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Morris, C. P.

Publications and source records attributed to Morris, C. P..

3 recordsLinked to original sources

High-throughput virus quantification using cytopathic effect area analysis by deep learning

Traditional infectivity-based virion quantification methods, such as 50% tissue culture infectious dose (TCID50) and plaque assays, are typically performed in 6-, 12-, 24-, or 48-well cell culture plates and require manual work and analysis based on legacy protocols. Adaptation of these methods to high-throughput formats (96-, 384- or 1,536-well plates) is challenging due to both assay automation constraints and the lack of well surface area available for reliable analysis. Here, we present a scalable alternative to traditional methods that uses whole-well image thresholding to quantify infectious virions by measuring virus-induced cytopathic effect (CPE) via cell lysis and detachment. The CPE area assay is best positioned as a practical high-throughput preliminary screening tool, effectively quantifying samples within the assay range and flagging samples above or below the concentration thresholds. To improve analysis efficiency and reduce user bias in CPE area selection, we evaluated an nnU-Net model for automated image segmentation against images segmented by manually defined brightness thresholds. The model achieved perfect correlation with manual thresholding (R2=1.00), showing minimal differences in the identified CPE area and thus validating nnU-Net as a reliable alternative to manual analysis. This approach provides two complementary pipelines: manual thresholding, which tolerates adjustments of hyperparameters, and fully automated segmentation via nnU-Net, which streamlines analysis and enhances throughput. This flexible CPE area assay enables accurate and automated quantification in high-throughput screening formats, thereby greatly accelerating a routine laboratory task while decreasing subjectivity and bias. Author summaryMeasuring the amount of virus in a biosample is a critical part of viral research and testing of new treatments. Traditional methods are slow, labor-intensive, and not easily scaled up to handle large numbers of samples. In this study, we developed a new approach that makes the process faster, more efficient, scalable, and less reliant on manual steps. We used microscopy imaging to capture how cells respond to virus infections and analyzed these images automatically to identify and measure areas where the virus had damaged cells. The analysis pipeline allows researchers to fine-tune settings or run the process using machine learning. This method is flexible and adaptable to a variety of viruses and experiments. By increasing the number of samples that can be tested at once while reducing the time and effort needed for analysis, our approach has the potential to accelerate research in virology, drug development, and public health.

microbiology↗

Bma-LAD-2, an intestinal cell adhesion protein, as a potential therapeutic target for lymphatic filariasis

Lymphatic filariasis (LF) is a debilitating disease that afflicts over 70 million people worldwide. It is caused by the parasitic nematodes Wuchereria bancrofti, Brugia malayi, and Brugia timori. While efforts to eliminate LF have seen substantial success, complete eradication will likely require more time and resources than predicted. Identifying new drug and vaccine targets in adult filariae could help elimination efforts. This studys aim was to evaluate intestinal proteins in adult Brugia malayi worms as possible therapeutic targets. Using siRNA, we successfully inhibited transcripts of four candidate genes: Bma-Serpin, Bma-ShTK, Bma-Reprolysin, and Bma-LAD-2. Of those, Bma-LAD-2, an immunoglobulin superfamily cell adhesion molecule (IgSF CAM), was determined to be essential for adult worm survival. We observed a 70.42% knockdown in Bma-LAD-2 transcript levels 1 day post-siRNA incubation and an 87.02% reduction in protein expression 2 days post-siRNA incubation. This inhibition of Bma-LAD-2 expression resulted in an 80% decrease in worm motility over 6 days, a 93.43% reduction in microfilaria release (Mf) by day 6 post-siRNA incubation, and a significant decrease in MTT reduction. Transmission electron microscopy revealed the loss of microvilli and unraveling of mitochondrial cristae in the intestinal epithelium of Bma-LAD-2 siRNA-treated worms. Strikingly, Bma-LAD-2 siRNA-treated worms exhibited an almost complete loss of pseudocoelomic fluid, suggesting that loss of these tight junctions led to the leakage and subsequent loss of the worms structural integrity. Luciferase immunoprecipitation system assay demonstrated that serum from 30 patients with LF did not have detectable IgE antibodies against Bma-LAD-2, indicating that LF exposure does not result in IgE sensitization to this antigen. These results indicate that Bma-LAD-2 is an essential protein for adult Brugia malayi and may be an effective drug or vaccine target. In addition, these findings further validate the strategy of targeting the worm intestine to prevent and treat helminthic infections. Author SummaryBrugia malayi is a parasitic nematode that can cause lymphatic filariasis, a debilitating disease prevalent in tropical and subtropical countries. Significant progress has been made towards eliminating the disease. However, complete eradication may require new therapeutics such as drugs or a vaccine that kill adult filariae. In this study, we identified an immunoglobulin superfamily cell adhesion molecule (Bma-LAD-2) as a potential drug and vaccine candidate. When we knocked down Bma-LAD-2 expression, we observed a decrease in worm motility, fecundity, and metabolism. We also visualized the loss of microvilli, destruction of the mitochondria in the intestinal epithelium, and loss of pseudocoelomic fluid contents after Bma-LAD-2 siRNA treatment. Finally, we demonstrated that serum from filaria-infected patients does not contain preexisting IgE to Bma-LAD-2, which indicates that this antigen would likely be safe to administer as a vaccine in endemic populations.

microbiology↗

Accelerated DNA methylation aging and increased resilience in veterans: the biological cost for soldiering on

Accelerated epigenetic aging, the difference between the DNA methylation-predicted age (DNAm age) and the chronological age, is associated with a myriad of diseases. This study investigates the relationship between epigenetic aging and risk and protective factors of PTSD. Genome-wide DNA methylation analysis was performed in 211 individuals including combat-exposed Australian veterans (discovery cohort, n = 96 males) and trauma-exposed civilian males from the Grady Trauma Project (replication cohort, n = 115 males). Primary measures included the Clinician Administered PTSD Scale for DSM-5 and the Connor-Davidson Resilience Scale (CDRISC). DNAm age prediction was performed using the validated epigenetic clock calculator. Veterans with PTSD had increased PTSD symptom severity (P-value = 3.75 x 10-34) and lower CDRISC scores (P-value = 7.5 x 10-8) than veterans without PTSD. DNAm age was significantly correlated with the chronological age (P-value = 3.3 x 10-6), but DNAm age acceleration was not different between the PTSD and non-PTSD groups (P-value = 0.24). Evaluating potential protective factors, we found that DNAm age acceleration was significantly associated with CDRISC resilience scores in veterans with PTSD, these results remained significant after multiple testing correction (P-value = 0.023; r = 0.32). This finding was also replicated in an independent trauma-exposed civilian cohort (P-value = 0.02; r = 0.23). Post-hoc factor analyses revealed that this association was driven by \"self-efficacy\" items within the CDRISC (P-value = 0.015). These results suggest that among individuals already suffering from PTSD, some aspects of increased resilience might come at a biological cost.

genomics↗