This is a report collecting publications that describe Drosophila models of infection by viruses that can infect humans. There are detailed reports available for Drosophila models of infection by specific viruses or families of viruses, see the 'Related Diseases' section below.
There are two prevalent methods to study infection using Drosophila: direct infection and transgenic expression of pathogenic proteins. For a review of fly models using transgenic expression of pathogenic proteins see Harnish et al., 2021 (FBrf02488558).
This report does not cover interactions with viruses that do not infect humans, or the mechanics of the innate immune system response in general rather than in response to a specific virus.
[updated May 2021 by FlyBase; FBrf0222196]
Cell-mediated immunity in insects includes phagocytosis, nodulation, encapsulation, and melanization, and is primarily mediated by the hemocytes or blood cells. The majority of blood cells constitute the macrophage-like plasmatocytes (90-95% of hemocytes in Drosophila that are specialized in the engulfment and degradation of cellular debris, debris and invading pathogens. (Swevers et al. 2018 and references therein, FBrf0238851.)
In Drosophila, the major RNAi pathway involved in antiviral immunity is initiated by the processing of virus-derived dsRNA molecules to viral small interfering RNAs (viral siRNAs or vsiRNAs) by Dicer-2 (Dcr-2) enzyme. Viral siRNAs are subsequently loaded in an effector complex named RISC (RNAi-induced silencing complex) with Argonaute 2 (AGO2) as central molecule. SiRNA-programmed RISC complexes subsequently scan cellular RNA populations for complementary sequences and cause specific RNA degradation after specific siRNA-mRNA hybridization. The central factors of the siRNA pathway, Dcr-2 and AGO2, were demonstrated to have undergone accelerated evolution as a consequence of adaptive virus-host arms races. (Swevers et al. 2018 and references therein, FBrf0238851.)