256C Poster - 02. Immunity and the microbiome
Saturday April 09, 1:30 PM - 3:30 PM

Age-dependent antiviral immunity in Wolbachia-infected Drosophila melanogaster


Authors:
Brian Kmiecik; Casey Goltz; Lakbira Sheffield; Stanislava Chtarbanova

Affiliation: The University of Alabama, Tuscaloosa, AL

Keywords:
l. Wolbachia; k. host/pathogen interactions

Wolbachia (Wolb) is an obligate, maternally-transmitted, intracellular bacterium known to infect ~50% of all insect species on Earth, including Drosophila. One aspect of Wolbachia-Drosophila interactions is a phenomenon called “pathogen blocking,” which corresponds to Wolbachia-mediated protection of Drosophila against pathogenic viral infections. The genetic and molecular mechanisms underlying this protection are not fully understood and are thus an ongoing area of investigation. Moreover, a gap in knowledge exists about the nature of the Wolbachia-Drosophila relationship as a function of host age. This is important to address as the aging process itself affects host physiology, including immunity to viral infections.
We have previously shown that aging impairs the ability of Drosophila to withstand the pathological consequences of infection (the viral ‘tolerance’ mechanism) with the RNA-containing Flock House Virus (FHV). Here, using 149 (66 Wolb-free and 83 Wolb-positive) lines from the Drosophila Genetic Reference Panel (DGRP), we demonstrate that the age-dependent survival of FHV infection is a continuous trait, and is significantly modulated by the presence of Wolb independently of underlying lifespan. For several of the Wolb-positive DGRP lines, we established Wolb-free stocks using standard tetracycline treatment. Our analysis of one line so far, DGRP320, indicates that age-dependent decrease in survival of FHV infection observed in Wolb-free flies is suppressed when Wolb is present in the stock. Using RT-qPCR, we show no significant changes in Wolb 16S gene expression, nor in FHV load between young and aged, Wolb-free and Wolb-positive hosts. Our results indicate that Wolb possibly modulates disease tolerance to FHV with aging, independently of Wolb load.