Inhibition of Herpesvirus-6B RNA Replication by Short Interference RNAs

Yoon, Jong-Sub; Kim, Sun-Hwa; Shin, Min-Chul; Lee, Dong Gun; Hong, Seong-Karp; Jung, Yong-Tae; Khang, In-Gu; Shin, Wan Shik; Kim, Chun-Choo; Paik, Soon-Young

doi:10.5483/bmbrep.2004.37.3.383

Cited by 14 publications

(5 citation statements)

References 15 publications

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“…An alternative approach for developing antiviral drugs targets specific host functions necessary for viral replication. A good example of this class of targets is the epidermal growth factor receptor family of tyrosine kinases [ 44 ], which disrupt viral maturation and replication cycle when antagonized. A member of this family (ErbB-1) was inhibited by CI-1033, a drug that has been developed originally for its anticancer properties, and led to significant reduction in poxvirus activity [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Monkeypox virus replication by RNA interference

Alkhalil

Strand

Mucker

et al. 2009

Virol J

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The Orthopoxvirus genus of Poxviridae family is comprised of several human pathogens, including cowpox (CPXV), Vaccinia (VACV), monkeypox (MPV) and Variola (VARV) viruses. Species of this virus genus cause human diseases with various severities and outcome ranging from mild conditions to death in fulminating cases. Currently, vaccination is the only protective measure against infection with these viruses and no licensed antiviral drug therapy is available. In this study, we investigated the potential of RNA interference pathway (RNAi) as a therapeutic approach for orthopox virus infections using MPV as a model. Based on genome-wide expression studies and bioinformatic analysis, we selected 12 viral genes and targeted them by small interference RNA (siRNA). Fortyeight siRNA constructs were developed and evaluated in vitro for their ability to inhibit viral replication. Two genes, each targeted with four different siRNA constructs in one pool, were limiting to viral replication. Seven siRNA constructs from these two pools, targeting either an essential gene for viral replication (A6R) or an important gene in viral entry (E8L), inhibited viral replication in cell culture by 65-95% with no apparent cytotoxicity. Further analysis with wild-type and recombinant MPV expressing green fluorescence protein demonstrated that one of these constructs, siA6-a, was the most potent and inhibited viral replication for up to 7 days at a concentration of 10 nM. These results emphasis the essential role of A6R gene in viral replication, and demonstrate the potential of RNAi as a therapeutic approach for developing oligonucleotidebased drug therapy for MPV and other orthopox viruses.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Monkeypox virus replication by RNA interference

Alkhalil

Strand

Mucker

et al. 2009

Virol J

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“…With the continuous development of biotechnology, new approaches to suppress herpesvirus at the gene level have been developed; for instance, RNA interference (RNAi) be could represented as a powerful tool to silence gene expression at the mRNA level and has demonstrated promise in combatting several herpesviruses, such as HSV-1, HHV-6B and CyHV-3 9 - 10 - . 11 At the DNA level, zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs) and clustered regularly interspersed short palindromic repeat (CRISPR)-associated protein 9 (Cas9) make editing viral DNA genomes feasible. 12 The specific editing of viral DNA may lead to better effects during the acute and latent periods with reduced virus-induced toxicity and a strong host immune response.…”

Section: Antiviral Strategies For Treating Herpesvirusesmentioning

confidence: 99%

Antiviral strategies targeting herpesviruses

Dong

Wang

Zhao

et al. 2021

Journal of Virus Eradication

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Herpesviruses, known as large DNA viruses, have a wide host range. In addition to human beings, cattle, and horses, even carp can be hosts for herpesvirus infection. Herpesviruses are pathogens possessing elaborate mechanisms that regulate host cell components for its replication, assembly and generating mature virus particles that can infect humans and most animals, usually causing multiple and lifelong infections. In addition, several human diseases, such as genital or mouth herpes, mononucleosis, and Burkitt lymphoma, are usually associated with herpesvirus infection. Blocking the steps of viral infection, such as entry, replication and assembly, may be an effective way for many different herpes viruses and their related diseases. Therefore, we aim to describe antiviral agents that are able to prevent herpesvirus entry, replication and assembly in host cells. We summarize antiviral strategies, including certain small molecular drugs, RNA interference and CRISPR/Cas9 system-based antiviral approaches, which represent promising approaches.

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“…siRNAs-based antiviral activity has been reported for many RNA and DNA viruses in vitro and in vivo (Ma et al, 2007). The siRNAs-based antiviral activity has been reported against different herpesviruses including Herpes simplex virus 1 (HSV-1) (Bhuyan et al, 2004;Yoon et al, 2004;Palliser et al, 2006;Zhang et al, 2007;Muylaert and Elias, 2007;Zhe et al, 2008), Human cytomegalovirus (Wiebusch et al, 2004), Anatid herpesvirus 1 (AnHV-1) (Mallanna et al, 2006) and Pseudorabies virus (Klupp et al, 2006). These studies targeted genes primarily involved in viral DNA synthesis, replication, assembly, and structural genes.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Bovine herpesvirus multiplication in MDBK cells by small interfering RNAs

Narute¹,

Raut²,

Saini³

et al. 2009

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Small interfering RNA (siRNA) mediated gene silencing is a promising approach in antiviral therapy. To investigate the antiviral effects of siRNAs on Bovine herpesvirus 1 (BoHV-1) multiplication, we designed and in vitro synthesized two siRNAs (siRNA-1 and siRNA-2) targeting the UL25 gene that is essential for BHV-1 multiplication. siRNA-1 and siRNA-2 inhibited the BoHV-1 multiplication in MDBK cells to a different extent, namely by 11% and 40%, respectively, as demonstrated by virus titers (TCID 50 /ml) determined in cell culture. This indicates that, in general, siRNAs can inhibit BHV-1 multiplication in vitro and could be used also against a BHV-1 infection in vivo following optimization of their application.

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Inhibition of Herpesvirus-6B RNA Replication by Short Interference RNAs

Cited by 14 publications

References 15 publications

Inhibition of Monkeypox virus replication by RNA interference

Inhibition of Monkeypox virus replication by RNA interference

Antiviral strategies targeting herpesviruses

Inhibition of Bovine herpesvirus multiplication in MDBK cells by small interfering RNAs

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