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

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 51971

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Prof. Dr. Maria Salomé Gomes

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Instituto de Investigação e Inovação em Saúde, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal
Interests: mycobacterium; innate immunity; iron metabolism; macrophages; hematopoiesis; antimicrobial molecules
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Prof. Dr. Luisa Pereira

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Guest Editor

1. Instituto de Patologia e Imunologia Molecular, Universidade do Porto, Porto, Portugal
2. i3S–Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
Interests: human population genetics; evolution; selection; genomics; mitochondrial DNA; genome-wide association studies; genetic susceptibility to complex diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the enormous progress that was achieved during the last century, infectious diseases still have a huge impact on human health worldwide.

Studies on host–pathogen interactions have been key in the identification of the most important determinants of infection outcome. From the pathogen side, these studies contribute to the identification of virulence factors. From the host side, they identify not only those factors more directly related to the immune system but also other aspects of host-metabolic and homeostatic status with an impact on resistance or susceptibility to infection. In this context, it is important to note that several high-throughput omics studies have revealed that infection has more diverse and subtle impacts on host health status, both immediate and life-long, than previously antecipated.

The identification of host targets of infection with a role in disease progression or resistance represents a new opportunity to envisage host-directed therapies. In a time when antibiotic treatments are being challenged by increasing bacterial resistance rates, host-directed therapies represent an appealing complementary strategy to combat infectious diseases.

In this Issue, we would like to reunite recent developments made by studies in host–pathogen interactions that may contribute to the proposal of host-targeted therapies to treat infectious diseases.

Prof. Dr. Maria Salomé Gomes
Prof. Dr. Luisa Luisa Pereira
Guest Editors

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Keywords

infection
host–pathogen interactions
host-directed therapy
high-throughput data regarding infection

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Published Papers (12 papers)

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Editorial

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4 pages, 200 KiB

Open AccessEditorial

Special Issue: From Host–Pathogen Interaction to Host-Directed Therapies

by Maria Salomé Gomes and Luisa Pereira

Microorganisms 2021, 9(12), 2606; https://doi.org/10.3390/microorganisms9122606 - 17 Dec 2021

Cited by 1 | Viewed by 1851

Abstract

Despite the enormous progress made in the last few decades, infectious diseases still represent a huge challenge to human society and health systems, as evidenced by the recent SARS-CoV-2 pandemic [...] Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

Research

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13 pages, 1994 KiB

Open AccessArticle

A Mucoralean White Collar-1 Photoreceptor Controls Virulence by Regulating an Intricate Gene Network during Host Interactions

by Carlos Pérez-Arques, María Isabel Navarro-Mendoza, Laura Murcia, Carlos Lax, Marta Sanchis, Javier Capilla, Eusebio Navarro, Victoriano Garre and Francisco Esteban Nicolás

Microorganisms 2021, 9(2), 459; https://doi.org/10.3390/microorganisms9020459 - 23 Feb 2021

Cited by 7 | Viewed by 2514

Abstract

Mucolares are an ancient group of fungi encompassing the causal agents for the lethal infection mucormycosis. The high lethality rates, the emerging character of this disease, and the broad antifungal resistance of its causal agents are mucormycosis features that are alarming clinicians and researchers. Thus, the research field around mucormycosis is currently focused on finding specific weaknesses and targets in Mucorales for developing new treatments. In this work, we tested the role of the white-collar genes family in the virulence potential of Mucor lusitanicus. Study of the three genes of this family, mcwc-1a, mcwc-1b, and mcwc-1c, resulted in a marked functional specialization, as only mcwc-1a was essential to maintain the virulence potential of M. lusitanicus. The traditional role of wc-1 genes regulating light-dependent responses is a thoroughly studied field, whereas their role in virulence remains uncharacterized. In this work, we investigated the mechanism involving mcwc-1a in virulence from an integrated transcriptomic and functional approach during the host–pathogen interaction. Our results revealed mcwc-1a as a master regulator controlling an extensive gene network. Further dissection of this gene network clustering its components by type of regulation and functional criteria disclosed a multifunctional mechanism depending on diverse pathways. In the absence of phagocytic cells, mcwc-1a controlled pathways related to cell motility and the cytoskeleton that could be associated with the essential tropism during tissue invasion. After phagocytosis, several oxidative response pathways dependent on mcwc-1a were activated during the germination of M. lusitanicus spores inside phagocytic cells, which is the first stage of the infection. The third relevant group of genes involved in virulence and regulated by mcwc-1a belonged to the “unknown function,” indicating that new and hidden pathways are involved in virulence. The unknown function category is especially pertinent in the study of mucormycosis, as it is highly enriched in specific fungal genes that represent the most promising targets for developing new antifungal compounds. These results unveil a complex multifunctional mechanism used by wc-1 genes to regulate the pathogenic potential in Mucorales that could also apply to other fungal pathogens. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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13 pages, 726 KiB

