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Turnip mosaic virus (TuMV) is a devastating potyvirus pathogen that infects a wide variety of both cultivated and wild Brassicaceae plants. We urgently need more information and understanding of TuMV pathogenesis and the host responses involved in disease development in cruciferous crops. TuMV displays great versatility in viral pathogenesis, especially in its replication and intercellular movement. Moreover, in the coevolutionary arms races between TuMV and its hosts, the virus has evolved to co-opt host factors to facilitate its infection and counter host defense responses. This review mainly focuses on recent advances in understanding the viral factors that contribute to the TuMV infection cycle and the host resistance mechanism in Brassica. Finally, we propose some future research directions on TuMV pathogenesis and control strategies to design durable TuMV-resistant Brassica crops.

Monkeypox virus (MPXV) is the etiological agent of monkeypox (mpox), a zoonotic disease. MPXV is endemic in the forested regions of West and Central Africa, but the virus has recently spread globally, causing outbreaks in multiple non-endemic countries. In this paper, we review the characteristics of the virus, including its ecology, genomics, infection biology, and evolution. We estimate by phylogenomic molecular clock that the B.1 lineage responsible for the 2022 mpox outbreaks has been in circulation since 2016. We interrogate the host-virus interactions that modulate the virus infection biology, signal transduction, pathogenesis, and host immune responses. We highlight the changing pathophysiology and epidemiology of MPXV and summarize recent advances in the prevention and treatment of mpox. In addition, this review identifies knowledge gaps with respect to the virus and the disease, suggests future research directions to address the knowledge gaps, and proposes a One Health approach as an effective strategy to prevent current and future epidemics of mpox. [ABSTRACT FROM AUTHOR]

Monkeypox virus (MPXV) is the etiological agent of monkeypox (mpox), a zoonotic disease. MPXV is endemic in the forested regions of West and Central Africa, but the virus has recently spread globally, causing outbreaks in multiple non-endemic countries. In this paper, we review the characteristics of the virus, including its ecology, genomics, infection biology, and evolution. We estimate by phylogenomic molecular clock that the B.1 lineage responsible for the 2022 mpox outbreaks has been in circulation since 2016. We interrogate the host-virus interactions that modulate the virus infection biology, signal transduction, pathogenesis, and host immune responses. We highlight the changing pathophysiology and epidemiology of MPXV and summarize recent advances in the prevention and treatment of mpox. In addition, this review identifies knowledge gaps with respect to the virus and the disease, suggests future research directions to address the knowledge gaps, and proposes a One Health approach as an effective strategy to prevent current and future epidemics of mpox.

ABSTRACT Machine learning and artificial intelligence (AI) are becoming more common in infection biology laboratories around the world. Yet, as they gain traction in research, novel frontiers arise. Novel artificial intelligence algorithms are capable of addressing advanced tasks like image generation and question answering. However, similar algorithms can prove useful in addressing advanced questions in infection biology like prediction of host-pathogen interactions or inferring virus protein conformations. Addressing such tasks requires large annotated data sets, which are often scarce in biomedical research. In this review, I bring together several successful examples where such tasks were addressed. I underline the importance of formulating novel AI tasks in infection biology accompanied by freely available benchmark data sets to address these tasks. Furthermore, I discuss the current state of the field and potential future trends. I argue that one such trend involves AI tools becoming more versatile.

On September 20–22 September 2023, the international conference 'Microbiology 2023: from single cell to microbiome and host' convened microbiologists from across the globe for a very successful symposium, showcasing cutting-edge research in the field. Invited lecturers delivered exceptional presentations covering a wide range of topics, with a major emphasis on phages and microbiomes, on the relevant bacteria within these ecosystems, and their multifaceted roles in diverse environments. Discussions also spanned the intricate analysis of fundamental bacterial processes, such as cell division, stress resistance, and interactions with phages. Organized by four renowned Academies, the German Leopoldina, the French Académie des sciences, the Royal Society UK, and the Royal Swedish Academy of Sciences, the symposium provided a dynamic platform for experts to share insights and discoveries, leaving participants inspired and eager to integrate new knowledge into their respective projects. The success of Microbiology 2023 prompted the decision to host the next quadrennial academic meeting in Sweden. This choice underscores the commitment to fostering international collaboration and advancing the frontiers of microbiological knowledge. The transition to Sweden promises to be an exciting step in the ongoing global dialogue and specific collaborations on microbiology, a field where researchers will continue to push the boundaries of knowledge, understanding, and innovation not only in health and disease but also in ecology. [ABSTRACT FROM AUTHOR]

