Yersinia pestis Biomolecules

A topical collection in Biomolecules (ISSN 2218-273X). This collection belongs to the section "Biological Factors".

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Guest Editor
Laboratory for Plague Microbiology, Especially Dangerous Infections Department, State Research Center for Applied Microbiology and Biotechnology, 142279 Obolensk, Russia
Interests: molecular bacteriology; infectious diseases; molecular biology of host-vector-pathogen interactions; microbial pathogenesis; virulence factors; vaccinology; biotechnology

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Guest Editor
Department of Molecular Medicine, USF Health Byrd Alzheimer’s Research Institute, Morsani College of Medicine, University of South Florida, 12901 Bruce B. Downs Blvd, MDC07, Tampa, FL 33612, USA
Interests: intrinsically disordered proteins; protein folding; protein misfolding; partially folded proteins; protein aggregation; protein structure; protein function; protein stability; protein biophysics; protein bioinformatics; conformational diseases; protein–ligand interactions; protein–protein interactions; liquid-liquid phase transitions
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Topical Collection Information

Dear Colleagues,

Although humanity first noticed the plague only when it began to ruthlessly reduce human populations, its causative agent, Yersinia pestis, did not come out of nowhere. Similar to its less pathogenic progenitor Yersinia pseudotuberculosis, it was the longtime inhabitant of wild rodents (e.g., marmots, voles, gerbils, and gophers) that had simply invaded a new accidental host—who happened to be human. Microevolution led to the formation of several phylogenetic lines of the plague pathogen, differing in their host specificity/pathogenicity. The strains circulating in populations of gophers, gerbils, and especially marmots are highly virulent for humans and guinea pigs, while voles’ (micro) strains are highly virulent for their natural hosts, Microtus spp., and laboratory mice, while exclusively conditionally pathogenic for people (and guinea pigs), causing rare infections only in immunocompromised human individuals. Our access to data on closely related strains with known genomes, transcriptomes, proteomes, methylomes, etc., differing not only in host specificity but also in isoforms of virulent proteins, gives us hope for the possibility of identifying new molecular targets for vaccine prevention and treatment of the plague.

This Topical Collection of Biomolecules aims to present a collection of papers submitted by experts working in the field of Yersinia research. We welcome both original articles and surveys that cover state-of-the-art advances in this important area.

Authors can submit their manuscripts online at www.mdpi.com by registering and logging in at the following website: https://susy.mdpi.com/user/login. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the Topical Collection’s website.

Prof. Dr. Andrey P. Anisimov
Dr. Vladimir N. Uversky
Collection Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the collection website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Yersinia pestis
  • Yersinia pseudotuberculosis complex
  • taxonomy
  • biomolecule
  • pathogenicity
  • immunity
  • protein
  • protein–protein interaction
  • lipopolysaccharide
  • paleomicrobiology

Published Papers (6 papers)