Open AccessArticle

HBcAb Positivity Is a Risk Factor for an Increased Detectability of HIV RNA after Switching to a Two-Drug Regimen Lamivudine-Based (2DR-3TC-Based) Treatment: Analysis of a Multicenter Italian Cohort

by Vincenzo Malagnino, Elisabetta Teti, Mirko Compagno, Luigi Coppola, Romina Salpini, Valentina Svicher, Monica Basso, Giuliana Battagin, Sandro Panese, Maria Cristina Rossi, Renzo Scaggiante, Daniela Zago, Marco Iannetta, Saverio Giuseppe Parisi, Massimo Andreoni and Loredana Sarmati

Microorganisms 2021, 9(2), 396; https://doi.org/10.3390/microorganisms9020396 - 15 Feb 2021

Cited by 7 | Viewed by 2301

Abstract

The aim of this study was to evaluate whether the presence of anti-hepatitis B (HBV) c antibodies (HBcAb positivity) could influence the control of Human Immunodeficiency Virus (HIV) viremia in patients living with HIV (PLWH) who switch a to two-drug antiretroviral therapy (2DR) containing lamivudine (3TC) (2DR-3TC). A retrospective observational multicenter study was conducted on 166 PLWH switching to the 2DR-3TC-based regimen: 58 HBcAb-positive and 108 HBcAb-negative patients. The HBcAb-positive PLWH group demonstrated a significantly higher percentage of subjects with very low-level viremia at all time points after switching (6th month: <31% vs. 17.6%, p = 0.047; 12th month 34% vs. 27.5%, p = 0.001; 24th month 37% vs. 34.2, p = 0.003 of the HBcAb-positive and HBcAb-negative groups, respectively) and a higher percentage of subjects with detectable HIV RNA greater than 20 copies/mL 12 and 24 months after switching (12 months 32% vs. 11%, p = 0.001; 24 months 37% vs. 13.9%, p = 0.003 of the HBcAb-positive and HBcAb-negative groups, respectively). Logistic regression analysis showed that an increase in age of ten years (OR 2.48 (95% CI 1.58–3.89), p < 0.0001) and the presence of HBcAb positivity (OR 2.7 (5% CI 1.05–6.9), p = 0.038) increased the risk of detectability of HIV RNA by nearly three-fold after switching to 2DR-3TC. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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10 pages, 2147 KiB

Open AccessArticle

Dynamics of a Dual SARS-CoV-2 Lineage Co-Infection on a Prolonged Viral Shedding COVID-19 Case: Insights into Clinical Severity and Disease Duration

by Nicole Pedro, Cláudio N. Silva, Ana C. Magalhães, Bruno Cavadas, Ana M. Rocha, Ana C. Moreira, Maria Salomé Gomes, Diogo Silva, Joana Sobrinho-Simões, Angélica Ramos, Maria J. Cardoso, Rita Filipe, Pedro Palma, Filipa Ceia, Susana Silva, João T. Guimarães, António Sarmento, Verónica Fernandes, Luisa Pereira and Margarida Tavares

Microorganisms 2021, 9(2), 300; https://doi.org/10.3390/microorganisms9020300 - 2 Feb 2021

