scholarly journals An Evolutionary Arms Race Between Burkholderia pseudomallei and Host Immune System: What Do We Know?

2021 ◽  
Vol 11 ◽  
Author(s):  
Chalita Chomkatekaew ◽  
Phumrapee Boonklang ◽  
Apiwat Sangphukieo ◽  
Claire Chewapreecha
Keyword(s):  
Genetic Diversity ◽  
Immune System ◽  
Burkholderia Pseudomallei ◽  
Host Population ◽  
Ecological Niches ◽  
Host Immune System ◽  
Structural Variations ◽  
Evolutionary Trajectory ◽  
Human Host ◽  
Host Pathogen

A better understanding of co-evolution between pathogens and hosts holds promise for better prevention and control strategies. This review will explore the interactions between Burkholderia pseudomallei, an environmental and opportunistic pathogen, and the human host immune system. B. pseudomallei causes “Melioidosis,” a rapidly fatal tropical infectious disease predicted to affect 165,000 cases annually worldwide, of which 89,000 are fatal. Genetic heterogeneities were reported in both B. pseudomallei and human host population, some of which may, at least in part, contribute to inter-individual differences in disease susceptibility. Here, we review (i) a multi-host—pathogen characteristic of the interaction; (ii) selection pressures acting on B. pseudomallei and human genomes with the former being driven by bacterial adaptation across ranges of ecological niches while the latter are driven by human encounter of broad ranges of pathogens; (iii) the mechanisms that generate genetic diversity in bacterial and host population particularly in sequences encoding proteins functioning in host—pathogen interaction; (iv) reported genetic and structural variations of proteins or molecules observed in B. pseudomallei—human host interactions and their implications in infection outcomes. Together, these predict bacterial and host evolutionary trajectory which continues to generate genetic diversity in bacterium and operates host immune selection at the molecular level.

scholarly journals Review on the Relationship between Human Polyomaviruses-Associated Tumors and Host Immune System

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Serena Delbue ◽  
Manola Comar ◽  
Pasquale Ferrante
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Human Population ◽  
Host Immune System ◽  
Dna Viruses ◽  
Human Host ◽  
Immunosuppressed Patients ◽  
The Relationship ◽  
Associated Tumors ◽  
Human Polyomaviruses

The polyomaviruses are small DNA viruses that can establish latency in the human host. The name polyomavirus is derived from the Greek rootspoly-, which means “many,” and -oma, which means “tumours.” These viruses were originally isolated in mouse (mPyV) and in monkey (SV40). In 1971, the first human polyomaviruses BK and JC were isolated and subsequently demonstrated to be ubiquitous in the human population. To date, at least nine members of thePolyomaviridaefamily have been identified, some of them playing an etiological role in malignancies in immunosuppressed patients. Here, we describe the biology of human polyomaviruses, their nonmalignant and malignant potentials ability, and their relationship with the host immune response.

Evolutionary causes and consequences of diversified CRISPR immune profiles in natural populations

2013 ◽  
Vol 41 (6) ◽  
pp. 1431-1436 ◽  
Author(s):  
Whitney E. England ◽  
Rachel J. Whitaker
Keyword(s):  
Immune System ◽  
Present Article ◽  
Natural Populations ◽  
Host Immunity ◽  
Microbial Populations ◽  
Evolutionary Trajectory ◽  
Host Diversity ◽  
Low Diversity ◽  
Host Pathogen ◽  
Immunity Mechanism

Host–pathogen co-evolution is a significant force which shapes the ecology and evolution of all types of organisms, and such interactions are driven by resistance and immunity mechanisms of the host. Diversity of resistance and immunity can affect the co-evolutionary trajectory of both host and pathogen. The microbial CRISPR (clustered regularly interspaced short palindromic repeats)–Cas (CRISPR-associated) system is one host immunity mechanism which offers a tractable model for examining the dynamics of diversity in an immune system. In the present article, we review CRISPR variation observed in a variety of natural populations, examine the forces which can push CRISPRs towards high or low diversity, and investigate the consequences of various levels of diversity on microbial populations.

scholarly journals Tools for Assessing Translation in Cryptococcus neoformans

2021 ◽  
Vol 7 (3) ◽  
pp. 159
Author(s):  
Corey M. Knowles ◽  
Kelcy M. McIntyre ◽  
John C. Panepinto
Keyword(s):  
Immune System ◽  
Cryptococcus Neoformans ◽  
Cellular Stress ◽  
Antifungal Drugs ◽  
Limited Resources ◽  
Host Immune System ◽  
Human Host ◽  
Rapid Changes ◽  
Host Infection ◽  
Translation State

