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Dengue virus serotypes 1-4 (DENV1-4) have spread through tropical and subtropical countries, causing endemic and epidemic diseases. Recently, a novel field approach using the Wolbachia symbiont was proposed to suppress DENV transmission via the mosquito vectors Aedes aegypti and Aedes albopictus. Previously, we showed that a Wolbachia strain, wMelPop, suppresses DENV2 replication in the C6/36 albopictus cell line, with the mutant DENV2 appearing and replacing the wild type DENV2. In this study, we expanded the analysis to include replications of all DENV serotypes 1-4, effects of wAu Wolbachia in C6/36 cells, and wMelPop-influences on the Aag2 aegypti cell line. It was revealed that both wAu and wMelPop reduce all DENV infectious titers without dominant appearances of the mutant viruses, despite varied effects on the viral copy numbers. The host transcriptomic profiles by RNA-seq were also variously altered by wAu and wMelPop (ranging from 10 to 30%, Log2FC > 2 or <−2, p < 0.05). Those transcripts were not further altered by DENV infection. In contrast, abundant transcriptomic alterations by DENV infection in naïve C6/36 and Aag2 cells were blocked by either wAu or wMelPop. These results indicate that Wolbachia prevents host cellular transcriptomic alterations which are induced by DENV infection, affecting the cellular homeostasis necessary for DENV replication.

Dengue virus serotypes 1-4 (DENV1-4) have spread through tropical and subtropical countries, causing endemic and epidemic diseases. Recently, a novel field approach using the symbiont was proposed to suppress DENV transmission via the mosquito vectors and . Previously, we showed that a strain, MelPop, suppresses DENV2 replication in the C6/36 cell line, with the mutant DENV2 appearing and replacing the wild type DENV2. In this study, we expanded the analysis to include replications of all DENV serotypes 1-4, effects of Au in C6/36 cells, and MelPop-influences on the Aag2 cell line. It was revealed that both Au MelPop reduce all DENV infectious titers without dominant appearances of the mutant viruses, despite varied effects on the viral copy numbers. The host transcriptomic profiles by RNA-seq were also variously altered by Au and MelPop (ranging from 10 to 30%, Log FC > 2 or <-2, < 0.05). Those transcripts were not further altered by DENV infection. In contrast, abundant transcriptomic alterations by DENV infection in naïve C6/36 and Aag2 cells were blocked by either Au MelPop. These results indicate that prevents host cellular transcriptomic alterations which are induced by DENV infection, affecting the cellular homeostasis necessary for DENV replication.

You may be wondering who Super Dave is! Well his real name is Dave Durepos, and this is his story . . . A number of years ago, Dave was just a regular guy travelling home on his motorcycle, until one night he hit a sharp turn and his world came crashing down before his eyes. He flipped his motorcycle into a rocky ravine. Dave became a paraplegic that night. Doctors weren't sure he'd make it, but he did.

The progressive impairment of immunity to pathogens and vaccines with aging is a significant public health problem as the world population shifts to an increased percentage of older adults (> 65). We have previously demonstrated that cells obtained from older volunteers have delayed and defective induction of type I interferons and T cell and B cell helper cytokines in response to TLR ligands when compared to those from adult subjects. However, the underlying intracellular mechanisms are not well described. Herein, we studied two critical pathways important in the production of type I interferon (IFN), the interferon response factor 7 (pIRF7), and TANK-binding kinase (pTBK-1). We show a decrease in pIRF7 and pTBK-1 in cross-priming dendritic cells (cDC1s), CD4 + T cell priming DCs (cDC2s), and CD14 dim CD16 + vascular patrolling monocytes from older adults ( n  = 11) following stimulation with pathway-specific agonists in comparison with young individuals ( n  = 11). The decrease in these key antiviral pathway proteins correlates with decreased phagocytosis, suggesting impaired function in Overall, our findings describe molecular mechanisms which explain the innate functional impairment in older adults and thus could inform us of novel approaches to restore these defects. Graphical abstract