Cited by 46 | Viewed by 5508

Abstract

A few molecularly proven severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cases of symptomatic reinfection are currently known worldwide, with a resolved first infection followed by a second infection after a 48 to 142-day intervening period. We report a multiple-component study of a clinically severe and prolonged viral shedding coronavirus disease 2019 (COVID-19) case in a 17-year-old Portuguese female. She had two hospitalizations, a total of 19 RT-PCR tests, mostly positive, and criteria for releasing from home isolation at the end of 97 days. The viral genome was sequenced in seven serial samples and in the diagnostic sample from her infected mother. A human genome-wide array (>900 K) was screened on the seven samples, and in vitro culture was conducted on isolates from three late samples. The patient had co-infection by two SARS-CoV-2 lineages, which were affiliated in distinct clades and diverging by six variants. The 20A lineage was absolute at the diagnosis (shared with the patient’s mother), but nine days later, the 20B lineage had 3% frequency, and two months later, the 20B lineage had 100% frequency. The 900 K profiles confirmed the identity of the patient in the serial samples, and they allowed us to infer that she had polygenic risk scores for hospitalization and severe respiratory disease within the normal distributions for a Portuguese population cohort. The early-on dynamic co-infection may have contributed to the severity of COVID-19 in this otherwise healthy young patient, and to her prolonged SARS-CoV-2 shedding profile. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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18 pages, 4106 KiB

Open AccessArticle

Shedding Light on the African Enigma: In Vitro Testing of Homo sapiens-Helicobacter pylori Coevolution

by Bruno Cavadas, Marina Leite, Nicole Pedro, Ana C. Magalhães, Joana Melo, Marcelo Correia, Valdemar Máximo, Rui Camacho, Nuno A. Fonseca, Ceu Figueiredo and Luísa Pereira

Microorganisms 2021, 9(2), 240; https://doi.org/10.3390/microorganisms9020240 - 25 Jan 2021

Cited by 10 | Viewed by 2756

Abstract

The continuous characterization of genome-wide diversity in population and case–cohort samples, allied to the development of new algorithms, are shedding light on host ancestry impact and selection events on various infectious diseases. Especially interesting are the long-standing associations between humans and certain bacteria, such as the case of Helicobacter pylori, which could have been strong drivers of adaptation leading to coevolution. Some evidence on admixed gastric cancer cohorts have been suggested as supporting Homo-Helicobacter coevolution, but reliable experimental data that control both the bacterium and the host ancestries are lacking. Here, we conducted the first in vitro coinfection assays with dual human- and bacterium-matched and -mismatched ancestries, in African and European backgrounds, to evaluate the genome wide gene expression host response to H. pylori. Our results showed that: (1) the host response to H. pylori infection was greatly shaped by the human ancestry, with variability on innate immune system and metabolism; (2) African human ancestry showed signs of coevolution with H. pylori while European ancestry appeared to be maladapted; and (3) mismatched ancestry did not seem to be an important differentiator of gene expression at the initial stages of infection as assayed here. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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18 pages, 2712 KiB

Open AccessArticle

Anti-Pathogenic and Immune-Modulatory Effects of Peroral Treatment with Cardamom Essential Oil in Acute Murine Campylobacteriosis

by Markus M. Heimesaat, Soraya Mousavi, Dennis Weschka and Stefan Bereswill

Microorganisms 2021, 9(1), 169; https://doi.org/10.3390/microorganisms9010169 - 14 Jan 2021

Cited by 22 | Viewed by 3541

Abstract

Human infections with enteropathogenic Campylobacter jejuni (C. jejuni) including multi-drug resistant isolates are emerging worldwide. Antibiotics-independent approaches in the combat of campylobacteriosis are therefore highly desirable. Since the health-beneficial including anti-inflammatory and anti-infectious properties of cardamom have been acknowledged for long, we here addressed potential anti-pathogenic and immune-modulatory effects of this natural compound during acute campylobacteriosis. For this purpose, microbiota-depleted IL-10^−/− mice were orally infected with C. jejuni strain 81–176 and subjected to cardamom essential oil (EO) via the drinking water starting on day 2 post-infection. Cardamom EO treatment resulted in lower intestinal pathogen loads and improved clinical outcome of mice as early as day 3 post-infection. Furthermore, when compared to mock controls, cardamom EO treated mice displayed less distinct macroscopic and microscopic inflammatory sequelae on day 6 post-infection that were paralleled by lower colonic numbers of macrophages, monocytes, and T cells and diminished pro-inflammatory mediator secretion not only in the intestinal tract, but also in extra-intestinal and, remarkably, systemic organs. In conclusion, our preclinical intervention study provides the first evidence that cardamom EO comprises a promising compound for the combat of acute campylobacteriosis and presumably prevention of post-infectious morbidities. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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14 pages, 2657 KiB

