Abstract
High-throughput approaches have opened new opportunities for understanding biological processes such as persistent virus infections, which are widespread. However, the potential of persistent infections to develop towards pathogenesis remains to be investigated, particularly with respect to the role of host metabolism. To explore the interactions between cellular metabolism and persistent/pathogenic virus infection, we performed untargeted and targeted metabolomic analysis to examine the effects of Cricket paralysis virus (CrPV, Dicistroviridae) in persistently infected silkworm Bm5 cells and acutely infected Drosophila S2 cells. Our previous study (Viruses 2019, 11, 861) established that both glucose and glutamine levels significantly increased during the persistent period of CrPV infection of Bm5 cells, while they decreased steeply during the pathogenic stages. Strikingly, in this study, an almost opposite pattern in change of metabolites was observed during different stages of acute infection of S2 cells. More specifically, a significant decrease in amino acids and carbohydrates was observed prior to pathogenesis, while their abundance significantly increased again during pathogenesis. Our study illustrates the occurrence of diametrically opposite changes in central carbon mechanisms during CrPV infection of S2 and Bm5 cells that is possibly related to the type of infection (acute or persistent) that is triggered by the virus.
Highlights
Infections with cytopathic viruses typically cause cellular lethality, which explains their acute character, leading either to the death of the organism or clearing of the infection by the immune response
A previous study by our group revealed that pathogenic infection of lepidopteran Bm5 cells and dipteran S2 cells with Cricket paralysis virus (CrPV) occurred with different kinetics [11]
Since differences in the kinetics of CrPV infections could serve as a model for studying the parameters that maintain viral persistence versus those that cause pathogenicity, we are interested to investigate how specific metabolites would change in the course of infection and which changes would be characteristic for the transition from persistence to pathogenicity
Summary
Infections with cytopathic viruses typically cause cellular lethality, which explains their acute character, leading either to the death of the organism or clearing of the infection by the immune response. Non-cytopathic viruses can establish readily long-lasting (persistent) infections that manage the evasion of elimination by the immune system for very long periods [1]. Mechanisms to establish viral persistence include modulation of viral gene expression, subversion of apoptosis and immune evasion but can involve the selection of particular cell types that are ideal. Most studies have focused on alterations in the viral genome during establishment of persistent virus infections (and loss of the cytopathic character) in cell lines, e.g., [3,4], evidence exists for the importance of the interaction between the genetic make-up of both host cells and virus [5]. Because of the importance of cellular entry in viral infection, viral tropism is usually distinguished between receptor-dependent and -independent (i.e., intracellular) mechanisms
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
