Producción y evaluación anti-herpética de una molécula recombinante de interferón beta

Jaime E. Castellanos; Sheilla Ledesma-Ortiz; Jeanette Prada-Arismendy

doi:10.17533/udea.hm.12649

Authors

Jaime E. Castellanos National university of Colombia
Sheilla Ledesma-Ortiz National University of Colombia
Jeanette Prada-Arismendy El Bosque University

DOI:

https://doi.org/10.17533/udea.hm.12649

Keywords:

herpes simplex virus , cell culture , interferon β, antiviral, bioassay

Abstract

INTRODUCTION

Herpes Simplex Virus Type 1 (HSV-1) is the main viral pathogen causing mouth and perioral epithelial

infections. After primary mucosal infection, virus goes through nerve endings toward trigeminal ganglion where it establishes latent infection and it can be reactivated when some stimuli or conditions favors the viral gene transcription resulting in a recurrent infection. Despite anti-herpetic drugs can reduce herpes morbidity and mortality, latency and recurrences are a lifespan threat which is little known. Interferons type 1 are recognized antiviral cytokines, even in HSV -1 infections, but it is not known its role during latency establishment or recurrences apparitions.

OBJECTIVE

In this work we standardized the production of recombinant Interferon B and tested its in vitro anti-herpetic activity.

RESULTS

It was found an antiviral effect against Vesicular Stomatitis Virus in a classical antiviral bioassay. Infection with HSV-1 caused cell, but treatment with supernatants from cells transfected with an IFN-B construct, did protect the neuronal cell line SH-SY5Y against cytopathic effect (cell death 2,5%) induced by HSV-1 without changesin virus yielding.

CONCLUSIONS

Recombinant IFN-B han a light but significant antiherpetic activity in SH-SY5Y neuroblastoma cells. is necessary to improve the molecule production to reach better activity of IFN-B.

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Author Biographies

Jaime E. Castellanos, National university of Colombia

Infectious Pathogenesis Group, School of Dentistry, National University of Colombia.

Sheilla Ledesma-Ortiz, National University of Colombia

Infectious Pathogenesis Group, School of Dentistry, National University of Colombia.

Jeanette Prada-Arismendy, El Bosque University

Virology Group, El Bosque University, Bogotá Colombia.

References

Akhtar J, Shukla D. Viral entry mechanisms: cellular and viral mediators of herpes simplex virus entry. FEBS J. 2009; 276: 7228-36.

Amir J, Harel L, Smetana Z, Varsano I. Treatment of herpes simplex gingivostomatitis with aciclovir in children: a randomised double blind placebo controlled study. Br Med J. 1997; 314: 1800-3.

Penfold ME, Armati P, Cunningham AL. Axonal transport of herpes simplex virions to epidermal cells: evidence for a specialized mode of virus transport and assembly. Proc Natl Acad Sci U S A. 1994; 91: 6529-33.

Sawtell NM, Thompson RL. Rapid in vivo reactivation of herpes simplex virus in latently infected murine ganglionic neurons after transient hyperthermia. J Virol. 1992; 66: 2150-6.

Ship II, Miller MF, Ram C. A retrospective study of recurrent herpes labialis (RHL) in a professional population, 1958-1971. Oral Surg Oral Med Oral Pathol. 1977; 44: 723-30.

Marín LM. Expresión de oligoadenilato sintetasa 1b (OAS-1b) en neuronas trigeminales infectadas con HSV-1. Trabajo de grado, Facultad de Odontología, Universidad Nacional de Colombia. 2007.

Sun, Y, Kum, R, Hoon, S, Pei, P. Detection and Genotyping of Human Herpes Simplex Viruses in Cu-taneous Lesions of Erythema Multiforme by Nested PCR. J Med Virol 2003; 71: 423-428.

Al-khatib K, Williams BR, Silverman RH, Halford W, Carr DJ. The murine double-stranded RNA-dependent protein kinase PKR and the murine 2’,5’-oli-goadenylate synthetase-dependent RNase L are required for IFN-beta-mediated resistance against herpes simplex virus type 1 in primary trigeminal ganglion culture. Virology 2003; 313:126-35.

Samuel S. Antiviral Actions of Interferons. Clin Microbiol Rev. 2006; 14: 778 – 809.

Poon AW, Gu H, Roizman B. ICP0 and the US3 protein kinase of herpes simplex virus 1 independently block histone deacetylation to enable gene expression. Proc Natl Acad Sci U S A. 2006; 103: 9995-99.

Chee AV, Roizman B. Herpes simplex virus 1 gene products occlude the interferon signaling pathway at multiple sites. J Virol. 2004; 78: 4185-96.

Maheshwari R, Friedman R. E!ect of interferon treatment on vesicular stomatitis virus (VSV): Release of unusual particles with low infectivity. Virology 1980; 101: 399 – 407.

McSharry J, Compans R and Choppin P. (1971). Proteins of Vesicular Stomatitis Virus and of Phenotypically Mixed Vesicular Stomatitis Virus-Simian Virus 5 Virions. J Virol. 1971; 8: 722-29.

Cui B, Carr DJ. A plasmid construct encoding murine interferon beta antagonizes the replication of herpes simplex virus type I in vitro and in vivo. J Neuroimmunol. 2000; 108: 92 - 102.

Härle P, Cull V, Agbaga M, Silverman R, Williams B, James C, Carr DJ. Di!erential e!ect of murine alpha/beta interferon transgenes on antagonization of herpes simplex virus type 1 replication. J Virol. 2002; 76: 6558-67.

Härle P, Noisakran S, Carr DJ. T h e a p p l i c a t i o n o f a plasmid DNA encoding IFN-alpha 1 postinfection enhances cumulative survival of herpes simplex virus type 2 vaginally infected mice. J Immunol. 2001; 166: 1803-12.

Sainz B, Halford W. Alpha/Beta interferon and gamma interferon synergize to inhibit the replication of herpes simplex virus type 1. J Virol. 2002; 76: 11541-50.

Pierce A, DeSalvo J, Foster T, Kosinski A, Weller S and Halford W. Beta interferon and gamma interferon synergize to block viral DNA and virion synthesis in herpes simplex virus-infected cells. J Gen Virol. 2005; 86: 2421–32.