FEMS microbiology reviews最新文献

Human oncogenic viruses contribute significantly to the global health burden and include seven types: Epstein-Barr virus, hepatitis B virus, human T-cell leukemia virus type 1, human papillomavirus, hepatitis C virus, Kaposi's sarcoma-associated herpesvirus, and Merkel cell polyomavirus. While the roles of latent or integrated viral genomes in cancer have been documented, emerging evidence highlights the contribution of defective viruses-those carrying intragenic deletions or loss-of-function mutations-in promoting viral oncogenesis. These altered genomes often lack genes essential for lytic replication or immune recognition, which enhances their persistence and immune evasion. In virus-associated diseases, specific patterns of gene retention and deletion suggest that host-driven selective pressures drive the emergence of these altered genomes. This review examines the generation, prevalence, and functional impact of these viruses, reframing them as active participants in disease development and progression. Recognizing their role offers new insights into viral tumor evolution and creates opportunities for applications in viral diagnostics and targeted intervention strategies.

Bacterial spores formed upon metabolic stress have minimal metabolic activity and can remain dormant for years. Nevertheless, they can sense the environment and germinate quickly upon exposure to various germinants. Germinated spores can then outgrow into vegetative cells. Germination of spores of some anaerobes, especially Clostridioides difficile, is triggered by cholic acid and taurocholic acid. Elevated levels of these bile acids are thought to correlate with a perturbed gut microbiome, which cannot efficiently convert primary bile acids into secondary bile acids. That bile acids are germination-triggers suggests these bacteria have a life cycle taking place partially in the mammalian digestive tract where bile acids are plentiful; notably bile acids can be made by all vertebrates. Thus, spores survive in the environment until taken up by a host where they encounter an environment suitable for germination and then proliferate in the largely anaerobic large intestine; some ultimately sporulate there, regenerating environmentally resistant spores in the C. difficile life cycle. This review summarizes current literature on the effects of bile acids and their metabolites on spore germination in the gut and evidence that adaptation to bile acids as germinants is a consequence of a life cycle both inside and outside the digestive tract.

Plant-microbiome symbiotic interactions play a crucial role in regulating plant health and productivity. To establish symbiotic relationships, the plant secretes a variety of substances to facilitate microbial community recruitment and assembly. In recent years, important progress has been made in studying how plant exudates attract beneficial microorganisms and regulate plant health. However, the mechanisms of plant exudates-mediated microbial community recruitment and assembly and their effects on plant health are no comprehensive review. Here, we summarize the interaction mechanisms among plant exudates, microbial community recruitment and assembly, and plant health. First, we systematically evaluate the type and distribution of plant exudates, as well as their role in microbiome recruitment and assembly. Second, we summarize the mechanisms of plant exudates in terms of microbiome recruitment, diversity regulation and chemotaxis. Finally, we list some typical examples for elucidating the importance of plant exudates in promoting plant health and development. This review contributes to utilizing plant exudate or beneficial microbiome resources to manage plant health and productivity.

Studies on the epidemiology and clinical relevance of Mycobacterium tuberculosis complex (MTBC) have immensely benefited from molecular typing methods, associated software applications, and bioinformatics tools. Over the last two decades, the Pasteur Institute of Guadeloupe has developed a range of bioinformatic resources, including databases and software, to advance understanding of TB epidemiology. Traditional methods, such as IS6110-RFLP, MIRU-VNTR typing, and spoligotyping, have been instrumental but are increasingly supplanted by more precise and high-throughput techniques. These typing methods offer relatively good discrimination and reproducibility, making them popular choices for epidemiological studies. However, the advent of whole-genome sequencing (WGS) has revolutionized Mycobacterium tuberculosis complex (MTBC) typing, providing unparalleled resolution and data analysis depth. WGS enables the identification of single nucleotide polymorphisms and other genetic variations, facilitating robust phylogenetic reconstructions, and detailed outbreak investigations. This review summarizes current molecular typing methods, as well as databases and software tools used for MTBC data analysis. A comprehensive comparison of available tools and databases is provided to guide future research on the epidemiology of TB and pathogen-associated variables (drug resistance or virulence) and public health initiatives.