The article discusses the 5th UK Cellular Microbiology Network Meeting, which took place in London in June 2023. The meeting aimed to support and enhance the cellular microbiology community in the UK and Europe, providing a platform for collaboration and research. The event featured keynote speakers, presentations from early career researchers, and discussions on various topics related to cellular microbiology, including host-pathogen interactions and innate immunity. The meeting concluded with a community discussion and the recognition of outstanding presentations. The article expresses gratitude to the sponsors and organizers of the event. [Extracted from the article]

Bacteriophages encode diverse anti-CRISPR (Acr) proteins that inhibit CRISPR-Cas immunity during infection of their bacterial hosts. Although detailed mechanisms have been characterized for multiple Acr proteins, an understanding of their role in phage infection biology is just emerging. Here, we review recent work in this area and propose a framework of "phage autonomy" to evaluate CRISPR-immune evasion strategies. During phage infection, Acr proteins are deployed by a tightly regulated "fast on-fast off" transcriptional burst, which is necessary, but insufficient, for CRISPR-Cas inactivation. Instead of a single phage shutting down CRISPR-Cas immunity, a community of acr-carrying phages cooperate to suppress bacterial immunity, displaying low phage autonomy. Enzymatic Acr proteins with novel mechanisms have been recently revealed and are predicted to enhance phage autonomy, while phage DNA protective measures offer the highest phage autonomy observed. These varied Acr mechanisms and strengths also have unexpected impacts on the bacterial populations and competing phages.

My scientific career has resulted from key decisions and reorientations, sometimes taken rapidly but not always, guided by discussions or collaborations with amazing individuals from whom I learnt a lot scientifically and humanly. I had never anticipated that I would accomplish so much in what appeared as terra incognita when I started to interrogate the mechanisms underlying the virulence of the bacterium Listeria monocytogenes. All this has been possible thanks to a number of talented team members who ultimately became friends. [ABSTRACT FROM AUTHOR]

In September 2022, an international summer course entitled 'The new microbiology' took place in Greece, on the island of Spetses. The organizers aimed to highlight the spectacular advances and the renaissance occurring in Microbiology, driven by developments in genomics, proteomics, imaging techniques, and bioinformatics. Combinations of these advances allow for single cell analyses, rapid and relatively inexpensive metagenomic and transcriptomic data analyses and comparisons, visualization of previously unsuspected mechanisms, and large-scale studies. A 'New Microbiology' is emerging which allows studies that address the critical roles of microbes in health and disease, in humans, animals, and the environment. The concept of one health is now transforming microbiology. The goal of the course was to discuss all these topics with members of the new generation of microbiologists all of whom were highly motivated and fully receptive. [ABSTRACT FROM AUTHOR]

Plasmodiophora brassicae (Wor.) is an obligate plant pathogen affecting Brassicae worldwide. To date, there is very little information available on the biology and molecular basis of P. brassicae primary and secondary zoospore infections. To examine their roles, we used microscope to systematically investigate the infection differences of P. brassicae between samples inoculated separately with resting spores and secondary zoospores. The obvious development of P. brassicae asynchrony that is characterized by secondary plasmodium, resting sporangial plasmodium, and resting spores was observed at 12 days in Brassica rapa inoculated with resting spores but not when inoculated with secondary zoospores at the same time. Inoculation with resting spores resulted in much more development of zoosporangia clusters than inoculation with secondary zoospores in non-host Spinacia oleracea. The results indicated that primary zoospore infection played an important role in the subsequent development. To improve our understanding of the infection mechanisms, RNA-seq analysis was performed. Among 18 effectors identified in P. brassicae, 13 effectors were induced in B. rapa seedlings inoculated with resting spores, which suggested that the pathogen and host first contacted, and more effectors were needed. Corresponding to those in B. rapa, the expression levels of most genes involved in the calcium-mediated signaling pathway and PTI pathway were higher in plants inoculated with resting spores than in those inoculated with secondary zoospores. The ETI pathway was suppressed after inoculation with secondary zoospores. The genes induced after inoculation with resting spores were suppressed in B. rapa seedlings inoculated with secondary zoospores, which might be important to allow a fully compatible interaction and contribute to a susceptible reaction in the host at the subsequent infection stage. The primary zoospores undertook an more important interaction with plants. [ABSTRACT FROM AUTHOR]

