Intracellular bacteria exploit host cell niches, such as lysosomes, phagosomes, cytosol, entire cells, and even erythrocytes, to evade immune clearance and escape conventional antibiotics. These environments pose numerous therapeutic challenges, including crossing host cell membranes, navigating endosomal trafficking, tolerating acidic and redox conditions, bypassing efflux mechanisms, and countering phenotypic tolerance. Although recent advancements in nanotechnology—such as carriers, prodrugs, and host‐directed therapies—offer promising solutions, current strategies remain narrowly focused on “getting the drug inside the cell”, leaving therapeutic agents vulnerable to off‐site targeting, degradation, and functional failure. This review introduces a next‐generation approach for intracellular antibacterial therapy, incorporating subcellular targeting, dual‐function delivery systems, innovative biomimetic carriers, precise intracellular pharmacokinetics/pharmacodynamics (PK/PD) assessment, and artificial intelligence‐assisted drug design. Highlighting frameworks for multimodal regimens targeting intracellular bacteria, we advocate a transition from solely facilitating cellular entry to achieving precise spatiotemporal regulation of drug activity within infected host cells. This paradigm informs the development of therapeutics designed to persist within the intracellular bacterial niche, minimizing relapse and reducing the emergence of antimicrobial resistance.

The global socioeconomic and health impacts of microbial diseases cannot be overemphasized. The emergence of the coronavirus in 2019 and the ongoing threat of infectious diseases, such as HIV/AIDS, tuberculosis, and hepatitis, remind us of the impact these infections have on economic stability and global health. Gaps in the treatment of microbial infections and their contribution to increased mortality necessitate holistic and long-term solutions, as opposed to antibiotics, which were previously relied upon. Immunotherapy is becoming increasingly promising for the treatment of microbial infections. This study reviews recent advances in immunotherapeutic strategies, particularly cytokine-based therapies, adoptive cell therapy, monoclonal antibodies, and immune checkpoint inhibitors, for the control of antimicrobial resistance. New inventive approaches, such as chimeric antigen receptor T cell therapy and mucosal-associated invariant T cells, have been discussed in the context of bacterial and viral infections, highlighting promising results from clinical trials and addressing the challenges of toxicity, immune evasion, and therapy resistance that are inherent in these diseases. Future priorities include optimizing combination therapies and exploring new immunomodulatory targets to improve the effectiveness of these interventions in treating antimicrobial resistance and other infectious diseases.

Migratory birds have been implicated in the spread of diverse emerging infectious pathogens, including West Nile virus, Usutu virus, Avian influenza viruses, Salmonella, Campylobacter, antimicrobial-resistant (AMR) bacteria, and antibiotic resistance genes (ARGs). Beyond their roles as vectors and reservoirs, migratory birds are also susceptible hosts whose own health may be compromised by these infections, reflecting their dual position in the ecology of pathogens. As facilitators of pathogen transmission during their long-distance migrations, often spanning thousands of kilometres and connecting ecosystems across continents, these birds can easily cross-national borders and circumvent traditional biosecurity measures, thereby acting as primary or secondary vectors in the transmission of cross-species diseases among wildlife, livestock, and humans. Africa occupies a pivotal position in global migratory bird networks, yet comprehensive data on pathogen carriage remain limited. Gaps in knowledge of pathogen diversity constrain current surveillance systems, resulting in insufficient genomic monitoring of pathogen evolution and a weak integration of avian ecology with veterinary and human health. These limitations hinder early detection of novel pathogens and reduce the continent’s preparedness to manage outbreaks. Therefore, this review provides a holistic assessment of these challenges by consolidating existing knowledge concerning the pathogens transmitted by migratory birds in Africa, while recognizing the adverse effect of pathogens, which potentiates population decline, extinction, and ecological imbalance. It further advocates for the adoption of a comprehensive One Health-omics approach that not only strengthens surveillance and technological capacity but also prioritizes the protection of avian health as an integral component of ecosystem and public health.

