Abstract
Single-cell RNA sequencing (scRNA-seq) offers the possibility to monitor both host and pathogens transcriptomes at the cellular level. Here, public scRNA-seq datasets from Drosophila melanogaster midgut cells were used to compare the differences in replication strategy and cellular responses between two fly picorna-like viruses, Thika virus (TV) and D. melanogaster Nora virus (DMelNV). TV exhibited lower levels of viral RNA accumulation but infected a higher number of cells compared to DMelNV. In both cases, viral RNA accumulation varied according to cell subtype. The cellular heat shock response to TV and DMelNV infection was cell-subtype- and virus-specific. Disruption of bottleneck genes at later stages of infection in the systemic response, as well as of translation-related genes in the cellular response to DMelNV in two cell subtypes, may affect the virus replication.
Highlights
Single-cell RNA sequencing offers the possibility to monitor both host and pathogens transcriptomes at the cellular level
Single-cell profiling of Ebola virus (EBOV)-infected immune cells from rhesus macaques revealed that interferon-stimulated genes (ISGs) are down-regulated in infected cells compared to bystanders [1], shedding light into previous seemingly contradictory results from studies of EBOV infection in culture and in vivo, where ISGs and downstream signaling genes were, respectively, down- and up-regulated compared to their healthy counterparts [2,3,4,5,6,7]
Studies using scRNA-seq found that bystander cells from mice infected with influenza virus A (IAV), and bystander cells from patients positive for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) show an over-expression of ISGs compared to cells from healthy individuals [8,9], stressing the importance of a systemic response to these respiratory viruses
Summary
Single-cell RNA sequencing (scRNA-seq) offers the possibility to monitor both host and pathogens transcriptomes at the cellular level. Studies using scRNA-seq found that bystander cells from mice infected with influenza virus A (IAV), and bystander cells from patients positive for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) show an over-expression of ISGs compared to cells from healthy individuals [8,9], stressing the importance of a systemic response to these respiratory viruses. This powerful technique has been largely applied to viral infections in mammalian cells, and studies in non-mammalian hosts are currently missing. Overexpression of the heat shock factor (Hsf) and Hsp induce resistance to viral infections in transgenic flies
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