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The COVID-19 pandemic has severely disrupted worldwide supplies of viral transport media (VTM) due to widespread demand for SARS-CoV-2 RT-PCR testing. In response to this ongoing shortage, we began production of VTM in-house in support of diagnostic testing in our hospital network. As our diagnostic laboratory was not equipped for reagent production, we took advantage of space and personnel that became available due to closure of the research division of our medical center. We utilized a formulation of VTM described by the CDC that was simple to produce, did not require filtration for sterilization, and used reagents that were available from commercial suppliers. Performance of VTM was evaluated by several quality assurance measures. Based on Ct values of spiking experiments, we found that our VTM supported highly consistent amplification of the SARS-CoV-2 target (coefficient of variation = 2.95%) using the Abbott RealTime SARS-CoV-2 EUA assay on the Abbott m2000 platform. VTM was also found to be compatible with multiple swab types and, based on accelerated stability studies, able to maintain functionality for at least four months at room temperature. We further discuss how we met logistical challenges associated with large-scale VTM production in a crisis setting including use of staged, assembly line for VTM transport tube production.
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http://dx.doi.org/10.1101/2020.04.29.20085514 | DOI Listing |
J Virol
September 2025
Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Double-stranded RNA (dsRNA), which induces an innate immune response against viral infections, is rarely detected in influenza A virus (IAV)-infected cells. Nevertheless, we previously reported that the influenza A viral ribonucleoprotein (vRNP) complex generates looped dsRNAs during RNA synthesis . This finding suggests that IAV possesses a specific mechanism for sequestering dsRNA within infected cells, thereby enabling viral evasion of the innate immune response.
View Article and Find Full Text PDFMicrobiol Spectr
September 2025
Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China.
Modulating cell endocytosis activity to reduce host susceptibility to virus represents a promising strategy for antiviral drug development. In this study, we reveal that lactate transporter SLC16A3 is a critical host factor for reducing diverse virus invasion. By performing metabolomics, proteomics, and thermal proteome profiling experiments, AP1G1, a pivotal protein involved in cellular endocytosis, was indiscriminately screened as a chaperone of SLC16A3.
View Article and Find Full Text PDFLung
September 2025
The Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, 97 Lisburn Road, Belfast, Belfast BT9 7BL, UK.
Introduction: Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV's effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly via the release of mediators from infected epithelial cells.
View Article and Find Full Text PDFPestic Biochem Physiol
November 2025
Newcastle University, School of Natural and Environmental Sciences, Newcastle upon Tyne, UK NE1 7RU. Electronic address:
RNA interference (RNAi) is an endogenous eukaryote viral defence mechanism representing a unique form of post-transcriptional gene silencing that can be induced via the exongenous application of dsRNA. Due to its high specificity, dsRNA-based biopesticides are being developed to control pest insects. Whilst many lepidopteran species are recalcitrant to RNAi, Tuta absoluta, a polyphagous insect responsible for extensive crop damage, is sensitive.
View Article and Find Full Text PDFCancer Res
September 2025
Zhongnan Hospital of Wuhan University, Wuhan, China.
Tumor metabolic reprogramming has been recognized as a critical determinant in tumor development and cancer immunotherapy response. Aberrant choline metabolism is emerging as a defining hallmark of cancer. Here, we found that carbohydrate responsive element binding protein (ChREBP)-mediated choline deprivation induced tumor-associated macrophage (TAM) reprogramming and maintained an immunosuppressive tumor microenvironment (TME).
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