Critical Reviews in Microbiology最新文献

Infections account for approximately 15% of human cancers worldwide. Viruses are the most predominant infectious agents and can infect and alter various types of human cells thereby leading to the development of various forms of cancer. Current studies have reported that Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HBC), human papillomavirus (HPV), Kaposi's sarcoma-associated herpesvirus (KSHV), human T-lymphotropic virus 1 (HTLV-1), Markel cell polyomavirus (MCPyV), and BK polyomavirus are the most important oncogenic viruses that are directly involved in the initiation and progression of cancer. Additionally, some recent studies have also reported that some non-oncogenic viruses, such as COVID-19 causing SARS-CoV-2, HIV and Dengue may potentially facilitate the onset of cancer. In this review, we outline the current knowledge of the molecular machinery of viral infection, and how viral oncogenic proteins play a specific role in cellular transformation as well as oncogenesis. Here, we have also discussed the available preventive and treatment approaches for viral infection and oncogenesis. This review will further help in the making of a roadmap for future research and the development of effective therapies such as precision medicine, gene therapies, vaccine development, and immunotherapy.

Dermatophytoses is a well-known name among dermatologists due to its high prevalence among various ages of humans. It is mainly caused by skin-infecting fungi called dermatophytes. From these dermatophytes, Trichophyton indotineae is a newly virulent species with high prevalence and multidrug properties. It was first described in the Indian subcontinent as a closely genetically related strain to Trichophyton interdigitale and Trichophyton mentagrophytes, and spread quickly worldwide. Terbinafine has been utilized for the treatment of dermatophytosis caused by T. indotineae owing to the development of resistance to azole in many of its strains. Wide use of terbinafine has also induced later the development of terbinafine-resistant strains of T. indotineae. Point mutations in the squalene epoxidase (SQLE) gene, which lead to single or multiple substitutions in amino acid positions in the encoded protein (SQLE), are the main reason for antifungal resistance in T. indotineae. This review aims to determine the background of terbinafine-resistant strains of T. indotineae and where they are currently located.

Candida albicans is a primary pathogen implicated in invasive fungal infections. Through its intricate iron uptake and regulatory systems, C. albicans adeptly adapts to various iron-rich environments, circumventing the growth and virulence restrictions imposed by the host's nutritional immunity and intensifying infection severity. This fungus activates the Sef1-Sfu1-Hap43 iron homeostasis regulatory circuit via iron bioavailability sensors (iron-sulfur cluster assembly system). This activation precisely regulates multiple iron uptake pathways, including the high-affinity iron reduction system, heme-iron uptake pathway, and siderophore uptake system, as well as genes involved in iron utilization and storage, thus ensuring effective iron acquisition and maintaining iron homeostasis across diverse environmental conditions and developmental stages. Conversely, disruptions in iron metabolism markedly diminish C. albicans's pathogenic potential by impairing mitochondrial function, suppressing hyphal formation, limiting fungal colonization, and reversing antifungal drug resistance. This review presents a comprehensive analysis of the mechanisms governing iron uptake and regulation in C. albicans and examines the consequences of impaired iron homeostasis on mitochondrial function, hyphal formation, infection progression, and drug resistance. Our goal is to provide a theoretical framework to better understand the pathogenesis of C. albicans and to support the development of targeted therapeutic strategies against this resilient pathogen.

Listeria monocytogenes (L. monocytogenes) is an opportunistic intracellular pathogen that causes listeriosis in human and leads to high mortality rate. L. monocytogenes is resistant to various antibiotics due to its ability to form biofilm. Designing a new generation of antibiotics is a very expensive and time-consuming process. Moreover, the protection of antibiotics via drug delivery system can promote their effectiveness and bioavailability. Nanomedicine can be a promising tool for treating intracellular bacteria and preventing the recurrence of infections. Nanocarriers can be employed as antibacterial agents or as a carrier for antibacterial agents. In the present review, the application of nanotechnology has been discussed for the prevention and treatment of Listeria infection. According to the studies, the application of nanomaterials can be a potential strategy to eradicate infections caused by L. monocytogenes.

The rise of antibiotic-resistant bacteria poses a grave threat to global health, with the ESKAPE pathogens, which comprise Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter spp. being among the most notorious. The World Health Organization has reserved a group of last-resort antibiotics for treating multidrug-resistant bacterial infections, including those caused by ESKAPE pathogens. This situation calls for a comprehensive understanding of the resistance mechanisms as it threatens public health and hinder progress toward the Sustainable Development Goal (SDG) 3: Good Health and Well-being. The present article reviews resistance mechanisms, focusing on emerging resistance mutations in multidrug-resistant ESKAPE pathogens, particularly against last-resort antibiotics, and describes the role of biofilm formation in multidrug-resistant ESKAPE pathogens. It discusses the latest therapeutic advances, including the use of antimicrobial peptides and CRISPR-Cas systems, and the modulation of quorum sensing and iron homeostasis, which offer promising strategies for countering resistance. The integration of CRISPR-based tools and biofilm-targeted approaches provides a potential framework for managing ESKAPE infections. By highlighting the spread of current resistance mutations and biofilm-targeted approaches, the review aims to contribute significantly to advancing our understanding and strategies in combatting this pressing global health challenge.