Antiphospholipid syndrome (APS), also known as Hughes syndrome, is a systemic autoimmune disorder characterized by recurrent thrombosis and pregnancy complications, accompanied by the presence of antiphospholipid antibodies (aPLs). These antibodies target anionic phospholipids or protein–phospholipid complexes within cell membranes, contributing to the underlying mechanisms of the disease. Although anticoagulation therapy remains the cornerstone of APS management, it often fails to prevent complications, particularly in obstetric and thrombotic cases. As autoimmune diseases become increasingly linked to alterations in the gut microbiome, this study investigates the complex interaction between gut bacteria and immune modulation in APS. We explore how disruptions in the gut microbiome may influence the development of autoimmune conditions, with a specific focus on APS. By identifying key microorganisms potentially involved in this gut–immune axis, we aim to provide insights into novel preventive and control approaches. Future research should focus on harnessing the gut microbiome to develop more effective treatments that target both the immune system and microbial populations in APS patients.

Sickle cell anaemia is one of the haemoglobin abnormalities resulting from a genetic mutation— it is caused by inheriting two faulty genes that result in an abnormal substitution of glutamate for valine on the beta chain of haemoglobin, which causes haemoglobin molecules to stick together. According to a World Health Organization (WHO) report, 20 out of every 1,000 births suffer from sickle-cell anaemia, and 24% of Nigerians are carriers of this mutant gene. Scientists have suggested several solutions, including stem cell transplantation and gene therapies, but these have faced opposition due to ethical beliefs, high cost, and the ensuing immune issues. Research is now centered on advancing genome editing techniques for gene therapy. Ongoing studies have proven that genetic differences can be corrected methodically by modifying the genome at specific sites instead of introducing a new copy of the affected gene into the cells; due to the effectiveness of this method, scientists are testing its applications in manipulating genes in various systems. This review correlates a few studies that used the recently developed technique—CRISPR-Cas9—as a novel approach to gene therapy, dissecting the different clinical studies about sickle cell origin to point out many of its ethical and medical limitations, the consequences of these limitations, and the advancements this technology has made possible.

Background Polycyclic aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs) are combustion-derived pollutants linked to cardiovascular disease. Prior NHANES analyses have evaluated these chemicals individually, failing to capture the correlated co-exposure structures that characterize real-world environmental burden, thereby underscoring the need for application. In this study, we applied an unsupervised machine learning pipeline to urinary biomarker data to identify multi-chemical exposure clusters and quantify their differential cardiovascular risk profiles in a nationally representative US sample. Methods We analyzed 2,979 participants from NHANES between 2017-2018, representing an estimated 36.8 million US adults after complex survey weighting. Twenty-five urinary biomarkers (6 PAH, 19 VOC metabolites) were log-transformed, imputed using Multivariate Imputation by Chained Equations (MICE), and standardized. Uniform Manifold Approximation and Projection (UMAP) was used for dimensionality reduction, followed by Gaussian Mixture Model (GMM) clustering. Survey-weighted prevalence estimates with 95% confidence intervals (CIs) were calculated for hypertension and high total cholesterol within each cluster. Weighted multivariable logistic regression was used to estimate odds ratios (OR) for hypertension, adjusting for age, sex, race/ethnicity, and income. Results Four exposure clusters were identified with a mean assignment probability of 0.948. The High combustion cluster (n=370; estimated 5.1 million US adults) exhibited the highest multi-chemical burden and a weighted hypertension prevalence of 39.3% (95% CI 37.2-41.4%), compared to 28.7% (95% CI 21.9-35.5%) in the Low exposure reference group. After demographic adjustment, High combustion cluster membership was independently associated with 38.4% higher odds of prevalent hypertension (OR 1.38). The prediction model achieved a cross-validated area under the receiver operating characteristic curve (AUC) of 0.849 (SD 0.017). Non-Hispanic Black participants constituted approximately 40% of the High combustion cluster, exceeding their representation in lower-risk clusters. Conclusions Multi-chemical exposome profiling identifies four cardiovascularly distinct subpopulations in the US adult population. Membership in the High combustion exposure cluster was associated with higher odds of prevalent hypertension and disproportionately affected Non-Hispanic Black participants. These findings support the use of multichemical approaches over single-pollutant analyses and highlight the relevance of environmental exposure patterns for making policy and targeted cardiovascular risk stratification.