Antiviral Activity of Sirna UL42 against Herpes Simplex Virus Type 1 in HeLa Cell Culture
- *Corresponding Author:
- Seyedhamidreza Monavari
Associated Professor in Medical Virology
Department of Medical Virology
Iran University of Medical Sciences, Tehran, Iran
E-mail: [email protected]
Received Date: June 05, 2014; Accepted Date: September 11, 2014; Published Date: September 13, 2014
Citation: Mollaei HR, Monavari SH, Arabzadeh S, Shahrabadi MS, Fazlalipour M (2014) Antiviral Activity of Sirna UL42 against Herpes Simplex Virus Type 1 in HeLa Cell Culture. J Antivir Antiretrovir 6:114-119. doi: 10.4172/jaa.10000106
Copyright: © 2014 Mollaei HR, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
RNA interference (RNAi) is a process by which introduced small interfering RNA (siRNA) can cause the specific
degradation of mRNA with identical sequences. In this study, we applied siRNAs targeting the UL42 gene of
human herpes simplex virus type 1 (HSV-1), which encodes a multifunctional polypeptide that is vital for virus DNA
replication, binding to DNA, stably associating with the virus DNA polymerase (Pol), and acting to increase the length
of DNA chains synthesized by Pol. HeLa cell line was used for HSV 1 infection and SiRNA transfection was done
to suppress UL-42 gene in cell culture. The decrease in titer of HSV 1 was observed by rReal Time PCR to detect
the drop in HSV 1 DNA synthesis and translation. The inhibition rates of siRNA1 and siRNA2 on HSV-1 plaque
formation were reported and Comparing with virus control, siRNA1 and siRNA2 reduced DNA replication HSV-1. The
decision whether the decrease in the number of HSV-1 plaques was due to siRNA silencing expression of the UL42
gene, a real-time PCR indicating that UL42-specific siRNAs blocked the expression of the UL42 gene significantly.
Comparing with virus control, siRNA1 and siRNA2 reduced the expression of UL42 gene. In this study the synthetic
siRNA silenced UL42 mRNA expression effectively and specifically and inhibited HSV-1 replication and also our data
offer new possibilities for RNAi as a genetic tool for inhibition of HSV-1 replication.