Abstract
The phosphatidylinositol-3-kinase (PI3K)/Akt/target of rapamycin (TOR) signalling pathway controls cell growth and survival, and is targeted by a number of viruses at different phases of their infection cycle to control translation. Whether and how insect viruses interact with this pathway remain poorly addressed. Here, we investigated the role of PI3K/Akt/TOR signalling during lethal infection of insect cells with an insect parvovirus. Using Junonia coenia densovirus (JcDV; lepidopteran ambidensovirus 1) and susceptible insect cells as experimental models, we first described JcDV cytopathology, and showed that viral infection affects cell size, cell proliferation and survival. We deciphered the role of PI3K/Akt/TOR signalling in the course of infection and found that non-structural (NS) protein expression correlates with the inhibition of TOR and the shutdown of cellular synthesis, concomitant with the burst of viral protein expression. Together, these results suggest that NS proteins control the cellular translational machinery to favour the translation of viral mRNAs at the expense of cellular mRNAs. As a consequence of TOR inhibition, cell autophagy is activated. These results highlight new functions for NS proteins in the course of multiplication of an insect parvovirus.
Highlights
Viruses are obligate intracellular parasites that rely entirely on host cell resources for their multiplication; one major challenge is to control translation
We deciphered the role of PI3K/Akt/target of rapamycin (TOR) signalling in the course of infection and found that non-structural (NS) protein expression correlates with the inhibition of TOR and the shutdown of cellular synthesis, concomitant with the burst of viral protein expression
We investigated the interaction of an insect parvovirus with the host PI3K/Akt/TOR signalling pathway
Summary
Viruses are obligate intracellular parasites that rely entirely on host cell resources for their multiplication; one major challenge is to control translation. Very different viruses may use convergent strategies to hijack translational components, either targeting key signal transduction pathways and/or antagonizing cell antiviral response (Buchkovich et al, 2008). The phosphatidylinositol-3-kinase (PI3K)/serine/ threonine kinase target of rapamycin (TOR) pathway is a major transduction signalling cascade controlling capdependent translation (Laplante & Sabatini, 2009); its activation propagates to downstream effectors through a coordinated cascade of phosphorylation. PI3K/Akt/TOR signalling controls cell death and survival, making this pathway a target of choice for many viruses that have developed exquisite strategies to maintain cell metabolic activity or counteract detrimental early death signalling (Cooray, 2004; Diehl & Schaal, 2013)
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