Gymnopus fusipes (syn. Collybia fusipes; syn. Agaricus fusipes) is an agaricomycete fungus known to cause root rot on a number of economically important tree species, including oak, where it has been linked to the development of chronic oak decline. Due to lack of correlation between above‐ground decline symptoms and G. fusipes infection, its presence can often go undiagnosed until mortality. Although G. fusipes was first described over 200 years ago, there is still a paucity of information on the biology and ecology of this species, which represents a barrier to understanding its impacts on tree health. The aim of this review was to synthesize existing knowledge on the biology, ecology, host range and host interactions of G. fusipes. Using a systematic search, five online databases were used to obtain published literature resulting from the search terms 'Gymnopus fusipes', 'Collybia fusipes' and 'Agaricus fusipes'. After a strict filtering process, the papers were examined for data pertaining to the biochemistry, distribution, ecology, genomic information, host range, infection biology, morphology and phylogeny of the species. The results reveal that there is a large amount of ambiguous and sometimes spurious citation of G. fusipes in the literature. However, it can be confirmed that G. fusipes is a facultative saproparasite, found in several countries, mainly in Europe, and is associated with several socioeconomically important host species, including oak, chestnut, and fir. Gymnopus fusipes has repeatedly been investigated with regard to oak decline in Europe, where it is believed to play a crucial role in the early stage of decline development. Key knowledge gaps highlighted in this review include a lack of information on the basic biology of the species, including its life cycle, which is crucial to fully understanding G. fusipes infection and epidemiology. Further work is needed to assess G. fusipes distribution, phylogeny and host range through molecular identification. There is also a need to characterize the pathogen–host interaction at a molecular level, with identification of active genes and therefore the mechanisms of infection. A combination of culture‐based and molecular techniques should be utilized in order to close these key knowledge gaps. [ABSTRACT FROM AUTHOR]

Deep understanding of the SARS-CoV-2 effects on host molecular pathways is paramount for the discovery of early biomarkers of outcome of coronavirus disease 2019 (COVID-19) and the identification of novel therapeutic targets. In that light, we generated metabolomic data from COVID-19 patient blood using high-throughput targeted nuclear magnetic resonance (NMR) spectroscopy and high-dimensional flow cytometry. We find considerable changes in serum metabolome composition of COVID-19 patients associated with disease severity, and response to tocilizumab treatment. We built a clinically annotated, biologically-interpretable space for precise time-resolved disease monitoring and characterize the temporal dynamics of metabolomic change along the clinical course of COVID-19 patients and in response to therapy. Finally, we leverage joint immuno-metabolic measurements to provide a novel approach for patient stratification and early prediction of severe disease. Our results show that high-dimensional metabolomic and joint immune-metabolic readouts provide rich information content for elucidation of the host’s response to infection and empower discovery of novel metabolic-driven therapies, as well as precise and efficient clinical action.

Deep understanding of the SARS-CoV-2 effects on host molecular pathways is paramount for the discovery of early biomarkers of outcome of coronavirus disease 2019 (COVID-19) and the identification of novel therapeutic targets. In that light, we generated metabolomic data from COVID-19 patient blood using high-throughput targeted nuclear magnetic resonance (NMR) spectroscopy and high-dimensional flow cytometry. We find considerable changes in serum metabolome composition of COVID-19 patients associated with disease severity, and response to tocilizumab treatment. We built a clinically annotated, biologically-interpretable space for precise time-resolved disease monitoring and characterize the temporal dynamics of metabolomic change along the clinical course of COVID-19 patients and in response to therapy. Finally, we leverage joint immuno-metabolic measurements to provide a novel approach for patient stratification and early prediction of severe disease. Our results show that high-dimensional metabolomic and joint immune-metabolic readouts provide rich information content for elucidation of the host's response to infection and empower discovery of novel metabolic-driven therapies, as well as precise and efficient clinical action. [ABSTRACT FROM AUTHOR]