2021

Jump to: 2020

23 pages, 7020 KiB  
Review
Lipopolysaccharide of the Yersinia pseudotuberculosis Complex
by Yuriy A. Knirel, Andrey P. Anisimov, Angelina A. Kislichkina, Anna N. Kondakova, Olga V. Bystrova, Anastasia S. Vagaiskaya, Konstantin Y. Shatalin, Alexander S. Shashkov and Svetlana V. Dentovskaya
Biomolecules 2021, 11(10), 1410; https://doi.org/10.3390/biom11101410 - 26 Sep 2021
Cited by 8 | Viewed by 3289
Abstract
Lipopolysaccharide (LPS), localized in the outer leaflet of the outer membrane, serves as the major surface component of the Gram-negative bacterial cell envelope responsible for the activation of the host’s innate immune system. Variations of the LPS structure utilized by Gram-negative bacteria promote [...] Read more.
Lipopolysaccharide (LPS), localized in the outer leaflet of the outer membrane, serves as the major surface component of the Gram-negative bacterial cell envelope responsible for the activation of the host’s innate immune system. Variations of the LPS structure utilized by Gram-negative bacteria promote survival by providing resistance to components of the innate immune system and preventing recognition by TLR4. This review summarizes studies of the biosynthesis of Yersinia pseudotuberculosis complex LPSs, and the roles of their structural components in molecular mechanisms of yersiniae pathogenesis and immunogenesis. Full article
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24 pages, 346 KiB  
Review
Antibiotic Therapy of Plague: A Review
by Florent Sebbane and Nadine Lemaître
Biomolecules 2021, 11(5), 724; https://doi.org/10.3390/biom11050724 - 12 May 2021
Cited by 14 | Viewed by 5394
Abstract
Plague—a deadly disease caused by the bacterium Yersinia pestis—is still an international public health concern. There are three main clinical forms: bubonic plague, septicemic plague, and pulmonary plague. In all three forms, the symptoms appear suddenly and progress very rapidly. Early antibiotic [...] Read more.
Plague—a deadly disease caused by the bacterium Yersinia pestis—is still an international public health concern. There are three main clinical forms: bubonic plague, septicemic plague, and pulmonary plague. In all three forms, the symptoms appear suddenly and progress very rapidly. Early antibiotic therapy is essential for countering the disease. Several classes of antibiotics (e.g., tetracyclines, fluoroquinolones, aminoglycosides, sulfonamides, chloramphenicol, rifamycin, and β-lactams) are active in vitro against the majority of Y. pestis strains and have demonstrated efficacy in various animal models. However, some discrepancies have been reported. Hence, health authorities have approved and recommended several drugs for prophylactic or curative use. Only monotherapy is currently recommended; combination therapy has not shown any benefits in preclinical studies or case reports. Concerns about the emergence of multidrug-resistant strains of Y. pestis have led to the development of new classes of antibiotics and other therapeutics (e.g., LpxC inhibitors, cationic peptides, antivirulence drugs, predatory bacteria, phages, immunotherapy, host-directed therapy, and nutritional immunity). It is difficult to know which of the currently available treatments or therapeutics in development will be most effective for a given form of plague. This is due to the lack of standardization in preclinical studies, conflicting data from case reports, and the small number of clinical trials performed to date. Full article
13 pages, 1162 KiB  
Review
Molecular and Genetic Mechanisms That Mediate Transmission of Yersinia pestis by Fleas
by B. Joseph Hinnebusch, Clayton O. Jarrett and David M. Bland
Biomolecules 2021, 11(2), 210; https://doi.org/10.3390/biom11020210 - 3 Feb 2021
Cited by 15 | Viewed by 4593
Abstract
The ability to cause plague in mammals represents only half of the life history of Yersinia pestis. It is also able to colonize and produce a transmissible infection in the digestive tract of the flea, its insect host. Parallel to studies of [...] Read more.
The ability to cause plague in mammals represents only half of the life history of Yersinia pestis. It is also able to colonize and produce a transmissible infection in the digestive tract of the flea, its insect host. Parallel to studies of the molecular mechanisms by which Y. pestis is able to overcome the immune response of its mammalian hosts, disseminate, and produce septicemia, studies of Y. pestis–flea interactions have led to the identification and characterization of important factors that lead to transmission by flea bite. Y. pestis adapts to the unique conditions in the flea gut by altering its metabolic physiology in ways that promote biofilm development, a common strategy by which bacteria cope with a nutrient-limited environment. Biofilm localization to the flea foregut disrupts normal fluid dynamics of blood feeding, resulting in regurgitative transmission. Many of the important genes, regulatory pathways, and molecules required for this process have been identified and are reviewed here. Full article
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2020