Cryptococcus neoformans is a ubiquitous environmental fungus capable of establishing an infection in a human host. Rapid changes in environments and exposure to the host immune system results in a significant amount of cellular stress, which is effectively combated at the level of translatome reprogramming. Repression of translation following stress allows for the specific reallocation of limited resources. Understanding the mechanisms involved in regulating translation in C. neoformans during host infection is critical in the development of new antifungal drugs. In this review, we discuss the main tools available for assessing changes in translation state and translational output during cellular stress.

scholarly journals Lessons from Toxoplasma: Host responses that mediate parasite control and the microbial effectors that subvert them

2021 ◽  
Vol 218 (11) ◽  
Author(s):  
Eva-Maria Frickel ◽  
Christopher A. Hunter
Keyword(s):  
Immune System ◽  
Toxoplasma Gondii ◽  
Experimental System ◽  
Host Responses ◽  
Host Immune System ◽  
Intracellular Parasite ◽  
Parasite Control ◽  
Host Pathogen ◽  
Ifn Γ ◽  
Intracellular Infections

The intracellular parasite Toxoplasma gondii has long provided a tractable experimental system to investigate how the immune system deals with intracellular infections. This review highlights the advances in defining how this organism was first detected and the studies with T. gondii that contribute to our understanding of how the cytokine IFN-γ promotes control of vacuolar pathogens. In addition, the genetic tractability of this eukaryote organism has provided the foundation for studies into the diverse strategies that pathogens use to evade antimicrobial responses and now provides the opportunity to study the basis for latency. Thus, T. gondii remains a clinically relevant organism whose evolving interactions with the host immune system continue to teach lessons broadly relevant to host–pathogen interactions.

scholarly journals Cryptococcus neoformans Rim101 Is Associated with Cell Wall Remodeling and Evasion of the Host Immune Responses

mBio ◽  
2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Teresa R. O'Meara ◽  
Stephanie M. Holmer ◽  
Kyla Selvig ◽  
Fred Dietrich ◽  
J. Andrew Alspaugh
Keyword(s):  
Immune Response ◽  
Cell Wall ◽  
Transcription Factor ◽  
Immune System ◽  
Immune Responses ◽  
Cryptococcus Neoformans ◽  
Host Immune Response ◽  
Host Immune System ◽  
Content Type ◽  
Host Pathogen

ABSTRACTInfectious microorganisms often play a role in modulating the immune responses of their infected hosts. We demonstrate thatCryptococcus neoformanssignals through the Rim101 transcription factor to regulate cell wall composition and the host-pathogen interface. In the absence of Rim101,C. neoformansexhibits an altered cell surface in response to host signals, generating an excessive and ineffective immune response that results in accelerated host death. This host immune response to therim101Δ mutant strain is characterized by increased neutrophil influx into the infected lungs and an altered pattern of host cytokine expression compared to the response to wild-type cryptococcal infection. To identify genes associated with the observed phenotypes, we performed whole-genome RNA sequencing experiments under capsule-inducing conditions. We defined the downstream regulon of the Rim101 transcription factor and determined potential cell wall processes involved in the capsule attachment defects and altered mechanisms of virulence in therim101Δ mutant. The cell wall generates structural stability for the cell and allows the attachment of surface molecules such as capsule polysaccharides. In turn, the capsule provides an effective mask for the immunogenic cell wall, shielding it from recognition by the host immune system.IMPORTANCECryptococcus neoformansis an opportunistic human pathogen that is a significant cause of death in immunocompromised individuals. There are two major causes of death due to this pathogen: meningitis due to uncontrolled fungal proliferation in the brain in the face of a weakened immune system and immune reconstitution inflammatory syndrome characterized by an overactive immune response to subclinical levels of the pathogen. In this study, we examined howC. neoformansuses the conserved Rim101 transcription factor to specifically remodel the host-pathogen interface, thus regulating the host immune response. These studies explored the complex ways in which successful microbial pathogens induce phenotypes that ensure their own survival while simultaneously controlling the nature and degree of the associated host response.

