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.
Highlights
Like all multicellular organisms, insects face a constant threat of infection from a wide array of microorganisms, including viral, bacterial, and fungal pathogens
While we know a great deal regarding how insects combat RNA viruses, we know little about their immune response to DNA virus infections
Studies of DNA virus infections may reveal novel immune mechanisms, which could be uniquely effective against DNA virus infections or could be broadly effective against many viruses
Summary
Insects face a constant threat of infection from a wide array of microorganisms, including viral, bacterial, and fungal pathogens Insects combat these infections with both static and inducible defenses, including a chitinous exoskeleton, circulating phagocytes and the induction of host defense genes, such as antimicrobial peptides [1]. The siRNA response is triggered when viral dsRNA intermediates, either derived directly from the viral genome or produced as an intermediate during replication or transcription, are recognized by Dicer-2, which processes these dsRNAs into 21 basepair fragments and loads them onto Argonaute-2 This complex, termed an RNA-Induced Silencing Complex (RISC), is able to destroy its complementary target sequence. While antiviral effects of Vago have only been shown upon Drosophila C virus (DCV) infection of flies, mosquito Vago was induced upon flavivirus infections of Culicine cell lines and animals and was suggested to be antiviral [10, 11]
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