In the context of host-pathogen interactions, gram-negative bacterial virulence factors, such as effectors, may be transferred from bacterial to eukaryotic host cytoplasm by multicomponent Type III protein secretion systems (T3SSs). Central to Salmonella enterica serovar Typhimurium (S. Typhimurium) pathogenesis is the secretion of over 40 effectors by two T3SSs encoded within pathogenicity islands SPI-1 and SPI-2. These effectors manipulate miscellaneous host cellular processes, such as cytoskeleton organization and immune signaling pathways, thereby permitting host colonization and bacterial dissemination. Recent research on effector biology provided mechanistic insights for some effectors. However, for many effectors, clearly defined roles and host target repertoires—further clarifying effector interconnectivity and virulence networks—are yet to be uncovered. Here we demonstrate the utility of the recently described viral-like particle trapping technology Virotrap as an effective approach to catalog S. Typhimurium effector-host protein complexes (EH-PCs). Mass spectrometry-based Virotrap analysis of the novel E3 ubiquitin ligase SspH2 previously shown to be implicated in modulating actin dynamics and immune signaling, exposed known host interactors PFN1 and−2 besides several putative novel, interconnected host targets. Network analysis revealed an actin (-binding) cluster among the significantly enriched hits for SspH2, consistent with the known localization of the S-palmitoylated effector with actin cytoskeleton components in the host. We show that Virotrap complements the current state-of-the-art toolkit to study protein complexes and represents a valuable means to screen for effector host targets in a high-throughput manner, thereby bridging the knowledge gap between effector-host interplay and pathogenesis.

The study aimed to monitor parasite and host gene expression during the early stages of Eimeria tenella infection of chicken cells using dual RNA-Seq analysis. For this, we used chicken macrophage-like cell line HD11 cultures infected in vitro with purified E. tenella sporozoites. Cultures were harvested between 2 and 72 h post-infection and mRNA was extracted and sequenced. Dual RNA-Seq analysis showed clear patterns of altered expression for both parasite and host genes during infection. For example, genes in the chicken immune system showed upregulation early (2–4 h), a strong downregulation of genes across the immune system at 24 h and a repetition of early patterns at 72 h, indicating that invasion by a second generation of parasites was occurring. The observed downregulation may be due to immune self-regulation or to immune evasive mechanisms exerted by E. tenella. Results also suggested pathogen recognition receptors involved in E. tenella innate recognition, MRC2, TLR15 and NLRC5 and showed distinct chemokine and cytokine induction patterns. Moreover, the expression of several functional categories of Eimeria genes, such as rhoptry kinase genes and microneme genes, were also examined, showing distinctive differences which were expressed in sporozoites and merozoites. [ABSTRACT FROM AUTHOR]

The potential infection biology of Plasmodiophora brassicae in resistant hosts and non-hosts is still not completely understood. Clubroot resistance assay on European clubroot differentials (ECD) set revealed that ECD10 (Brassica napus) and ECD4 (Brassica rapa) show a complete resistance to the tested P. brassicae isolate in contrast to highly susceptible hosts Westar (B. napus) and ECD5 (B. rapa). Previously, we used fluorescent probe-based confocal microscopy (FCM) to refine the life cycle of P. brassicae and indicate the important time points during its infection in Arabidopsis. Here, we used FCM to systematically investigate the infection of P. brassicae in two resistant host species ECD10 and ECD4 and two non-host crops wheat and barley at each indicated time points, compared with two susceptible hosts Westar and ECD5. We found that P. brassicae can initiate the primary infection phase and produce uninucleate primary plasmodia in both resistant hosts and non-hosts just like susceptible hosts at 2 days post-inoculation (dpi). Importantly, P. brassicae can develop into zoosporangia and secondary zoospores and release the secondary zoospores from the zoosporangia in resistant hosts at 7 dpi, comparable to susceptible hosts. However, during the secondary infection phase, no secondary plasmodium was detected in the cortical cells of both resistant hosts in contrast to massive secondary plasmodia present in the cortex tissue of two susceptible hosts leading to root swelling at 15 dpi. In both non-host crops, only uninucleate primary plasmodia were observed throughout roots at 7 and 15 dpi. Quantitative PCR based on DNA revealed that the biomass of P. brassicae has no significant increase from 2 dpi in non-host plants and from 7 dpi in resistant host plants, compared to the huge biomass increase in susceptible host plants from 2 to 25 dpi. Our study reveals that the primary infection phase in the root epidermis and the secondary infection phase in the cortex tissue are, respectively, blocked in non-hosts and resistant hosts, contributing to understanding of cellular and molecular mechanisms underlying clubroot non-host and host resistance.