Open AccessArticle

Mycobacterium tuberculosis Infection Up-Regulates Sialyl Lewis X Expression in the Lung Epithelium

by Rita Matos, Kaori L. Fonseca, Stefan Mereiter, Ana Raquel Maceiras, Joana Gomes, Cristina Vilaplana, Fátima Gartner, Pedro N. S. Rodrigues, Celso A. Reis, Margarida Saraiva and Ana Magalhães

Microorganisms 2021, 9(1), 99; https://doi.org/10.3390/microorganisms9010099 - 4 Jan 2021

Cited by 10 | Viewed by 3514

Abstract

Glycans display increasingly recognized roles in pathological contexts, however, their impact in the host-pathogen interplay in many infectious diseases remains largely unknown. This is the case for tuberculosis (TB), one of the ten most fatal diseases worldwide, caused by infection of the bacteria Mycobacterium tuberculosis. We have recently reported that perturbing the core-2 O-glycans biosynthetic pathway increases the host susceptibility to M. tuberculosis infection, by disrupting the neutrophil homeostasis and enhancing lung pathology. In the present study, we show an increased expression of the sialylated glycan structure Sialyl-Lewis X (SLeX) in the lung epithelium upon M. tuberculosis infection. This increase in SLeX glycan epitope is accompanied by an altered lung tissue transcriptomic signature, with up-regulation of genes codifying enzymes that are involved in the SLeX core-2 O-glycans biosynthetic pathway. This study provides novel insights into previously unappreciated molecular mechanisms involving glycosylation, which modulate the host response to M. tuberculosis infection, possibly contributing to shape TB disease outcome. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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15 pages, 748 KiB

Open AccessArticle

An Evolutionary Model of Progression to AIDS

by Igor M. Rouzine

Microorganisms 2020, 8(11), 1714; https://doi.org/10.3390/microorganisms8111714 - 31 Oct 2020

Cited by 4 | Viewed by 2877

Abstract

The time to the onset of AIDS symptoms in an HIV infected individual is known to correlate inversely with viremia and the level of immune activation. The correlation exists against the background of strong individual fluctuations demonstrating the existence of hidden variables depending on patient and virus parameters. At the moment, prognosis of the time to AIDS based on patient parameters is not possible. In addition, it is of paramount importance to understand the reason of progression to AIDS in untreated patients to be able to learn to control it by means other than anti-retroviral therapy. Here we develop a mechanistic mathematical model to predict the speed of progression to AIDS in individual untreated patients and patients treated with suboptimal therapy, based on a single-time measurement of several virological and immunological parameters. We show that the gradual increase in virus fitness during a chronic infection causes slow gradual depletion of CD4 T cells. Using the existing evolution models of HIV, we obtain general expressions predicting the time to the onset of AIDS symptoms in terms of the patient parameters, for low-viremia and high-viremia patients separately. We show that the evolution model of AIDS fits the existing data on virus-time correlations better than the alternative model of the deregulation of homeostatic response. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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15 pages, 4137 KiB

Open AccessArticle

Gastric Microbiome Diversities in Gastric Cancer Patients from Europe and Asia Mimic the Human Population Structure and Are Partly Driven by Microbiome Quantitative Trait Loci

by Bruno Cavadas, Rui Camacho, Joana C. Ferreira, Rui M. Ferreira, Ceu Figueiredo, Alvis Brazma, Nuno A. Fonseca and Luísa Pereira

Microorganisms 2020, 8(8), 1196; https://doi.org/10.3390/microorganisms8081196 - 6 Aug 2020

Cited by 17 | Viewed by 4022

Abstract

The human gastrointestinal tract harbors approximately 100 trillion microorganisms with different microbial compositions across geographic locations. In this work, we used RNASeq data from stomach samples of non-disease (164 individuals from European ancestry) and gastric cancer patients (137 from Europe and Asia) from public databases. Although these data were intended to characterize the human expression profiles, they allowed for a reliable inference of the microbiome composition, as confirmed from measures such as the genus coverage, richness and evenness. The microbiome diversity (weighted UniFrac distances) in gastric cancer mimics host diversity across the world, with European gastric microbiome profiles clustering together, distinct from Asian ones. Despite the confirmed loss of microbiome diversity from a healthy status to a cancer status, the structured profile was still recognized in the disease condition. In concordance with the parallel host-bacteria population structure, we found 16 human loci (non-synonymous variants) in the European-descendent cohorts that were significantly associated with specific genera abundance. These microbiome quantitative trait loci display heterogeneity between population groups, being mainly linked to the immune system or cellular features that may play a role in enabling microbe colonization and inflammation. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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Review

