Dataset Information

Previous exposure to an RNA virus does not protect against subsequent infection in Drosophila melanogaster.

ABSTRACT:

Background

Immune priming has been shown to occur in a wide array of invertebrate taxa, with individuals exposed to a pathogen showing increased protection upon subsequent exposure. However, the mechanisms underlying immune priming are poorly understood. The antiviral RNAi response in Drosophila melanogaster is an ideal candidate for providing a specific and acquired response to subsequent infection. We exposed D. melanogaster to two challenges of a virus known to produce an antiviral RNAi response, to examine whether any protective effects of prior exposure on survival were observed.

Results

In this experiment we found no evidence that prior exposure to Drosophila C Virus (DCV) protects flies from a subsequent lethal challenge, with almost identical levels of mortality in flies previously exposed to DCV or a control.

Conclusions

Our results confirm the finding that 'acquired' immune responses are not ubiquitous across all invertebrate-pathogen interactions. We discuss why we may have observed no effect in this study, with focus on the mechanistic basis of the RNAi pathway.

SUBMITTER: Longdon B

PROVIDER: S-EPMC3770682 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Publications

Previous exposure to an RNA virus does not protect against subsequent infection in Drosophila melanogaster.

Longdon Ben B Cao Chuan C Martinez Julien J Jiggins Francis M FM

PloS one 20130911 9

<h4>Background</h4>Immune priming has been shown to occur in a wide array of invertebrate taxa, with individuals exposed to a pathogen showing increased protection upon subsequent exposure. However, the mechanisms underlying immune priming are poorly understood. The antiviral RNAi response in Drosophila melanogaster is an ideal candidate for providing a specific and acquired response to subsequent infection. We exposed D. melanogaster to two challenges of a virus known to produce an antiviral RN ...[more]

PMID: 24040086

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Project description:Mosquito-borne dengue virus (DENV, genus Flavivirus) has emerged as a major threat to global human health in recent decades, and novel strategies to contain the escalating dengue fever pandemic are urgently needed. RNA interference (RNAi) induced by exogenous small interfering RNAs (siRNAs) has shown promise for treatment of flavivirus infections in hosts and prevention of transmission by vectors. However, the impact of RNAi triggered by authentic virus infection on replication of DENV, or any flavivirus, has received little study. The objectives of the current study were threefold: first, to assess the utility of Drosophila melanogaster S2 cells for the study of DENV, second to investigate the impact of multiple enzymes in the RNAi pathway on DENV replication; and third to test for variation in the response of the four serotypes of DENV to modulation of RNAi.Three strains from each of the four DENV serotypes showed replication in S2 cells following infection at multiplicity of infection (MOI) 0.1 and MOI 10; each strain achieved titers > 4.0 log10pfu/ml five days after infection at MOI 10. The four serotypes did not differ in mean titer. S2 cells infected with DENV-1, 2, 3 or 4 produced siRNAs, indicating that infection triggered an RNAi response. Knockdown of one of the major enzymes in the RNAi pathway, Dicer-2 (Dcr-2), resulted in a 10 to 100-fold enhancement of replication of all twelve strains of DENV in S2 cells. While serotypes did not differ in their average response to Dcr-2 knockdown, strains within serotypes showed significant differences in their sensitivity to Dcr-2 knockdown. Moreover, knockdown of three additional components of the RNAi pathway, Argonaute 2 (Ago-2), Dcr-1 and Ago-1, also resulted in a significant increase in replication of the two DENV strains tested, and the magnitude of this increase was similar to that resulting from Dcr-2 knockdown.These findings indicate that DENV can replicate in Drosophila S2 cells and that the RNAi pathway plays a role in modulating DENV replication in these cells. S2 cells offer a useful cell culture model for evaluation of the interaction between DENV and the RNAi response.

Dataset Information

Previous exposure to an RNA virus does not protect against subsequent infection in Drosophila melanogaster.

Background

Results

Conclusions

Publications

Previous exposure to an RNA virus does not protect against subsequent infection in Drosophila melanogaster.

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