The potential infection biology of Plasmodiophora brassicae in resistant hosts and non-hosts is still not completely understood. Clubroot resistance assay on European clubroot differentials (ECD) set revealed that ECD10 (Brassica napus) and ECD4 (Brassica rapa) show a complete resistance to the tested P. brassicae isolate in contrast to highly susceptible hosts Westar (B. napus) and ECD5 (B. rapa). Previously, we used fluorescent probe-based confocal microscopy (FCM) to refine the life cycle of P. brassicae and indicate the important time points during its infection in Arabidopsis. Here, we used FCM to systematically investigate the infection of P. brassicae in two resistant host species ECD10 and ECD4 and two non-host crops wheat and barley at each indicated time points, compared with two susceptible hosts Westar and ECD5. We found that P. brassicae can initiate the primary infection phase and produce uninucleate primary plasmodia in both resistant hosts and non-hosts just like susceptible hosts at 2 days post-inoculation (dpi). Importantly, P. brassicae can develop into zoosporangia and secondary zoospores and release the secondary zoospores from the zoosporangia in resistant hosts at 7 dpi, comparable to susceptible hosts. However, during the secondary infection phase, no secondary plasmodium was detected in the cortical cells of both resistant hosts in contrast to massive secondary plasmodia present in the cortex tissue of two susceptible hosts leading to root swelling at 15 dpi. In both non-host crops, only uninucleate primary plasmodia were observed throughout roots at 7 and 15 dpi. Quantitative PCR based on DNA revealed that the biomass of P. brassicae has no significant increase from 2 dpi in non-host plants and from 7 dpi in resistant host plants, compared to the huge biomass increase in susceptible host plants from 2 to 25 dpi. Our study reveals that the primary infection phase in the root epidermis and the secondary infection phase in the cortex tissue are, respectively, blocked in non-hosts and resistant hosts, contributing to understanding of cellular and molecular mechanisms underlying clubroot non-host and host resistance. [ABSTRACT FROM AUTHOR]

Metabolic adaptation to the host cell is important for obligate intracellular pathogens such as Chlamydia trachomatis (Ct). Here we infer the flux differences for Ct from proteome and qRT-PCR data by comprehensive pathway modeling. We compare the comparatively inert infectious elementary body (EB) and the active replicative reticulate body (RB) systematically using a genome-scale metabolic model with 321 metabolites and 277 reactions. This did yield 84 extreme pathways based on a published proteomics dataset at three different time points of infection. Validation of predictions was done by quantitative RT-PCR of enzyme mRNA expression at three time points. Ct’s major active pathways are glycolysis, gluconeogenesis, glycerol-phospholipid (GPL) biosynthesis (support from host acetyl-CoA) and pentose phosphate pathway (PPP), while its incomplete TCA and fatty acid biosynthesis are less active. The modeled metabolic pathways are much more active in RB than in EB. Our in silico model suggests that EB and RB utilize folate to generate NAD(P)H using independent pathways. The only low metabolic flux inferred for EB involves mainly carbohydrate metabolism. RB utilizes energy -rich compounds to generate ATP in nucleic acid metabolism. Validation data for the modeling include proteomics experiments (model basis) as well as qRT-PCR confirmation of selected metabolic enzyme mRNA expression differences. The metabolic modeling is made fully available here. Its detailed insights and models on Ct metabolic adaptations during infection are a useful modeling basis for future studies.

Metabolic adaptation to the host cell is important for obligate intracellular pathogens such as Chlamydia trachomatis (Ct). Here we infer the flux differences for Ct from proteome and qRT-PCR data by comprehensive pathway modeling. We compare the comparatively inert infectious elementary body (EB) and the active replicative reticulate body (RB) systematically using a genome-scale metabolic model with 321 metabolites and 277 reactions. This did yield 84 extreme pathways based on a published proteomics dataset at three different time points of infection. Validation of predictions was done by quantitative RT-PCR of enzyme mRNA expression at three time points. Ct 's major active pathways are glycolysis, gluconeogenesis, glycerol-phospholipid (GPL) biosynthesis (support from host acetyl-CoA) and pentose phosphate pathway (PPP), while its incomplete TCA and fatty acid biosynthesis are less active. The modeled metabolic pathways are much more active in RB than in EB. Our in silico model suggests that EB and RB utilize folate to generate NAD(P)H using independent pathways. The only low metabolic flux inferred for EB involves mainly carbohydrate metabolism. RB utilizes energy -rich compounds to generate ATP in nucleic acid metabolism. Validation data for the modeling include proteomics experiments (model basis) as well as qRT-PCR confirmation of selected metabolic enzyme mRNA expression differences. The metabolic modeling is made fully available here. Its detailed insights and models on Ct metabolic adaptations during infection are a useful modeling basis for future studies. [ABSTRACT FROM AUTHOR]

