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Microorganisms
Special Issues
Adaptation of Pathogenic Microbes to the Host Environment
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Adaptation of Pathogenic Microbes to the Host Environment

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 23929

Special Issue Editor

Dr. Kylie Boyce

E-Mail Website
Guest Editor
RMIT University, PO Box 71, Bundoora VIC 3083, Australia
Interests: mycology; medical mycology; host–pathogen interactions; pathogenesis; morphology; dimorphic switching; genetics; epigenetics; microevolution; antibiotic resistance; fungi in biotechnology

Special Issue Information

Dear Colleagues,

Microbial pathogens are capable of adapting rapidly to the hostile environment of the host in order to survive, colonize and proliferate. Adaptation enables pathogens to avoid recognition by the host immune system and can facilitate survival by the initiation of pathways leading to tolerance to the destructive mechanisms of the innate immune system, resulting in latency and long-term pathogen persistence. Adaptation also expedites the emergence of resistance to antimicrobial agents, leading to subsequent treatment failure and high patient mortality.

In this Special Issue of Microorganisms, dedicated to adaptation to the host environment, we invite you to send in your contributions concerning any aspects related to the adaptation of pathogenic microbes to the host environment, from avoidance or tolerance of the immune system and the emergence of antimicrobial resistance, to changes in the genome, epigenome, signaling or physiology of species, and from fundamental to applied aspects.

Dr. Kylie Boyce
Guest Editor

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 special issue 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. Microorganisms 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

  • microbiology
  • host pathogen interactions
  • pathogen
  • fungi
  • adaptation
  • immune system
  • antimicrobials
  • antibiotics
  • antifungals
  • genomics
  • epigenomics
  • genetics

Published Papers (2 papers)

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Research

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20 pages, 31797 KiB  
Article
Snf1 Kinase Differentially Regulates Botrytis cinerea Pathogenicity according to the Plant Host
by Szabina Lengyel, Christine Rascle, Nathalie Poussereau, Christophe Bruel, Luca Sella, Mathias Choquer and Francesco Favaron
Microorganisms 2022, 10(2), 444; https://doi.org/10.3390/microorganisms10020444 - 15 Feb 2022
Cited by 4 | Viewed by 2236
Abstract
The Snf1 kinase of the glucose signaling pathway controls the response to nutritional and environmental stresses. In phytopathogenic fungi, Snf1 acts as a global activator of plant cell wall degrading enzymes that are major virulence factors for plant colonization. To characterize its role [...] Read more.
The Snf1 kinase of the glucose signaling pathway controls the response to nutritional and environmental stresses. In phytopathogenic fungi, Snf1 acts as a global activator of plant cell wall degrading enzymes that are major virulence factors for plant colonization. To characterize its role in the virulence of the necrotrophic fungus Botrytis cinerea, two independent deletion mutants of the Bcsnf1 gene were obtained and analyzed. Virulence of the Δsnf1 mutants was reduced by 59% on a host with acidic pH (apple fruit) and up to 89% on hosts with neutral pH (cucumber cotyledon and French bean leaf). In vitro, Δsnf1 mutants grew slower than the wild type strain at both pH 5 and 7, with a reduction of 20–80% in simple sugars, polysaccharides, and lipidic carbon sources, and these defects were amplified at pH 7. A two-fold reduction in secretion of xylanase activities was observed consequently to the Bcsnf1 gene deletion. Moreover, Δsnf1 mutants were altered in their ability to control ambient pH. Finally, Δsnf1 mutants were impaired in asexual sporulation and did not produce macroconidia. These results confirm the importance of BcSnf1 in pathogenicity, nutrition, and conidiation, and suggest a role in pH regulation for this global regulator in filamentous fungi. Full article
(This article belongs to the Special Issue Adaptation of Pathogenic Microbes to the Host Environment)
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Review

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14 pages, 4972 KiB  
Review
Evolutionary Genetics of Mycobacterium Tuberculosis and HIV-1: “The Tortoise and the Hare”
by Ana Santos-Pereira, Carlos Magalhães, Pedro M. M. Araújo and Nuno S. Osório
Microorganisms 2021, 9(1), 147; https://doi.org/10.3390/microorganisms9010147 - 11 Jan 2021
Cited by 7 | Viewed by 20160
Abstract
The already enormous burden caused by Mycobacterium tuberculosis and Human Immunodeficiency Virus type 1 (HIV-1) alone is aggravated by co-infection. Despite obvious differences in the rate of evolution comparing these two human pathogens, genetic diversity plays an important role in the success of [...] Read more.
The already enormous burden caused by Mycobacterium tuberculosis and Human Immunodeficiency Virus type 1 (HIV-1) alone is aggravated by co-infection. Despite obvious differences in the rate of evolution comparing these two human pathogens, genetic diversity plays an important role in the success of both. The extreme evolutionary dynamics of HIV-1 is in the basis of a robust capacity to evade immune responses, to generate drug-resistance and to diversify the population-level reservoir of M group viral subtypes. Compared to HIV-1 and other retroviruses, M. tuberculosis generates minute levels of genetic diversity within the host. However, emerging whole-genome sequencing data show that the M. tuberculosis complex contains at least nine human-adapted phylogenetic lineages. This level of genetic diversity results in differences in M. tuberculosis interactions with the host immune system, virulence and drug resistance propensity. In co-infected individuals, HIV-1 and M. tuberculosis are likely to co-colonize host cells. However, the evolutionary impact of the interaction between the host, the slowly evolving M. tuberculosis bacteria and the HIV-1 viral “mutant cloud” is poorly understood. These evolutionary dynamics, at the cellular niche of monocytes/macrophages, are also discussed and proposed as a relevant future research topic in the context of single-cell sequencing. Full article
(This article belongs to the Special Issue Adaptation of Pathogenic Microbes to the Host Environment)
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