Jump to: 2021

23 pages, 1401 KiB  
Review
Yersinia Outer Membrane Vesicles as Potential Vaccine Candidates in Protecting against Plague
by Andrey A. Byvalov, Ilya V. Konyshev, Vladimir N. Uversky, Svetlana V. Dentovskaya and Andrey P. Anisimov
Biomolecules 2020, 10(12), 1694; https://doi.org/10.3390/biom10121694 - 18 Dec 2020
Cited by 8 | Viewed by 3468
Abstract
Despite the relatively low incidence of plague, its etiological agent, Yersinia pestis, is an exceptional epidemic danger due to the high infectivity and mortality of this infectious disease. Reports on the isolation of drug-resistant Y. pestis strains indicate the advisability of using [...] Read more.
Despite the relatively low incidence of plague, its etiological agent, Yersinia pestis, is an exceptional epidemic danger due to the high infectivity and mortality of this infectious disease. Reports on the isolation of drug-resistant Y. pestis strains indicate the advisability of using asymmetric responses, such as phage therapy and vaccine prophylaxis in the fight against this problem. The current relatively effective live plague vaccine is not approved for use in most countries because of its ability to cause heavy local and system reactions and even a generalized infectious process in people with a repressed immune status or metabolic disorders, as well as lethal infection in some species of nonhuman primates. Therefore, developing alternative vaccines is of high priority and importance. However, until now, work on the development of plague vaccines has mainly focused on screening for the potential immunogens. Several investigators have identified the protective potency of bacterial outer membrane vesicles (OMVs) as a promising basis for bacterial vaccine candidates. This review is aimed at presenting these candidates of plague vaccine and the results of their analysis in animal models. Full article
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11 pages, 450 KiB  
Review
Autophagy and Intracellular Membrane Trafficking Subversion by Pathogenic Yersinia Species
by Marion Lemarignier and Javier Pizarro-Cerdá
Biomolecules 2020, 10(12), 1637; https://doi.org/10.3390/biom10121637 - 4 Dec 2020
Cited by 7 | Viewed by 6031
Abstract
Yersinia pseudotuberculosis, Y. enterocolitica and Y. pestis are pathogenic bacteria capable of causing disease in humans by growing extracellularly in lymph nodes and during systemic infections. While the capacity of these bacteria to invade, replicate, and survive within host cells has been [...] Read more.
Yersinia pseudotuberculosis, Y. enterocolitica and Y. pestis are pathogenic bacteria capable of causing disease in humans by growing extracellularly in lymph nodes and during systemic infections. While the capacity of these bacteria to invade, replicate, and survive within host cells has been known for long, it is only in recent years that their intracellular stages have been explored in more detail. Current evidence suggests that pathogenic Yersinia are capable of activating autophagy in both phagocytic and epithelial cells, subverting autophagosome formation to create a niche supporting bacterial intracellular replication. In this review, we discuss recent results opening novel perspectives to the understanding of intimate host-pathogens interactions taking place during enteric yersiniosis and plague. Full article
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32 pages, 3331 KiB  
Review
Yersinia pestis Plasminogen Activator
by Florent Sebbane, Vladimir N. Uversky and Andrey P. Anisimov
Biomolecules 2020, 10(11), 1554; https://doi.org/10.3390/biom10111554 - 14 Nov 2020
Cited by 12 | Viewed by 5190
Abstract
The Gram-negative bacterium Yersinia pestis causes plague, a fatal flea-borne anthropozoonosis, which can progress to aerosol-transmitted pneumonia. Y. pestis overcomes the innate immunity of its host thanks to many pathogenicity factors, including plasminogen activator, Pla. This factor is a broad-spectrum outer membrane protease [...] Read more.
The Gram-negative bacterium Yersinia pestis causes plague, a fatal flea-borne anthropozoonosis, which can progress to aerosol-transmitted pneumonia. Y. pestis overcomes the innate immunity of its host thanks to many pathogenicity factors, including plasminogen activator, Pla. This factor is a broad-spectrum outer membrane protease also acting as adhesin and invasin. Y. pestis uses Pla adhesion and proteolytic capacity to manipulate the fibrinolytic cascade and immune system to produce bacteremia necessary for pathogen transmission via fleabite or aerosols. Because of microevolution, Y. pestis invasiveness has increased significantly after a single amino-acid substitution (I259T) in Pla of one of the oldest Y. pestis phylogenetic groups. This mutation caused a better ability to activate plasminogen. In paradox with its fibrinolytic activity, Pla cleaves and inactivates the tissue factor pathway inhibitor (TFPI), a key inhibitor of the coagulation cascade. This function in the plague remains enigmatic. Pla (or pla) had been used as a specific marker of Y. pestis, but its solitary detection is no longer valid as this gene is present in other species of Enterobacteriaceae. Though recovering hosts generate anti-Pla antibodies, Pla is not a good subunit vaccine. However, its deletion increases the safety of attenuated Y. pestis strains, providing a means to generate a safe live plague vaccine. Full article
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Y. pestis biomolecules, potential components of plague subunit vaccines
Authors: Diane Williamson; et al
Affiliation: Biomedical Sciences, DSTL, Porton Down, Salisbury, Wilts SP4 0JQ, UK

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