The use of zebrafish as a model for human conditions is widely recognized. Within the last couple of decades, the zebrafish has furthermore increasingly been utilized as a model for diseases in aquacultured fish species. The unique tools available in zebrafish present advantages compared to other animal models and unprecedented in vivo imaging and the use of transgenic zebrafish lines have contributed with novel knowledge to this field. In this review, investigations conducted in zebrafish on economically important diseases in aquacultured fish species are included. Studies are summarized on bacterial, viral and parasitic diseases and described in relation to prophylactic approaches, immunology and infection biology. Considerable attention has been assigned to innate and adaptive immunological responses. Finally, advantages and drawbacks of using the zebrafish as a model for aquacultured fish species are discussed.

Anthracnose, caused by Colletotrichum sublineolum Henn. ex Sacc. & Trotter, is one of the most important sorghum [Sorghum bicolor (L.) Moench] diseases in Brazil. This fungus exhibits conidial dimorphism, producing either falcate or oval conidia on solid and liquid media, respectively. We compared patterns of the initial infection events by these two types of conidia on sorghum leaves using light microscopy and scanning electron microscopy. The infection events during the first 24 h were similar for both oval and falcate conidia. Globose and melanized apressoria were formed at 24 h after inoculation (hai) regardless of the conidia type. Dense mycelium and oval conidia developed from germinated falcate conidia at 32 hai. Hyphal mass displaying acervuli filled with falcate conidia and surrounded by setae, developed from germinated oval conidia at 48 hai. Oval conidia were as capable as falcate conidia of infecting sorghum leaves. The inherent ability to grow faster and the easeness with which oval conidia can be produced in vitro as compared to falcate, make the former a preferred choice for studies on the C. sublineolum-sorghum interaction. It would be instructive to further investigate the potential role of the oval conidia in epidemics.

Abstract The surveillance and pathogen fighting functions of the complement system have evolved to protect mammals from life-threatening infections. In turn, pathogens have developed complex molecular mechanisms to subvert, divert and evade the effector functions of the complement. The study of complement immunoevasion by pathogens sheds light on their infection drivers, knowledge that is essential to implement therapies. At the same time, complement evasion also acts as a discovery ground that reveals important aspects of how complement works under physiological conditions. In recent years, complex interrelationships between infection insults and the onset of autoimmune and complement dysregulation diseases have led to propose that encounters with pathogens can act as triggering factors for disease. The correct management of these diseases involves the recognition of their triggering factors and the development and administration of complement-associated molecular therapies. Even more recently, unsuspected proteins from pathogens have been shown to possess moonlighting functions as virulence factors, raising the possibility that behind the first line of virulence factors there be many more pathogen proteins playing secondary, helping and supporting roles for the pathogen to successfully establish infections. In an era where antibiotics have a progressively reduced effect on the management and control of infectious diseases worldwide, knowledge on the mechanisms of pathogenic invasion and evasion look more necessary and pressing than ever. [ABSTRACT FROM AUTHOR]

The HtrA family of chaperones and serine proteases is important for regulating stress responses and controlling protein quality in the periplasm of bacteria. HtrA is also associated with infectious diseases since inactivation of htrA genes results in significantly reduced virulence properties by various bacterial pathogens. These virulence features of HtrA can be attributed to reduced fitness of the bacteria, higher susceptibility to environmental stress and/or diminished secretion of virulence factors. In some Gram-negative and Gram-positive pathogens, HtrA itself can be exposed to the extracellular environment promoting bacterial colonisation and invasion of host tissues. Most of our knowledge on the function of exported HtrAs stems from research on Helicobacter pylori, Campylobacter jejuni, Borrelia burgdorferi, Bacillus anthracis, and Chlamydia species. Here, we discuss recent progress showing that extracellular HtrAs are able to cleave cell-to-cell junction factors including E-cadherin, occludin, and claudin-8, as well as extracellular matrix proteins such as fibronectin, aggrecan, and proteoglycans, disrupting the epithelial barrier and producing substantial host cell damage. We propose that the export of HtrAs is a newly discovered strategy, also applied by additional bacterial pathogens. Consequently, exported HtrA proteases represent highly attractive targets for antibacterial treatment by inhibiting their proteolytic activity or application in vaccine development. [ABSTRACT FROM AUTHOR]