Staphylococcus aureus (S. aureus) is a clinically significant opportunistic pathogen, and its colonization of the nasal cavity increases the risk of S. aureus infections in humans. Elucidating the mechanisms of nasal colonization by S. aureus would be beneficial in preventing infections, although this is intricate. The colonization of the nasal cavity by S. aureus depends firstly on the organism's ability to adhere to the nasal cavity, with surface components such as ClfB, IsdA, and wall teichoic acid playing an important role. Secondly, S. aureus must continuously adapt to the unfavorable environment in the nasal cavity, including epithelial cell shedding, weak acids, low nutrients, and mechanical forces, which is a prerequisite for maintaining reproduction. Furthermore, S. aureus evades the host immune system's clearance mechanisms by resisting antimicrobial substances and interfering with immune cells. Concurrently, there are interfering, competitive, or mutually beneficial relationships between the nasal microbiota and S. aureus that influence colonization.

AbstractsLactoferrin (LF) is a glycoprotein, a member of the transferrin family, and is present in a variety of secretory fluids, including milk, saliva, tears, and mucosal secretions. Iron binding, immunological regulation, antibacterial action, and intestinal nutrition absorption are only a few of its important biological roles. Although much research has been done on human lactoferrin (hLF), LF derived from different animals is equally essential for physiology and health. Depending on the intended application and mechanism of action, goods containing LF and its peptide derivatives may be classified as medical devices under FDA rules or EU Directives. For EU and FDA regulations, a product may be categorized as a medical device if it primarily provides antimicrobial or health advantages. However, LFs are not considered as medical device when used as a food addition or supplement without particular medicinal claims. Safety and efficacy data are examined for regulatory approval in this category to guarantee its appropriate usage and usefulness in clinical settings. When utilized in various medicinal applications, including wound healing, gastrointestinal problems, and immune system stimulation, the complex nature and potential health advantages of LFs and their derivatives would be consistent with their categorization as a class II medical device. The role of LFs of several species (especially cameloids) is discussed in this paper as biological products with particular biological activities and intended medical applications, where LF satisfies the requirements to be classified as a class II medical device.

Aryl hydrocarbon receptor (AhR) is a ligand-dependent transcriptional factor that is activated by a plethora of exogenous and endogenous compounds, including environmental pollutants, drugs, and microbial metabolites. The AhR plays an important role in modulating immunity. Current findings suggest that AhR activation serves as a mechanism for evasion of host antiviral immune response and promotes viral replication. This review will focus on AhR's role in RNA virus infection because they show high mutation rates compared with DNA viruses, and therefo pose one of the greatest threats to humans in terms of potential pandemic risk. Indeed, they include human immunodeficiency virus (HIV), influenza A virus (IAV), coronaviruses (CoVs), Zika virus, and others. Understanding the mechanisms by which AhR influences the immune response to these viruses is critical for developing effective therapeutic strategies. By focusing on the interplay between AhR signaling and RNA virus infections, this review aims to contribute to the growing body of knowledge regarding host-pathogen interactions and the implications for antiviral immunity.

Hepatocellular carcinoma (HCC), one of the leading causes of death worldwide, is a consequence of persistent liver injury, inflammation, and fibrosis. Recent research has demonstrated that the gut-liver axis plays a crucial role in the pathological mechanisms of HCC development. Given the overall paucity of data available, we examined both clinical and animal studies investigating the influence of gut microbiota and their metabolites on the development of HCC in light of current scientific understanding. In this review, we concentrate on the mechanism by which intestinal dysbiosis facilitates the hepatocarcinogenesis pathway and offer a detailed account of the specific pathways involved in the promotion of HCC by the microbiome and its metabolites. Based on this, researchers might extrapolate which strains would be beneficial or harmful to restore gut homeostasis by targeting gut-liver axis in the pathogenesis of HCC.

There is growing evidence that microbial dysbiosis is intimately related to carcinogenesis across several types of human cancer. Neisseria gonorrhoeae is best known for causing acute exudative genitourinary infection in males. N. gonorrhoeae can also cause chronic, asymptomatic infection of the female genitourinary tract along with the oropharynx and rectum of both sexes. Epidemiological studies suggest that N. gonorrhoeae is an independent risk factor for cancer of the anus, bladder, cervix, prostate, and oropharynx. It is not clear however if this association is causal. The purpose of this review is to appraise epidemiological, experimental, and clinical data in order to understand the possible carcinogenic potential of this sexually transmitted bacterium.