Mycobacterium tuberculosis does not show evidence of molecular DNA in human cadaveric ocular tissues in an endemic setting

2019 ◽  
Vol 48 (1) ◽  
pp. 69-77 ◽  
Author(s):  
Harish Chauhan ◽  
Reema Bansal ◽  
Aman Kumar ◽  
Surya P. Sharma ◽  
Geethanjali Gude ◽  
...  
2014 ◽  
Vol 7 (1) ◽  
pp. 512 ◽  
Author(s):  
Wassihun Wedajo ◽  
Thomas Schön ◽  
Ahmed Bedru ◽  
Teklu Kiros ◽  
Elena Hailu ◽  
...  

2001 ◽  
Vol 69 (5) ◽  
pp. 3264-3270 ◽  
Author(s):  
J. Turner ◽  
M. Gonzalez-Juarrero ◽  
B. M. Saunders ◽  
J. V. Brooks ◽  
P. Marietta ◽  
...  

ABSTRACT In this study different inbred strains of mice appeared to control and contain a low dose aerosol infection with Mycobacterium tuberculosis in a similar manner, giving rise to a chronic state of disease. Thereafter, however, certain strains gradually began to show evidence of regrowth of the infection, whereas others consistently did not. Using C57BL/6 mice as an example of a resistant strain and CBA/J mice as an example of a strain susceptible to bacterial growth, we found that these animals revealed distinct differences in the cellular makeup of lung granulomas. The CBA/J mice exhibited a generally poor lymphocyte response within the lungs and vastly increased degenerative pathology at a time associated with regrowth of the infection. As a possible explanation for these events, it was then observed that the CBA/J mouse strain was also less able to upregulate adhesion molecules, including CD11a and CD54, on circulating lymphocytes. These results therefore suggest that a failure to control a chronic infection with M. tuberculosis may reflect an inability to localize antigen-specific lymphocytes within the lung.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Aditi Gupta ◽  
David Alland

AbstractMycobacterium tuberculosis can adapt to changing environments by non-heritable mechanisms. Frame-shifting insertions and deletions (indels) may also participate in adaptation through gene disruption, which could be reversed by secondary introduction of a frame-restoring indel. We present ScarTrek, a program that scans genomic data for indels, including those that together disrupt and restore a gene’s reading frame, producing “frame-shift scars” suggestive of reversible gene inactivation. We use ScarTrek to analyze 5977 clinical M. tuberculosis isolates. We show that indel frequency inversely correlates with genomic linguistic complexity and varies with gene-position and gene-essentiality. Using ScarTrek, we detect 74 unique frame-shift scars in 48 genes, with a 3.74% population-level incidence of unique scar events. We find multiple scars in the ESX-1 gene cluster. Six scars show evidence of convergent evolution while the rest shared a common ancestor. Our results suggest that sequential indels are a mechanism for reversible gene silencing and adaptation in M. tuberculosis.


2010 ◽  
Vol 105 (6) ◽  
pp. 779-785 ◽  
Author(s):  
Erika Noda Noguti ◽  
Clarice Queico Fujimura Leite ◽  
Ana Carolina Malaspina ◽  
Adolfo Carlos Barreto Santos ◽  
Rosário Dominguez Crespo Hirata ◽  
...  

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