How do Persistent Viruses Modulate the Host Immune Response to Maintain Lifelong Infections?
Category: Research Poster
Author(s): Taylor Gelpi
Presenter(s): Taylor Gelpi
Mentors(s): Mark Stenglein
Galbut virus is a segmented double-stranded RNA virus that ubiquitously infects wild Drosophila melanogaster. Little is known about the biology of insect infecting partitiviruses like galbut virus, but this natural infection of a premier model organism provides an excellent opportunity to study persistent virus-host interactions. The role of galbut virus RNA segment 3 is currently unknown. We hypothesize that RNA 3 encodes a viral suppressor of RNAi (VSR), possibly a helicase-like protein that allows the virus to downregulate the insect’s innate immune response and remain dominant in wild D. melanogaster populations. RNA interference (RNAi) in insects serves as an innate anti-viral defense mechanism triggered by dsRNA. When dsRNA is detected, it is cleaved by Dicer-2 into small interfering RNAs which are incorporated into the RNA-induced silencing complex (RISC). Argonaute-2 (Ago-2) can then recognize complementary RNAs to cleave and therefore interfere with viral replication. We aim to test our hypothesis by expressing galbut virus proteins in stably transfected cells and use GFP as a reporter system. GFP fluorescence will decrease in the presence of GFP dsRNA when RNAi is activated. However, any RNAi inhibiting activity of the galbut proteins would inhibit the inhibition, resulting in the persistence of fluorescence. If results suggest suppression of RNAi, additional assays and experiments can be done to determine which step of the RNAi pathway is being targeted. This study ultimately allows for better understanding of how viral infections can modulate the host immune response and remain persistent during lifelong infection.