Drosophila melanogaster depends upon the innate immune system to regulate and combat viral infection. This is a complex, yet widely conserved process that involves a number of immune pathways and gene interactions. In addition, expression of genes involved in immunity are differentially regulated as the organism ages. This is particularly true for viruses that demonstrate chronic infection, as is seen with Nora virus. Nora virus is a persistent non-pathogenic virus that replicates in a horizontal manner in D. melanogaster. The genes involved in the regulation of the immune response to Nora virus infection are largely unknown. In addition, the temporal response of immune response genes as a result of infection has not been examined. In this study, D. melanogaster either infected with Nora virus or left uninfected were aged for 2, 10, 20 and 30 days. The RNA from these samples was analyzed by next generation sequencing (NGS) and the resulting immune-related genes evaluated by utilizing both the PANTHER and DAVID databases, as well as comparison to lists of immune related genes and FlyBase. The data demonstrate that Nora virus infected D. melanogaster exhibit an increase in immune related gene expression over time. In addition, at day 30, the data demonstrate that a persistent immune response may occur leading to an upregulation of specific immune response genes. These results demonstrate the utility of NGS in determining the potential immune system genes involved in Nora virus replication, chronic infection and involvement of antiviral pathways.

An azide appended 2,3-naphtahlimide (AHS) is functionalized as a fluorescence approach for quantitative detection of H2S in the range of 0–100 μM. In the presence of H2S, AHS displayed a 17-fold fluorescence enhancement that showed a highly linear correlation with H2S level.

The fruit fly, Drosophila melanogaster, is an extremely useful model to study innate immunity mechanisms. A fundamental understanding of these mechanisms as they relate to various pathogens has come to light over the past 30 years. The discovery of Toll-like receptors and their recognition of shared molecules (pathogen-associated molecular patterns or PAMPs) among pathogenic bacteria were the first detailed set of receptors to be described that act in innate immunity. The immune deficiency pathway (Imd) described in D. melanogaster functions in a very similar way to the Toll pathway in recognizing PAMPs primarily from Gram-negative bacteria. The discovery of small interfering RNAs (RNAi) provided a means by which antiviral immunity was accomplished in invertebrates. Another related pathway, the JAK/STAT pathway, functions in a similar manner to the interferon pathways described in vertebrates, also providing antiviral defense. Recently, autophagy was also shown to function as a protective pathway against virus infection in D. melanogaster. At least three of these pathways (Imd, JAK/STAT, and RNAi) show signal integration in response to viral infection, demonstrating a coordinated immune response against viral infection. The number of pathways and the integration of them reflect the diversity of pathogens to which innate immune mechanisms must be able to respond. The viral pathogens that infect invertebrates have developed countermeasures to some of these pathways, in particular to RNAi. The evolutionary arms race of pathogen vs. host is ever ongoing.

S. aureus accounts for approximately 80,000 infections every year, resulting in 11,000 deaths. While antibiotic resistance has been researched heavily, antibiotic tolerance has not. Persister cells are dormant like cells that are tolerant to antibiotic treatment. Persister cells could be the cause of many chronic and relapsing infections. Recent experiments have shown central metabolism is a critical component of persister cell formation. Results suggest that interruptions in the tricarboxylic acid (TCA) cycle increase persister cell formation. While many studies have been performed concerning the mechanism of formation of persister cells, few have been done to analyze how persister cells react in in vivo models or against aspects of the innate immune system. Antimicrobial peptides (AMPs) are a key component of the innate immune system. Challenging wild type S. aureus with AMPs, LL-37 and hBD-3, showed several logs of killing. Interruption of the TCA cycle (fumC) resulted in 100-fold more surviving cells compared to wild type. Following infection in Drosophila melanogaster, the fumC knockout exhibited increased survival. Furthermore, D. melanogaster that were infected with fumC had reduced survival. Interruption of the TCA cycle also led to increased survival within a macrophage suggesting persister cells represent a multifaceted problem for the immune system. These data suggest that persisters not only present a challenge during antimicrobial therapy but also for the innate immune system.