To evaluate the use of wastewater-based surveillance and epidemiology to monitor and predict SARS-CoV-2 virus trends, over the 2020–2021 academic year we collected wastewater samples twice weekly from 17 manholes across Virginia Tech’s main campus. We used data from external door swipe card readers and student isolation/quarantine status to estimate building-specific occupancy and COVID-19 case counts at a daily resolution. After analyzing 673 wastewater samples using reverse transcription quantitative polymerase chain reaction (RT-qPCR), we reanalyzed 329 samples from isolation and nonisolation dormitories and the campus sewage outflow using reverse transcription digital droplet polymerase chain reaction (RT-ddPCR). Population-adjusted viral copy means from isolation dormitory wastewater were 48% and 66% higher than unadjusted viral copy means for N and E genes (1846/100 mL to 2733/100 mL/100 people and 2312/100 mL to 3828/100 mL/100 people, respectively; n = 46). Prespecified analyses with random-effects Poisson regression and dormitory/cluster-robust standard errors showed that the detection of N and E genes were associated with increases of 85% and 99% in the likelihood of COVID-19 cases 8 days later (incident–rate ratio (IRR) = 1.845, p = 0.013 and IRR = 1.994, p = 0.007, respectively; n = 215), and one-log increases in swipe card normalized viral copies (copies/100 mL/100 people) for N and E were associated with increases of 21% and 27% in the likelihood of observing COVID-19 cases 8 days following sample collection (IRR = 1.206, p < 0.001, n = 211 for N ; IRR = 1.265, p < 0.001, n = 211 for E ). One-log increases in swipe normalized copies were also associated with 40% and 43% increases in the likelihood of observing COVID-19 cases 5 days after sample collection (IRR = 1.403, p = 0.002, n = 212 for N ; IRR = 1.426, p < 0.001, n = 212 for E ). Our findings highlight the use of building-specific occupancy data and add to the evidence for the potential of wastewater-based epidemiology to predict COVID-19 trends at subsewershed scales.

Following the adventive arrival, subsequent spread, and ensuing impact of Adelges tsugae Annand (Hemiptera: Adelgidae), the hemlock woolly adelgid (HWA) in the eastern United States, a robust initiative was launched with the goal of decreasing ecosystem impacts from the loss of eastern hemlock (Pinales: Pinaceae). This initiative includes the use of biological control agents, including Laricobius spp. (Insecta: Coleoptera). Laboratory production of these agents is limited by subterranean mortality and early emergence. Therefore, the subterranean survivorship and timing of emergence of a mixture of Laricobius spp. was investigated. PVC traps internally lined with a sticky card and covered with a mesh screen were inserted into the soil to measure the percent emergence of adults based on the number of larvae placed within. The number of emerged adults in the field and laboratory-reared larval treatments was adjusted based on emergence numbers in the control and used as the response variable. Independent variables included in the final model were: treatment (field-collected vs. laboratory-reared), organic layer depth (cm), soil pH, and April-to-December mean soil moisture. No differences were found in survivorship between field-collected and laboratory-reared treatments. As pH and organic layer increased survivorship decreased, significantly. Although the majority of emergence occurred in the fall, emergence also occurred in spring and summer. The occurrence of spring and summer emergence and low survivorship (17.1 ± 0.4%) in the field across all treatments suggests that these are characteristics of Laricobius spp. field biology in their introduced range and not artifacts of the laboratory rearing process.

A variety of pulmonary insults can result in the necessity for mechanical ventilation, which, when misused, used for prolonged periods of time, or associated with an excessive inflammatory response, can result in ventilator-induced lung injury. Older patients have been observed to have an increased risk for respiratory distress with ventilation and more recent studies suggest that this could be linked to disparities in the inflammatory response. To address this, we ventilated young (2-3 months) and old (20-25 months) mice for 2 hours using high pressure mechanical ventilation and extracted data for inflammatory cell ratios, namely macrophage phenotypes, and lung tissue integrity. A large difference in naive macrophages at baseline, alternatively-activated (M2) macrophages at baseline, and airspace enlargement after ventilation was observed in the old mice. The experimental data was used to fit a mathematical model for the inflammatory response to lung injury. Model variables include inflammatory markers and cells, namely neutrophils and macrophages, epithelial cells at varying states, and repair mediators. Parameter sampling was performed using an iterative sampling method and parameter sets were selected based on their ability to fit either the old or young macrophage phenotype percentages and epithelial variables at zero and two hours. Classification methods were performed to identify influential parameters separating the old and young parameter sets as well as user-defined health states. Parameters involved in repair and damage to epithelial cells and parameters regulating the pro-inflammatory response were shown to be important. Local sensitivity analysis preformed for the different epithelial cell variables produced similar results. A pseudo-intervention was also performed on the parameter sets. The results were most influential for the old parameter sets, specifically those with poorer lung health. These results indicate potential targets for therapeutic interventions prior to and during ventilation, particularly for old subjects.Author summaryA variety of inhaled pathogens and other pulmonary insults prompt the need for mechanical ventilation; a procedure that has become increasingly necessary following the 2019 coronavirus pandemic. A proportion of patients respond poorly to ventilation, some resulting in ventilator-induced lung injury. Observational data has shown increased instance of severe disease in older patients as well as differences in the inflammatory response to injury, although more research is needed to confirm this. We performed high-pressure ventilation on young (2-3 months) and old (20-25 months) mice and observed large disparities in inflammatory cell ratios at baseline and lung tissue integrity after ventilation. The experimental data was then used to fit a mathematical model of the inflammatory response to lung injury. We used a variety of analysis methods to identify important parameters separating the young and old parameter sets and user-defined health states of the resulting simulations. Parameters involved in damage and repair of epithelial cells in the lung as well as parameters controlling the pro-inflammatory response to injury were important in both classifying between old and young sets and determining predicted health after ventilation. These results indicate potential targets for therapeutic interventions prior to and during ventilation.