ArticlePLoS pathogens2018
p38b and JAK-STAT signaling protect against Invertebrate iridescent virus 6 infection in Drosophila.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 78 citations in OpenAlex.
- The JAK-STAT pathway in invertebrates: An emerging battleground for host‒virus warfare.Insect science · 2026Review
- A non-canonical JAK/STAT pathway promotes viral replication through the lipoprotein receptor-related protein in ticks.PLoS biology · 2026Article
- Tissue- and time-dependent modulation of JAK/STAT pathway genes in Tenebrio molitor during Listeria monocytogenes infection.World journal of microbiology & biotechnology · 2026Article
- Rethinking Disease Control in Aquaculture Invertebrates: Harnessing Innate Immunity in Molluscs and Crustaceans.Pathogens (Basel, Switzerland) · 2026Review
- CircRNA-encoded protein fine-tunes ROS homeostasis and engages conserved JAK-STAT antiviral defenses inJournal of virology · 2026Article
- From gatekeeper to target: MAPK cascades as control circuits at the insect-microbe interface.FEMS microbiology reviews · 2026Review
- Cytosolic mtDNA and associated EYA-mediated pro-inflammatory signaling modulate healthspan in Drosophila.Research square · 2025Article
- The Function of TER94 of Spodoptera frugiperda 9 Cells When Infected With Invertebrate Iridescent Virus-6.Journal of basic microbiology · 2025Article
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- Downregulation ofFrontiers in microbiology · 2024Article
- Double-edged sword of JAK/STAT signaling pathway in viral infections: novel insights into virotherapy.Cell communication and signaling : CCS · 2023Review
- Population mixing mediates the intestinal flora composition and facilitates invasiveness in a globally invasive fruit fly.Microbiome · 2023Article
- Unraveling the Role of Antimicrobial Peptides in Insects.International journal of molecular sciences · 2023Review
- The JAK-STAT pathway promotes persistent viral infection by activating apoptosis in insect vectors.PLoS pathogens · 2023Article
- Drosophila caspases as guardians of host-microbe interactions.Cell death and differentiation · 2023Review
- The Intestinal Immune Defense System in Insects.International journal of molecular sciences · 2022Review
- A balance between vector survival and virus transmission is achieved through JAK/STAT signaling inhibition by a plant virus.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The fruit fly Drosophila melanogaster is a powerful model system for the study of innate immunity in vector insects as well as mammals. For vector insects, it is particularly important to understand all aspects of their antiviral immune defenses, which could eventually be harnessed to control the transmission of human pathogenic viruses. The immune responses controlling RNA viruses in insects have been extensively studied, but the response to DNA virus infections is poorly characterized. Here, we report that infection of Drosophila with the DNA virus Invertebrate iridescent Virus 6 (IIV-6) triggers JAK-STAT signaling and the robust expression of the Turandots, a gene family encoding small secreted proteins. To drive JAK-STAT signaling, IIV-6 infection more immediately induced expression of the unpaireds, a family of IL-6-related cytokine genes, via a pathway that required one of the three Drosophila p38 homologs, p38b. In fact, both Stat92E and p38b were required for the survival of IIV-6 infected flies. In addition, in vitro induction of the unpaireds required an NADPH-oxidase, and in vivo studies demonstrated Nox was required for induction of TotA. These results argue that ROS production, triggered by IIV-6 infection, leads to p38b activation and unpaired expression, and subsequent JAK-STAT signaling, which ultimately protects the fly from IIV-6 infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.