2019
DOI: 10.1016/j.chom.2019.08.001
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Salmonella enterica serovar Typhi causes typhoid fever only in humans. Murine infection with S. Typhimurium is used as a typhoid model, but its relevance to human typhoid is limited. Non-obese diabetic-scid IL2rgnull mice engrafted with human hematopoietic stem cells (hu-SRC-SCID) are susceptible to lethal S. Typhi infection. In this study, we use a high-density S. Typhi transposon library in hu-SRC-SCID mice to identify virulence loci using transposon-directed insertion site sequencing (TraDIS). Vi capsule, l… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

1
36
0

Year Published

2019
2019
2024
2024

Publication Types

Select...
6
3
1

Relationship

0
10

Authors

Journals

citations
Cited by 43 publications
(37 citation statements)
references
References 56 publications
1
36
0
Order By: Relevance
“…In the humanized mouse model of typhoid fever, the PhoPQ regulators are dispensable for S . Typhi virulence, while the periplasmic domain of PbgA is critical (77). Therefore, we speculate that additional S.…”
Section: Discussionmentioning
confidence: 99%
“…In the humanized mouse model of typhoid fever, the PhoPQ regulators are dispensable for S . Typhi virulence, while the periplasmic domain of PbgA is critical (77). Therefore, we speculate that additional S.…”
Section: Discussionmentioning
confidence: 99%
“…Many bacteria possess TPS and TPP enzymes. However, with the exception of the Mycobacteria, trehalose biosynthesis pathways do not appear to play an important role in disease.For example, an otsA mutant of Salmonella enterica Typhimurium was reported to show no reduction in virulence in mice [ 35 ] and global mutagenesis studies have confirmed that otsA and otsB do not play roles in virulence of S. enterica in humanized mice [ 71 ]. In a global mutagenesis study of B. pseudomallei neither otsA nor otsB were found to be required for growth or virulence [ 72 , 73 ].…”
Section: Introductionmentioning
confidence: 99%
“…The deletion of the Ttr system of S. Dublin caused a higher level of invasion, but in S. Typhi, the ttrS sensor is a pseudogene (see below), which may explain why no phenotypes were observed. It may be surprising that the SsrAB system, which is the principal regulator of SPI-2, demonstrated no defect, but we have previously demonstrated that the entire SPI-2 deletion was not essential for S. Typhi survival in macrophages [23], and SPI-2 was not required for S. Typhi infection in a humanized mice model [111], highlighting one of the major differences with S. Typhimurium.…”
Section: Discussionmentioning
confidence: 90%