cancers. Oncolytic VSV and reovirus induced differential responses in our models which may relate to differences in virus activity or tumor susceptibility.

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