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Review Article
Yersinia pestis antibiotic resistance: a systematic review
Chen Lei, Suresh Kumar
Osong Public Health Res Perspect. 2022;13(1):24-36.   Published online February 18, 2022
DOI: https://doi.org/10.24171/j.phrp.2021.0288
  • 9,967 View
  • 301 Download
  • 13 Web of Science
  • 16 Crossref
AbstractAbstract PDF
Yersinia pestis, the cause of plague and a potential biological weapon, has always been a threatening pathogen. Some strains of Y. pestis have varying degrees of antibiotic resistance. Thus, this systematic review was conducted to alert clinicians to this pathogen’s potential antimicrobial resistance. A review of the literature was conducted for experimental reports and systematic reviews on the topics of plague, Y. pestis, and antibiotic resistance. From 1995 to 2021, 7 Y. pestis isolates with 4 antibiotic resistance mechanisms were reported. In Y. pestis 17/95, 16/95, and 2180H, resistance was mediated by transferable plasmids. Each plasmid contained resistance genes encoded within specific transposons. Strain 17/95 presented multiple drug resistance, since plasmid 1202 contained 10 resistance determinants. Strains 16/95 and 2180H showed single antibiotic resistance because both additional plasmids in these strains carried only 1 antimicrobial determinant. Strains 12/87, S19960127, 56/13, and 59/13 exhibited streptomycin resistance due to an rpsl gene mutation, a novel mechanism that was discovered recently. Y. pestis can acquire antibiotic resistance in nature not only via conjugative transfer of antimicrobial-resistant plasmids from other bacteria, but also by gene point mutations. Global surveillance should be strengthened to identify antibiotic-resistant Y. pestis strains by whole-genome sequencing and drug susceptibility testing.

Citations

Citations to this article as recorded by  
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  • Integrated Computational Analysis of Physicochemical Features, Biological Properties, Kinase Target Prediction and Biotransformation Pathways in Drug Discovery
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    Archives of Microbiology.2024;[Epub]     CrossRef
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    Umairah Natasya Mohd Omeershffudin, Suresh Kumar
    Genomics & Informatics.2023; 21(1): e5.     CrossRef
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    Joanna H. Bonczarowska, Julian Susat, Ben Krause-Kyora, Dorthe Dangvard Pedersen, Jesper Boldsen, Lars Agersnap Larsen, Lone Seeberg, Almut Nebel, Daniel Unterweger
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  • A situation analysis of the current plague outbreak in the Demographic Republic of Congo and counteracting strategies – Correspondence
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    Umairah Natasya Mohd Omeershffudin, Suresh Kumar
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Original Article
Cell Death Mechanisms in Esophageal Squamous Cell Carcinoma Induced by Vesicular Stomatitis Virus Matrix Protein
Yousef Douzandegan, Alireza Tahamtan, Zahra Gray, Hadi Razavi Nikoo, Alijan Tabarraei, Abdolvahab Moradi
Osong Public Health Res Perspect. 2019;10(4):246-252.   Published online August 31, 2019
DOI: https://doi.org/10.24171/j.phrp.2019.10.4.08
  • 7,177 View
  • 154 Download
  • 9 Crossref
AbstractAbstract PDF
Objectives

Vesicular stomatitis virus (VSV) is under development as an oncolytic virus due to its preferential replication in cancer cells and oncolytic activity, however the viral components responsible have not yet been determined. In this study the effects of VSV wild-type (wt) and M51R-mutant matrix proteins (M51R-mMP) on apoptosis, pyroptosis, necroptosis, and autophagy pathways, in an esophagus cancer cell line (KYSE-30) were investigated.

Methods

The KYSE-30 cells were transfected with pcDNA3.1 plasmids encoding wt or M51R-mMP, and apoptosis, pyroptosis, necroptosis, and autophagy were evaluated 48 and 72 hours after transfection.

Results

KYSE-30 cells transfected with VSV wt and M51R-mMPs significantly reduced cell viability to < 50% at 72 hours post-transfection. M51R-MP significantly increased the concentration of caspase-8 and caspase-9 at 48 and 72 hours post-transfection, respectively ( p < 0.05). In contrast, no significant changes were detected following transfection with the VSV wt plasmid. Moreover, VSV wt and M51R-mMP transfected cells did not change the expression of caspase-3. VSV wt and M51R-mMPs did not mMP change caspase-1 expression (a marker of pyroptosis) at 48 and 72 hours post-transfection. However, M51R-mMP and VSV wt transfected cells significantly increased RIP-1 (a marker of necroptosis) expression at 72 hours post-infection ( p < 0.05). Beclin-1, a biomarker of autophagy, was also induced by transfection with VSV wt or M51R-mMPs at 48 hours post-transfection.

Conclusion

The results in this study indicated that VSV exerts oncolytic activity in KYSE-30 tumor cells through different cell death pathways, suggesting that M51R-mMP may potentially be used to enhance oncolysis.

Citations

Citations to this article as recorded by  
  • Evoking pyroptosis with nanomaterials for cancer immunotherapy: Current boom and novel outlook
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    Qingbo Li, Patrick Kwabena Oduro, Rui Guo, Ruiqiao Li, Ling Leng, Xianbin Kong, Qilong Wang, Long Yang
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  • Live-attenuated poliovirus-induced extrinsic apoptosis through Caspase 8 within breast cancer cell lines expressing CD155
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    Takehiro Kanda, Madoka Sakai, Akiko Makino, Keizo Tomonaga
    Journal of General Virology .2022;[Epub]     CrossRef
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    César Sierra Martín
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    Isshu Kojima, Fumiki Izumi, Makoto Ozawa, Yoshikazu Fujimoto, Misuzu Okajima, Naoto Ito, Makoto Sugiyama, Tatsunori Masatani
    Journal of General Virology .2021;[Epub]     CrossRef
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