Viruses in Laboratory Drosophila and Their Impact on Host Gene Expression

Abstract

Drosophila melanogaster has one of the best characterized antiviral immune responses among invertebrates. However, relatively few easily transmitted natural virus isolates are available, and so many Drosophila experiments have been performed using artificial infection routes and artificial host–virus combinations. These may not reflect natural infections, especially for subtle phenotypes such as gene expression. Here, to explore the laboratory virus community and to better understand how natural virus infections induce changes in gene expression, we have analysed seven publicly available D. melanogaster transcriptomic sequencing datasets that were originally sequenced for projects unrelated to virus infection. We have found ten known viruses—including five that have not been experimentally isolated—but no previously unknown viruses. Our analysis of host gene expression revealed that numerous genes were differentially expressed in flies that were naturally infected with a virus. For example, flies infected with nora virus showed patterns of gene expression consistent with intestinal vacuolization and possible host repair via the upd3 JAK/STAT pathway. We also found marked sex differences in virus-induced differential gene expression. Our results show that natural virus infection in laboratory Drosophila does indeed induce detectable changes in gene expression, suggesting that this may form an important background condition for experimental studies in the laboratory.

Viral infection disrupts intestinal homeostasis via Sting-dependent NF-kB signaling

“…Persistent viral infections are common in arthropods and are known to be widespread in laboratory reared D. melanogaster , where Nora virus and DAV have reported prevalence of up to 52% and 18%, respectively 28 . Persistent viral infections are generally considered to pose no or only minor fitness costs for the host 27 , but there is relatively little published experimental data to support this claim and emerging studies demonstrate significant fitness impacts of persistent viral infection in D. melanogaster 90,91 .…”

“…Persistent viral infections are generally considered to pose no or only minor fitness costs for the host 27 , but there is relatively little published experimental data to support this claim and emerging studies demonstrate significant fitness impacts of persistent viral infection in D. melanogaster 90,91 . Moreover, re-analyses of published RNA-seq data from laboratory reared flies revealed previously undetected infections with several viruses including Nora virus, Thika virus, and DAV that induced significant changes in the host transcriptome 28,92 . Here we found that persistent infections with DAV, DCV, Nora virus, and Bloomfield virus all promote ISC proliferation and are associated with intestinal dysplasia (Figure S1).…”

“…It is made available under a preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in The copyright holder for this this version posted November 16, 2023. ; https://doi.org/10.1101/2023.11. 16.567400 doi: bioRxiv preprint impacts on host fitness and physiology [27][28][29] . Some of the most prevalent viruses of D. melanogaster, including Drosophila C virus (DCV), Nora virus, and Galbut virus [30][31][32] , are known to infect the intestinal epithelium, but the potential impacts of viral infection on intestinal homeostasis have not been examined.…”