Synthetic C1 assimilation holds the promise of facilitating carbon capture while mitigating greenhouse gas emissions, yet practical implementation in microbial hosts remains relatively limited. Despite substantial progress in pathway design and prototyping, most efforts stay at the proof-of-concept stage, with frequent failures observed even under in vitro conditions. This review identifies seven major barriers constraining the deployment of synthetic C1 metabolism in microorganisms and proposes targeted strategies for overcoming these issues. A primary limitation is the low catalytic activity of carbon-fixing enzymes, particularly carboxylases, which restricts the overall pathway performance. In parallel, challenges in expressing multiple heterologous genes-especially those encoding metal-dependent or oxygen-sensitive enzymes-further hinder pathway functionality. At the systems level, synthetic C1 pathways often exhibit poor flux distribution, limited integration with the host metabolism, accumulation of toxic intermediates, and disruptions in redox and energy balance. These factors collectively reduce biomass formation and compromise product yields in biotechnological setups. Overcoming these interconnected challenges is essential for moving synthetic C1 assimilation beyond conceptual stages and enabling its application in scalable, efficient bioprocesses towards a circular bioeconomy.

Enteropathogens cause many gastrointestinal infections every year. However, it is often overlooked that many individuals remain asymptomatic despite exposure to these pathogens. The mechanisms underlying this effective protection against infection may hold important clues for disease prevention or therapy. Here, we focus on Salmonella enterica serovar Typhimurium (S. Tm), a well-studied enteropathogen closely related to commensal Escherichia coli. We discuss the host's multi-layered defence mechanisms that protect against S. Tm infection of the intestine, with an emphasis on the microbiota, epithelial barrier, and immune system. Perturbations in these defences, such as microbiota dysbiosis, variability in epithelial barrier integrity, or immune defects, can impair protection and increase susceptibility to disease. Additionally, we review the virulence mechanisms and metabolic adaptations that S. Tm has evolved to overcome these protective layers. This complex interplay between host defence layers and pathogen traits, shaped by both intrinsic and extrinsic factors, ultimately determines whether exposure results in asymptomatic carriage or symptomatic disease. Understanding these dynamics is critical for developing targeted interventions to prevent S. Tm infections and mitigate their impact on public health.

In the innovative field of engineered living materials (ELMs) microbiology and material sciences meet. These materials incorporate living organisms, such as bacteria, fungi, plants, or algae, to enable unique functions like self-assembly, actuation, and dynamic interaction. By utilizing (micro)biological systems in material design, ELMs promise to transform industries including healthcare, construction, and agriculture. In the early phase of ELM technology development, researchers implemented a single living strain in an already established user material. However, the complexity and potential of these materials is limited by the abilities of this single strain. Even though synthetic biology brings the opportunity to add a range of nonnative bioactivities to these cells and thus the material, the increasing metabolic burden upon implementation of multiple nonnative pathways limits the capacity of a single strain. Furthermore, higher organisms and nonstandard hosts are often desired in material settings for their native physical or metabolic advantages. However these are not always straightforward to further engineer. Thus, the use of multiple, specialized strains broadens the functionalities and thus the applicability of ELMs. Multistrain ELMs are a brand-new technology, with many promising applications.

The exquisite ability of bacteria to adapt to their environment is essential for their capacity to colonize hostile niches. In the cystic fibrosis (CF) lung, hypoxia is among several environmental stresses that opportunistic pathogens must overcome to persist and chronically colonize. Although the role of hypoxia in the host has been widely reviewed, the impact of hypoxia on bacterial pathogens has not yet been studied extensively. This review considers the bacterial oxygen-sensing mechanisms in three species that effectively colonize the lungs of people with CF, namely Pseudomonas aeruginosa, Burkholderia cepacia complex, and Mycobacterium abscessus and draws parallels between their three proposed oxygen-sensing two-component systems: BfiSR, FixLJ, and DosRS, respectively. Moreover, each species expresses regulons that respond to hypoxia: Anr, Lxa, and DosR, and encode multiple proteins that share similar homologies and function. Many adaptations that these pathogens undergo during chronic infection, including antibiotic resistance, protease expression, or changes in motility, have parallels in the responses of the respective species to hypoxia. It is likely that exposure to hypoxia in their environmental habitats predispose these pathogens to colonization of hypoxic niches, arming them with mechanisms than enable their evasion of the immune system and establish chronic infections. Overcoming hypoxia presents a new target for therapeutic options against chronic lung infections.