Virus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense

Abstract Recent high annual losses of honey bee colonies are associated with many factors, including RNA virus infections. Honey bee antiviral responses include RNA interference and immune pathway activation, but their relative roles in antiviral defense are not well understood. To better characteri...

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Autores principales: Laura M. Brutscher, Katie F. Daughenbaugh, Michelle L. Flenniken
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/827c2b14addc4b71b1fbb31261abbadd
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spelling oai:doaj.org-article:827c2b14addc4b71b1fbb31261abbadd2021-12-02T15:05:32ZVirus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense10.1038/s41598-017-06623-z2045-2322https://doaj.org/article/827c2b14addc4b71b1fbb31261abbadd2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06623-zhttps://doaj.org/toc/2045-2322Abstract Recent high annual losses of honey bee colonies are associated with many factors, including RNA virus infections. Honey bee antiviral responses include RNA interference and immune pathway activation, but their relative roles in antiviral defense are not well understood. To better characterize the mechanism(s) of honey bee antiviral defense, bees were infected with a model virus in the presence or absence of dsRNA, a virus associated molecular pattern. Regardless of sequence specificity, dsRNA reduced virus abundance. We utilized next generation sequencing to examine transcriptional responses triggered by virus and dsRNA at three time-points post-infection. Hundreds of genes exhibited differential expression in response to co-treatment of dsRNA and virus. Virus-infected bees had greater expression of genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially expressed genes are not well characterized. To confirm the virus limiting role of two genes, including the well-characterized gene, dicer, and a probable uncharacterized cyclin dependent kinase in honey bees, we utilized RNAi to reduce their expression in vivo and determined that virus abundance increased, supporting their involvement in antiviral defense. Together, these results further our understanding of honey bee antiviral defense, particularly the role of a non-sequence specific dsRNA-mediated antiviral pathway.Laura M. BrutscherKatie F. DaughenbaughMichelle L. FlennikenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Laura M. Brutscher
Katie F. Daughenbaugh
Michelle L. Flenniken
Virus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense
description Abstract Recent high annual losses of honey bee colonies are associated with many factors, including RNA virus infections. Honey bee antiviral responses include RNA interference and immune pathway activation, but their relative roles in antiviral defense are not well understood. To better characterize the mechanism(s) of honey bee antiviral defense, bees were infected with a model virus in the presence or absence of dsRNA, a virus associated molecular pattern. Regardless of sequence specificity, dsRNA reduced virus abundance. We utilized next generation sequencing to examine transcriptional responses triggered by virus and dsRNA at three time-points post-infection. Hundreds of genes exhibited differential expression in response to co-treatment of dsRNA and virus. Virus-infected bees had greater expression of genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially expressed genes are not well characterized. To confirm the virus limiting role of two genes, including the well-characterized gene, dicer, and a probable uncharacterized cyclin dependent kinase in honey bees, we utilized RNAi to reduce their expression in vivo and determined that virus abundance increased, supporting their involvement in antiviral defense. Together, these results further our understanding of honey bee antiviral defense, particularly the role of a non-sequence specific dsRNA-mediated antiviral pathway.
format article
author Laura M. Brutscher
Katie F. Daughenbaugh
Michelle L. Flenniken
author_facet Laura M. Brutscher
Katie F. Daughenbaugh
Michelle L. Flenniken
author_sort Laura M. Brutscher
title Virus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense
title_short Virus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense
title_full Virus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense
title_fullStr Virus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense
title_full_unstemmed Virus and dsRNA-triggered transcriptional responses reveal key components of honey bee antiviral defense
title_sort virus and dsrna-triggered transcriptional responses reveal key components of honey bee antiviral defense
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/827c2b14addc4b71b1fbb31261abbadd
work_keys_str_mv AT laurambrutscher virusanddsrnatriggeredtranscriptionalresponsesrevealkeycomponentsofhoneybeeantiviraldefense
AT katiefdaughenbaugh virusanddsrnatriggeredtranscriptionalresponsesrevealkeycomponentsofhoneybeeantiviraldefense
AT michellelflenniken virusanddsrnatriggeredtranscriptionalresponsesrevealkeycomponentsofhoneybeeantiviraldefense
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