Influenza viruses are respiratory pathogens that represent a significant threat to public health, despite the large-scale implementation of vaccination programs. It is necessary to understand the detailed and complex interactions between influenza virus and its host cells in order to identify successful strategies for therapeutic intervention. During viral entry, the cellular microenvironment presents invading pathogens with a series of obstacles that must be overcome to infect permissive cells. Influenza hijacks numerous host cell proteins and associated biological pathways during its journey into the cell, responding to environmental cues in order to successfully replicate. The cellular cytoskeleton and its constituent microtubules represent a heavily exploited network during viral infection. Cytoskeletal filaments provide a dynamic scaffold for subcellular viral trafficking, as well as virus-host interactions with cellular machineries that are essential for efficient uncoating, replication, and egress. In addition, influenza virus infection results in structural changes in the microtubule network, which itself has consequences for viral replication. Microtubules, their functional roles in normal cell biology, and their exploitation by influenza viruses will be the focus of this review.

Western blots are a commonly used method for protein detection and quantification in biological samples. Compensation of loading variations is achieved by housekeeping protein (HKP) normalization and/or total protein normalization (TPN). However, under infection conditions, HKP normalization, traditionally used in cell biology for quantification of western blots, can be problematic. Binding of microbes to target cells via specific receptors can induce signal transduction events resulting in drastic changes in the level of expression of HKPs. Additionally, samples collected after infection assays will include cellular and microbial proteins altering the analysis with TPN. Here we demonstrate under experimental infection conditions, how a reliable semi-quantitative analysis of proteins in western blots can be achieved using the Stain-Free technology. [ABSTRACT FROM AUTHOR]

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By providing useful tools to study host–pathogen interactions, next-generation omics has recently enabled the study of gene expression changes in both pathogen and infected host simultaneously. However, since great discriminative power is required to study pathogen and host simultaneously throughout the infection process, the depth of quantitative gene expression profiling has proven to be unsatisfactory when focusing on bacterial pathogens, thus preferentially requiring specific strategies or the development of novel methodologies based on complementary omics approaches. In this review, we focus on the difficulties encountered when making use of proteogenomics approaches to study bacterial pathogenesis. In addition, we review different omics strategies (i.e., transcriptomics, proteomics and secretomics) and their applications for studying interactions of pathogens with their host.

Using parasites as sentinel organisms has received increased attention due to their responses toward environmental degradation. In some sections of the Vaal River, South Africa, water quality is altered and biota distribution affected. The aims of this study were to assess and compare infection variables of Paradipolozoon ichthyoxanthonAvenant-Oldewage, 2014 in Avenant- Oldewage et al. (2014) at two sites along the Vaal River and compare the water quality and trace element levels at the sites. Infection variables of the parasite, physico-chemical variables, and sediment and water samples for trace element analysis were collected at each site. Conductivity and trace element concentrations were higher at the Vaal River site than the Vaal Dam. Temporal variances in water quality and parasite prevalence, mean intensity and mean abundance, at intervals over a 14 year period occurred, P. ichthyoxanthon was absent at the Vaal River site though the host fish are present. Prevalence peaks in summer and winter. Comparison of infection data to water quality and trace elements indicated that conductivity and trace element levels negatively affected/correlated with the infection variables. Higher trace elements concentration and conductivity at the Vaal River site are thought to be driving factors responsible for absence of the parasite. [ABSTRACT FROM AUTHOR]

Cell biological research in the wheat pathogen Zymoseptoria tritici (formerly Mycosphaerella graminicola ) has led to a good understanding of the histology of the infection process. Expression profiling and bioinformatic approaches, combined with molecular studies on signaling pathways, effectors and potential necrosis factors provides first insight into the complex interplay between the host and the pathogen. Cell biological studies will help to further our understanding of the infection strategy of the fungus. The cellular organization and intracellular dynamics of the fungus itself is largely unexplored. Insight into essential cellular processes within the pathogen will expand our knowledge of the basic biology of Z. tritici , thereby providing putative new anti-fungal targets. [ABSTRACT FROM AUTHOR]