Turner, E. A. | Search bioRxiv

bioRxiv2024

The good, the BATV, and the ugly - first report of BATV vector competence in Culex quinquefasciatus from the Southern United States

Batai virus is an arbovirus with wide geographic, host, and climactic ranges. BATV infects primarily avian species but can cause disease in ruminants and humans. Louisiana is at particular risk for overlaps in natural and agricultural systems as the Mississippi Flyway passes through the state. We assessed the vector competence of Louisiana Cx. quinquefasciatus for BATV and found infection and dissemination rates of 22% and 11.1% at 7 days post-exposure (dpe), and 15.8% and 5.3% at 21dpe. The current H5N1 avian influenza outbreak in dairy cows demonstrates the importance of understanding the overlap in avian and other vertebrate species to inform public health and agricultural biosecurity. Results indicate a moderate vector competence of regional Louisiana Cx. quinquefasciatus for BATV. This study presents the first known report of vector competence of BATV in US mosquitoes and establishes the non-zero risk of its emergence in the southern US.

ecology↗

bioRxiv2020

Early-life mitochondrial DNA damage results in lifelong deficits in energy production mediated by redox signaling in Caenorhabditis elegans

The consequences of damage to the mitochondrial genome (mtDNA) are poorly understood, although mtDNA is more susceptible to damage than nuclear DNA (nucDNA), and many environmental toxicants target the mitochondria. Reports from the toxicological literature suggest that exposure to early-life mitochondrial damage could lead to deleterious consequences later in life (the "Developmental Origins of Health and Disease" paradigm) but reports from other fields often report beneficial ("mitohormetic") responses to such damage. Here, we test the effects of low (causing no change in lifespan) levels of ultraviolet C (UVC)-induced, irreparable mtDNA damage during early development in Caenorhabditis elegans. This exposure led to life-long reductions in mtDNA copy number and steady-state ATP levels, accompanied by increased oxygen consumption and altered metabolite profiles, suggesting inefficient mitochondrial function. Exposed nematodes were also developmentally delayed, reached smaller adult size, and were rendered more susceptible to subsequent exposure to chemical mitotoxicants. Metabolomic and genetic analysis of key signaling and metabolic pathways supported redox signaling during early development as a mechanism for establishing these persistent alterations. Our results highlight the importance of early-life exposures to environmental pollutants, especially in the context of exposure to chemicals that target mitochondria.

cell biology↗