Proteomic profiling of the Macrobrachium rosenbergii nodavirus infection: A study of early to late-stage infection in vitro

The Macrobrachium rosenbergii nodavirus ( Mr NV), belonging to the Nodaviridae family, is responsible for a deadly infection in freshwater prawns, especially impacting the post-larvae of Macrobrachium rosenbergii with a mortality rate reaching 100 %. Recent research has shed light on the typical process of Mr NV trafficking within the host, illustrating how the virus navigates through cells as the infection advances and the subsequent cellular alterations. Yet, the specific cellular pathways disrupted by Mr NV, leading to these alterations, are underexplored. Furthermore, the precise effects of the Mr NV capsid protein, known for its strong immune response, on the host cells are not well understood. This study seeks to clarify these impacts by analysing and comparing the protein expression profiles in healthy, Mr NV virus-like particle (VLP) invaded, and Mr NV-infected Sf9 cells over a 24-h period using a mass spectrometry based proteomics approach. Our findings show that the protein expression in Mr NV VLP-invaded and Mr NV-infected Sf9 cells during the mid-infection stages is similar, involving key signalling pathways like the eukaryotic translation system, cell cycle, actin cytoskeleton regulation, and the mTOR pathway. However, changes in protein expression for key proteins such as 40S and 60S ribosomal subunits, 14–3-3 protein epsilon, and tubulin beta chain persisted only within the Mr NV-infection group whilst the protein expression in the VLP-invasion group reverted to baseline levels over time, underscoring the transient nature of VLP effects due to their inability to replicate. Additionally, a reduction in peroxiredoxin levels was observed in the later stages of Mr NV infection, indicating a potential viral strategy to trigger apoptosis and release virions. Our results suggest that Mr NV increases expression of 40S ribosome activity to boost viral protein synthesis while suppressing 60S ribosome expression, which impedes the synthesis of host proteins. Mr NV also appears to extend the lifespan of host cells by interfering with their cell cycle and blocking apoptotic pathways, thus facilitating viral replication. This research enhances our comprehension of Mr NV's infectious mechanism, delineates the pathways exploited by the virus, and identifies crucial molecular targets for potential therapeutic intervention. • There are overlaps in protein expression changes induced by Mr NV capsid and full-length Mr NV. • Mr NV infection alters host protein translation to prioritize the synthesis of viral proteins. • Mr NV infection inhibits cell cycle progression via overexpression of 14–3-3 protein epsilon. • Mr NV induced overexpression of tubulins indicate high viral translocation. • Mr NV capsid induced expression changes for key pathways are transient in nature.