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Expression of key components of theRNAi machinery are suppressed in Apis mellifera that suffer a high virus infection.

Authors :
De Smet, Lina
Ravoet, Jorgen
Wenseleers, Tom
Graaf, Dirk C.
Source :
Entomological Science. Jan2017, Vol. 20 Issue 1, p76-85. 10p.
Publication Year :
2017

Abstract

Viruses are one of the major threats for honeybees and until now more than 20 different viruses have been discovered. Viruses and their hosts are engaged in a continuous arms race in which viral defense mechanisms drive the adaptive evolution of host immune genes, which in turn results in counter-adaptations of the viral immune antagonists. The honeybee immune responses to non-viral pathogens have been extensively studied, but little is known about the antiviral responses. Recent evidence suggests that the main mechanism of antiviral defense in insects is the RNA interference (RNAi) pathway. Furthermore, there is evidence that some viruses suppress this RNAi pathway in order to evade antiviral immunity. In the present study, we test this hypothesis by comparing the gene expression levels of some key components of the RNAi response of honeybees that were naturally infected with at least five viruses with those who were infected with only two or three viruses using a colorimetric microarray developed in-house, called BeeClinic, and subsequently confirmed by quantitative reverse-transcription-polymerase chain reaction (qRT-PCR). Our results show that key components of the RNAi pathway are indeed downregulated in highly infected bees. We were able to show that high virus loads suppress key RNAi components, which results in a counteraction of the host RNAi antiviral defense. As the RNAi is a primary defense against viruses, these findings shed new light on pathogen-host interactions and can help mitigate escalating colony losses worldwide. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
13438786
Volume :
20
Issue :
1
Database :
Academic Search Index
Journal :
Entomological Science
Publication Type :
Academic Journal
Accession number :
120718171
Full Text :
https://doi.org/10.1111/ens.12227