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18 pages, 10697 KiB

Open AccessReview

The Crossroads between Infection and Bone Loss

by Tiago Carvalho Oliveira, Maria Salomé Gomes and Ana Cordeiro Gomes

Microorganisms 2020, 8(11), 1765; https://doi.org/10.3390/microorganisms8111765 - 10 Nov 2020

Cited by 29 | Viewed by 6337

Abstract

Bone homeostasis, based on a tight balance between bone formation and bone degradation, is affected by infection. On one hand, some invading pathogens are capable of directly colonizing the bone, leading to its destruction. On the other hand, immune mediators produced in response to infection may dysregulate the deposition of mineral matrix by osteoblasts and/or the resorption of bone by osteoclasts. Therefore, bone loss pathologies may develop in response to infection, and their detection and treatment are challenging. Possible biomarkers of impaired bone metabolism during chronic infection need to be identified to improve the diagnosis and management of infection-associated osteopenia. Further understanding of the impact of infections on bone metabolism is imperative for the early detection, prevention, and/or reversion of bone loss. Here, we review the mechanisms responsible for bone loss as a direct and/or indirect consequence of infection. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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20 pages, 777 KiB

Open AccessReview

Ferritin: An Inflammatory Player Keeping Iron at the Core of Pathogen-Host Interactions

by Ana C. Moreira, Gonçalo Mesquita and Maria Salomé Gomes

Microorganisms 2020, 8(4), 589; https://doi.org/10.3390/microorganisms8040589 - 18 Apr 2020

Cited by 81 | Viewed by 13131

Abstract

Iron is an essential element for virtually all cell types due to its role in energy metabolism, nucleic acid synthesis and cell proliferation. Nevertheless, if free, iron induces cellular and organ damage through the formation of free radicals. Thus, iron levels must be firmly controlled. During infection, both host and microbe need to access iron and avoid its toxicity. Alterations in serum and cellular iron have been reported as important markers of pathology. In this regard, ferritin, first discovered as an iron storage protein, has emerged as a biomarker not only in iron-related disorders but also in inflammatory diseases, or diseases in which inflammation has a central role such as cancer, neurodegeneration or infection. The basic research on ferritin identification and functions, as well as its role in diseases with an inflammatory component and its potential as a target in host-directed therapies, are the main considerations of this review. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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Other

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8 pages, 1263 KiB

Open AccessBrief Report

Association of Leukotriene A4 Hydrolase with Tuberculosis Susceptibility Using Genomic Data in Portugal

by Teresa Rito, Joana Ferreira, Bruno Cavadas, Pedro Soares, Olena Oliveira, Martin B. Richards, Raquel Duarte, Luísa Pereira and Margarida Correia-Neves

Microorganisms 2019, 7(12), 650; https://doi.org/10.3390/microorganisms7120650 - 4 Dec 2019

Cited by 5 | Viewed by 2773

Abstract

Leukotriene A4 hydrolase (LTA4H) is a key enzyme in the eicosanoid pathway. lta4h locus polymorphisms have previously been linked to tuberculosis (TB) susceptibility and disease outcome in a Vietnamese dataset, but further studies suggested that those results were poorly reproducible. We, therefore, compared the full set of variants (113 SNPs) within the gene in a Portuguese dataset of 112 TB patients and 120 controls, using both the frequency of SNPs and haplotypes, in order to assess their association with TB susceptibility. Although we obtained no significant differences between the TB patients and the control group, linkage analysis showed that an extensively typed polymorphism, rs17525495, was associated with 21 other SNPs, all displaying evidence of association to lower LTA4H expression. While the derived alleles of these SNPs showed a moderately higher frequency in the TB group, differences were not significant. In contrast to Asian populations, where these SNPs are much more frequent, the low frequencies of candidate SNPs in Europeans render them less pertinent in a public health context. Consequently, the typing of specific polymorphisms as a strategy to establish preventive measures and differential TB drug treatments is important but needs to take into consideration that haplotypic background and structure can be substantially different in distinct geographic regions. Full article

(This article belongs to the Special Issue From Host-Pathogen Interaction to Host-Directed Therapies)

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