Silent control: microbial plant pathogens evade host immunity without coding sequence changes

2021 ◽  
Author(s):  
Han Chen ◽  
Sylvain Raffaele ◽  
Suomeng Dong
Keyword(s):  
Immune System ◽  
Plant Pathogens ◽  
Immune Surveillance ◽  
Host Immunity ◽  
Host Recognition ◽  
Host Immune System ◽  
Structural Variations ◽  
Coding Sequence ◽  
Biochemical Modification ◽  
Successful Infection

ABSTRACT Both animals and plants have evolved a robust immune system to surveil and defeat invading pathogenic microbes. Evasion of host immune surveillance is the key for pathogens to initiate successful infection. To evade the host immunity, plant pathogens evolved a variety of strategies such as masking themselves from host immune recognitions, blocking immune signaling transductions, reprogramming immune responses and adapting to immune microenvironmental changes. Gain of new virulence genes, sequence and structural variations enables plant pathogens to evade host immunity through changes in the genetic code. However, recent discoveries demonstrated that variations at the transcriptional, post-transcriptional, post-translational and glycome level enable pathogens to cope with the host immune system without coding sequence changes. The biochemical modification of pathogen associated molecular patterns and silencing of effector genes emerged as potent ways for pathogens to hide from host recognition. Altered processing in mRNA activities provide pathogens with resilience to microenvironment changes. Importantly, these hiding variants are directly or indirectly modulated by catalytic enzymes or enzymatic complexes and cannot be revealed by classical genomics alone. Unveiling these novel host evasion mechanisms in plant pathogens enables us to better understand the nature of plant disease and pinpoints strategies for rational diseases management in global food protection.

scholarly journals Glycomaterials for probing host–pathogen interactions and the immune response

2016 ◽  
Vol 241 (10) ◽  
pp. 1042-1053 ◽  
Author(s):  
Mia L Huang ◽  
Christopher J Fisher ◽  
Kamil Godula
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Cell Surface ◽  
Host Response ◽  
Host Immune Response ◽  
Host Cells ◽  
Host Immune System ◽  
Host Pathogen Interactions ◽  
Host Pathogen ◽  
Functional Complexity

The initial engagement of host cells by pathogens is often mediated by glycan structures presented on the cell surface. Various components of the glycocalyx can be targeted by pathogens for adhesion to facilitate infection. Glycans also play integral roles in the modulation of the host immune response to infection. Therefore, understanding the parameters that define glycan interactions with both pathogens and the various components of the host immune system can aid in the development of strategies to prevent, interrupt, or manage infection. Glycomaterials provide a unique and powerful tool with which to interrogate the compositional and functional complexity of the glycocalyx. The objective of this review is to highlight some key contributions from this area of research in deciphering the mechanisms of pathogenesis and the associated host response.

scholarly journals Corrigendum: An Evolutionary Arms Race Between Burkholderia pseudomallei and Host Immune System: What Do We Know?

2021 ◽  
Vol 12 ◽  
Author(s):  
Chalita Chomkatekaew ◽  
Phumrapee Boonklang ◽  
Apiwat Sangphukieo ◽  
Claire Chewapreecha
Keyword(s):  
Immune System ◽  
Burkholderia Pseudomallei ◽  
Arms Race ◽  
Host Immune System ◽  
Evolutionary Arms Race

scholarly journals VARIABILITY OF NEUTROPHIL-ACTIVATING PROTEIN AMONG HELICOBACTER PYLORI STRAINS

2021 ◽  
Vol 80 (1) ◽  
pp. 43-50
Author(s):  
Cecília R.C. Calado
Keyword(s):  
Genetic Diversity ◽  
Helicobacter Pylori ◽  
Immune System ◽  
Virulence Factors ◽  
Immunomodulatory Activity ◽  
Host Immune System ◽  
High Genetic Diversity ◽  
Vacuolating Cytotoxin ◽  
Synonymous Substitutions ◽  
H Pylori

The Helicobacter pylori neutrophil activating protein (NAP) presents relevant inflammatory and immunomodulatory activity and has consequently been explored as a diagnosis and therapeutic target. In the present work, nap gene sequences, retrieved from H. pylori isolated world-wide, were analyzed, a high genetic diversity (with 88% of alleles) being observed in accordance with other virulence factors. The phylogenetic analysis did not reveal the separation of strains per geographical region according to a bacterial panmictic population. When compared to other genes of virulence factors of H. pylori, such as the vacuolating cytotoxin A (vacA), nap presents slightly lower genetic variability, concerning the number of alleles and polymorphic sites, pointing to a possible lower pressure of the host immune system. The nap genetic diversity is associated to a high proportion of synonymous substitutions in relation to non-synonymous substitutions, pointing to equilibrium between the need for antigenic diversity as a mechanism to escape the host immune system and the maintenance of the proteins function. All this information could be put to good use when planning the NAP application as a therapeutic or diagnostic target.

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