Publications by authors named "Gregory W Hopkins"
Article Synopsis
- Researchers used a new ultra-low dose (ULD) aerosol model to study tuberculosis in mice, which better simulates natural exposure compared to the traditional low dose (LD) model.
- The ULD model showed that lower doses resulted in infection rates of 27-95%, with an ID50 of 1.6 CFU, indicating a dose-response relationship.
- Differences in lung bacterial loads were significant, with ULD exposed mice showing persistently lower CFU levels and greater variability, suggesting this model may offer insights into human pulmonary tuberculosis.
Article Synopsis
- Multiple factors affect the viability of aerosolized bacteria, including chamber conditions and characteristics of the bioaerosols, highlighting the importance of measuring viable aerosol concentration and particle size for effective lung delivery.
- A multiplex sampling port was added to the Madison chamber to analyze the conditions and bioaerosol characteristics of three pathogens (B. anthracis, Y. pestis, M. tuberculosis) and determine their impact on dose accuracy in small animal models.
- Results showed specific aerosol sizes and viable concentrations for each pathogen, allowing for the calculation of doses presented to mice, and discussed whether the challenge presented optimal conditions for effective bioaerosol exposure.
Organisms within the Mycobacterium avium complex (MAC) may have differential virulence. We compared 33 subjects with MAC pulmonary disease to 75 subjects with a single positive culture without disease. M.
View Article and Find Full Text PDFCCR5 is a chemokine receptor used by HIV-1 to enter cells and has recently been found to act as a pathogen associated molecule pattern receptor. Current positive selection for the high frequency of a CCR5-Delta32 allele in humans has been attributed to resistance to HIV, smallpox, and plague infections. Using an intranasal mouse model of Y.
View Article and Find Full Text PDFArticle Synopsis
- Yersinia pestis, the bacterium responsible for the plague, can kill the roundworm Caenorhabditis elegans (C. elegans) through different mechanisms, including a biofilm-dependent one and a newly discovered biofilm-independent one.
- Research using a specific mutant strain of Y. pestis lacking biofilm-forming genes revealed that the bacteria can still kill C. elegans by accumulating in its intestine, highlighting the complexity of its pathogenic mechanisms.
- The study identified both known and previously unknown virulence-related genes essential for Y. pestis's effectiveness, including a novel gene linked to reduced virulence in mice, suggesting that this model system could help uncover new virulence factors relevant to mammalian infections