Abstract
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.
Highlights
Melioidosis is a serious and often fatal neglected tropical infectious disease caused by Burkholderia pseudomallei, an intracellular bacterial pathogen and ubiquitous in the environment (Holden et al, 2004)
For the rest of the bacterial factors that do not get recognized by any specific innate pattern recognition receptors, these antigens will be processed and presented on Human Leukocyte Antigen (HLA) of antigenpresenting cells such as dendritic cells before getting recognized by appropriate T cell receptors (TCR) of the adaptive immune axis; this HLA-peptide-TCR interaction kicks start the adaptive immune response
There are three different classes of HLA: class I interacts with TCRs on CD8 + T cells while class II binds to TCRs on CD4 + T cells, and the less well-established class III which is not involved in antigen processing and presentation (Dendrou et al, 2018)
Summary
Melioidosis is a serious and often fatal neglected tropical infectious disease caused by Burkholderia pseudomallei, an intracellular bacterial pathogen and ubiquitous in the environment (Holden et al, 2004). Host-Pathogen Co-evolution in Melioidosis that B. pseudomallei has not evolved virulence mechanisms through consecutive passage in human hosts. B. pseudomallei within-host evolution observed in chronic infections are often linked to attenuated virulence (Price et al, 2013; Viberg et al, 2017; Pearson et al, 2020), which is possibly mediated by host immune evasion. It is likely that B. pseudomallei has acquired virulence genes for human infection before being exposed to the human hosts, and that these virulence factors are most effective when the host has underlying health issues. It is possible that a successful human infection is mediated by bacterial redundant virulence mechanisms that were acquired and maintained in the environment. We will leverage recent pieces of genomic studies to better understand the evolution of virulence mechanisms in B. pseudomallei and host defense system
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
