Innate responses to small interfering RNA pools inhibiting herpes simplex virus infection in astrocytoid and epithelial cells

Herpes simplex virus (HSV) is a human pathogen that can cause severe diseases such as encephalitis, keratitis and neonatal herpes. Control of HSV infection may be achieved by using small interfering (si)RNAs. We have designed and enzymatically produced pools of siRNAs targeting HSV. In addition to t...

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Bibliographic Details
Published in:Innate immunity (London, England) England), 2015-05, Vol.21 (4), p.349-357
Main Authors: Paavilainen, Henrik, Romanovskaya, Alesia, Nygårdas, Michaela, Bamford, Dennis H, Poranen, Minna M, Hukkanen, Veijo
Format: Article
Language:English
Subjects:
Astrocytes - immunology
Astrocytes - virology
Cell Line
Epithelial Cells - immunology
Epithelial Cells - virology
Gene Expression Regulation, Viral - genetics
Herpes Simplex - genetics
Herpes Simplex - immunology
Humans
Immunity, Innate
Interferon Type I - metabolism
Interferons
Interleukins - metabolism
Organ Specificity - immunology
RNA, Small Interfering - genetics
Simplexvirus - genetics
Simplexvirus - physiology
Toll-Like Receptor 3 - metabolism
Virus Replication - genetics
Virus Shedding - genetics
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Summary:Herpes simplex virus (HSV) is a human pathogen that can cause severe diseases such as encephalitis, keratitis and neonatal herpes. Control of HSV infection may be achieved by using small interfering (si)RNAs. We have designed and enzymatically produced pools of siRNAs targeting HSV. In addition to the target-specific effects, such siRNAs may induce innate immunity responses that may contribute to antiviral effects. HSV has versatile ways of modulating innate immunity, and it remains unclear whether HSV-specific antiviral treatment would benefit from the potential immunostimulatory effects of siRNAs. To address this, cell lines derived from epithelium and nervous system were studied for innate immunity reactions to HSV infection, to siRNA treatment, and to a combination of treatment and infection. In addition, the outcome of HSV infection was quantitated. We show that innate immunity reactions vary drastically between the cell lines. Moreover, our findings indicate only a minimal relation between the antiviral effect and the treatment-induced innate immunity responses. Thus, the antiviral effect is mainly sequence specific and the inhibition of HSV infection is not ascribed to the slight innate immunity induction.
ISSN:1753-4259
1753-4267
DOI:10.1177/1753425914537921