Physiological and metabolic consequences of viral infection in Drosophila melanogaster

Arnold, Pieter A., Johnson, Karyn N. and White, Craig R. (2013) Physiological and metabolic consequences of viral infection in Drosophila melanogaster. Journal of Experimental Biology, 216 17: 3350-3357. doi:10.1242/jeb.088138

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Author Arnold, Pieter A.
Johnson, Karyn N.
White, Craig R.
Title Physiological and metabolic consequences of viral infection in Drosophila melanogaster
Journal name Journal of Experimental Biology   Check publisher's open access policy
ISSN 0022-0949
Publication date 2013-09
Year available 2013
Sub-type Article (original research)
DOI 10.1242/jeb.088138
Open Access Status File (Publisher version)
Volume 216
Issue 17
Start page 3350
End page 3357
Total pages 8
Place of publication Cambridge, United Kingdom
Publisher The Company of Biologists Ltd.
Collection year 2014
Language eng
Formatted abstract
An extensively used model system for investigating anti-pathogen defence and innate immunity involves Drosophila C virus (DCV) and Drosophila melanogaster. While there has been a significant effort to understand infection consequences at molecular and genetic levels, an understanding of fundamental higher-level physiology of this system is lacking. Here, we investigate the metabolic rate, locomotory activity, dry mass and water content of adult male flies injected with DCV, measured over the 4?days prior to virus-induced mortality. DCV infection resulted in multiple pathologies, notably the depression of metabolic rate beginning 2?days post-infection as a response to physiological stress. Even in this depressed metabolic state, infected flies did not decrease their activity until 1?day prior to mortality, which further suggests that cellular processes and synthesis are disrupted because of viral infection. Growth rate was also reduced, indicating that energy partitioning is altered as infection progresses. Microbial infection in insects typically results in an increase in excretion; however, water appeared to be retained in DCV-infected flies. We hypothesise that this is due to a fluid intake-output imbalance due to disrupted transport signalling and a reduced rate of metabolic processing. Furthermore, infected flies had a reduced rate of respiration as a consequence of metabolic depression, which minimised water loss, and the excess mass as a result of water retention is concurrent with impaired locomotory ability. These findings contribute to developing a mechanistic understanding of how pathologies accumulate and lead to mortality in infected flies
Keyword Drosophila C virus
Innate Immune Responses
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2014 Collection
School of Biological Sciences Publications
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