RNA interference as a cellular defense mechanism against the DNA virus, baculovirus

Jayachandran, Balanchandran, Hussain, Mazhar and Sassan, Asgari (2012) RNA interference as a cellular defense mechanism against the DNA virus, baculovirus. Journal of Virology, 86 24: 13729-13734. doi:10.1128/JVI.02041-12


Author Jayachandran, Balanchandran
Hussain, Mazhar
Sassan, Asgari
Title RNA interference as a cellular defense mechanism against the DNA virus, baculovirus
Journal name Journal of Virology   Check publisher's open access policy
ISSN 0022-538X
1098-5514
Publication date 2012-12
Year available 2012
Sub-type Article (original research)
DOI 10.1128/JVI.02041-12
Open Access Status DOI
Volume 86
Issue 24
Start page 13729
End page 13734
Total pages 6
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Collection year 2013
Language eng
Formatted abstract
In insects, the RNA interference (RNAi) pathway plays a major role in anti-viral responses as shown against many RNA viruses. The response includes the cleavage of double stranded RNA genome or intermediates, produced during replication, into viral short interfering RNAs (v-siRNAs). Using deep sequencing, we found that a large number of small reads of ∼20 nucleotides from Helicoverpa armigera larvae infected with Helicoverpa armigera single nucleopolyhedrovirus (HaSNPV) were mapped to certain open reading frames in the viral genome (hotspots) that are mostly structural and auxiliary late genes. After excluding the possibility of these small RNAs to be microRNAs, it was determined that Dicer-2, the main enzyme implicated in the RNAi response in insects, is involved in the generation of v-siRNAs. In Dicer-2, but not Dicer-1 silenced cells, higher transcript levels of the hotspot genes were detected and as a consequence the virus replicated more efficiently. The results suggest that the viral transcripts are degraded by the RNAi response of the host. This may, however, be to the advantage of the virus by preventing over-replication of the virus, which may otherwise lead to the premature death of the host cells.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2013 Collection
School of Biological Sciences Publications
 
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Created: Wed, 07 Nov 2012, 15:12:17 EST by Gail Walter on behalf of School of Biological Sciences