Mycobacterium tuberculosis genes Rv2557 and Rv2558 have no known function. However, proteome, transcriptome and in situ hybridization studies have shown that these genes are significantly upregulated under carbon-starved conditions and in human granulomas, suggesting that they may play a role in persistence. Single and double deletion mutants of M. tuberculosis H37Rv in Rv2557 and/or Rv2558 were generated to explore their individual and/or collective role(s) in growth and survival. The mutants were assessed for growth and survival in vitro under normal and nutrient-deprived conditions and for virulence in the SCID mouse model. Although highly induced by carbon starvation, loss of Rv2557 and/or Rv2558 affected neither the long-term survival of M. tuberculosis under carbon-starved conditions in vitro, nor its virulence in SCID mice.
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http://dx.doi.org/10.1016/j.tube.2005.11.001 | DOI Listing |
Front Immunol
November 2024
Laboratory of Genomic Medicine, Center of Experimental Research, Hospital de Clínicas de Porto Alegre (HCPA), Porto Alegre, Rio Grande do Sul, Brazil.
J Allergy Clin Immunol
January 2025
Department of Medicine, Division of Rheumatology and Immunology, Duke University School of Medicine, Durham, NC; Department of Biochemistry, Duke University School of Medicine, Durham, NC. Electronic address:
Background: Deficiency of adenosine deaminase (ADA or ADA1) has broad clinical and genetic heterogeneity. Screening techniques can identify asymptomatic infants whose phenotype and prognosis are indeterminate, and who may carry ADA variants of unknown significance.
Objective: We systematically assessed the pathogenic potential of rare ADA missense variants to better define the relationship of genotype to red blood cell (RBC) total deoxyadenosine nucleotide (dAXP) content and to phenotype.
Front Immunol
August 2024
Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.
bioRxiv
June 2024
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202.
(or ) , the causative agent of Lyme disease, is a motile and invasive zoonotic pathogen, adept at navigating between its arthropod vector and mammalian host. While motility and chemotaxis are well established as essential for its enzootic cycle, the function of methyl-accepting chemotaxis proteins (MCPs) in the infectious cycle of remains unclear. In this study, we demonstrate that MCP5, one of the most abundant MCPs in , is differentially expressed in response to environmental signals as well as at different stages of the pathogen's enzootic cycle.
View Article and Find Full Text PDFPathogens
May 2024
Department of Molecular Microbiology and Immunology, University of Texas at San Antonio, San Antonio, TX 78249, USA.
is an obligate intracellular Gram-negative bacterium that causes Q fever, a life-threatening zoonotic disease. replicates within an acidified parasitophorous vacuole derived from the host lysosome. The ability of to replicate and achieve successful intracellular life in the cell cytosol is vastly dependent on the Dot/Icm type 4B secretion system (T4SSB).
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