Antimicrobial resistance (AMR) represents a major global health threat, largely driven by antibiotic overuse and the protective role of bacterial biofilms. Quorum sensing (QS), a bacterial communication system regulating virulence and biofilm formation, has emerged as a promising therapeutic target. Quorum quenching (QQ), which disrupts QS without directly inhibiting bacterial growth, is considered a potential anti-virulence strategy that may reduce selective pressure for resistance. This review critically evaluates recent advances in QQ research, focusing on its clinical applicability, limitations, and risks. We analyzed studies from the last five years involving natural compounds, synthetic molecules, nanoparticles (NPs), and combination therapies targeting key pathogens such as Pseudomonas aeruginosa and Staphylococcus aureus in models of lung diseases, mainly cystic fibrosis, chronic wounds, burns, and implant-associated infections. While numerous compounds demonstrate significant in vitro anti-biofilm and anti-virulence activity, major challenges remain, including limited in vivo validation, pharmacokinetic constraints, toxicity concerns, microbiome disruption, and the potential development of tolerance or functional resistance. Although QQ offers a promising adjunctive approach to conventional antibiotics, its long-term clinical feasibility requires comprehensive evaluation of evolutionary dynamics, host–microbe interactions, and safety profiles.

Candida biofilms associated with medical devices represent a major clinical challenge due to their high resistance to conventional antifungal therapies. In this study, we investigated the structure–activity relationship of a homologous series of dicephalic cationic surfactants branched on carbon atom (Cn-DCNMe3Br, n= 10, 12, 14), with a focus on the effect of alkyl chain length on antifungal, antibiofilm, and cytotoxic properties. Planktonic susceptibility assays revealed a non-linear “cut-off” effect, with the C12 homologue exhibiting maximal fungicidal efficacy across the tested strains (C. albicans, C. glabrata, C. krusei, and C. tropicalis). In contrast, adhesion and biofilm-related assays demonstrated that the less hydrophobic C10 homologue showed superior performance in inhibiting initial cell attachment and disrupting mature biofilms. These findings highlight the critical role of early-stage surface interactions in determining overall antibiofilm efficacy. Mechanistically, the activity of these amphiphiles appears to be strongly associated with their ability to modulate cell–surface interactions, likely through a combination of physicochemical effects, including surface adsorption, alteration of wettability, and electrostatic interactions with microbial cell envelopes. While oxidative stress was observed as a secondary effect, it is not considered the primary determinant of antifungal activity. Crucially, biocompatibility assessment based on hemolysis assays demonstrated a clear chain-length-dependent toxicity profile. While C10 and C12 exhibited concentration-dependent hemolytic activity above 0.5 mM, the C14 derivative showed negligible hemolysis across the tested concentration range (up to 5 mM). These findings underscore the importance of fine-tuning alkyl chain length to balance antimicrobial efficacy, anti-adhesive performance, and host cytotoxicity, positioning this novel class of dicephalic surfactants as promising candidates for surface-functionalization strategies aimed at preventing device-associated infections.

Acinetobacter baumannii (A. baumannii) is a major nosocomial pathogen that poses a significant threat to global health owing to its remarkable capacity for antimicrobial resistance, environmental persistence, and virulence. These adaptive traits are closely associated with its quorum-sensing (QS) network, particularly the AbaI/AbaR system. Current evidence indicates that AbaI/AbaR-mediated signalling coordinates biofilm formation, surface-associated motility, antimicrobial tolerance via modulation of efflux pump activity, oxidative stress responses, and membrane integrity, as well as biofilm-associated antibiotic resistance and stress adaptation, thereby enhancing bacterial survival and fitness. Furthermore, QS signalling contributes to epithelial cell injury and to the modulation of innate immune responses during infection, whereas its effects on adaptive immunity remain poorly understood. This review summarises current knowledge of the molecular mechanisms underlying AbaI/AbaR-mediated signalling, its role in regulating A. baumannii infection-relevant phenotypes and host–pathogen interactions, as well as the therapeutic potential of quorum quenching (QQ) strategies in attenuating A. baumannii virulence, while highlighting key knowledge gaps that warrant further mechanistic and translational investigation.

Hantaviruses are members of the Hantaviridae family, which can cause hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS). At present, no specific antiviral treatment is available for hantavirus infection, while licensed hantavirus vaccines are restricted to a limited number of countries in Asia. This review summarizes recent advances in hantavirus deoxyribonucleic acid (DNA) and messenger RNA (mRNA) vaccines, focusing on antigen design, delivery systems, immunogenicity, safety and translational development. Peer-reviewed studies published primarily within the past 10 years were evaluated together with available hantavirus vaccine trials registered in ClinicalTrials.gov, with emphasis on Hantaan virus (HTNV), Puumala virus (PUUV) and Andes virus (ANDV). DNA vaccine candidates have demonstrated immunogenicity in preclinical and early clinical studies, with an acceptable safety profile. mRNA vaccines represent a newer approach with promising preclinical evidence of humoral and cellular immune responses. However, they have not yet been evaluated clinically. Studies have also reported the potential for varying degrees of cross-protection between hantavirus species, although protection remains limited by antigenic diversity. Overall, current evidence supports further development of nucleic acid-based hantavirus vaccines, particularly multivalent strategies, with emphasis on standardized evaluation and clinical efficacy.

Antibiofilm strategies targeting Candida glabrata increasingly focus on membrane-active compounds capable of disrupting biofilm formation and mature biofilm structure. Building on previous work identifying alkylamidobetaine C9 (AAB C9)—[(3-decanoylmethylamino)propyl]dimethylammonium acetate—and β-escin as antibiofilm agents against C. glabrata, this study examined the biochemical and physiological basis of their efficacy in a reference strain (ATCC 90030) and a clinical isolate (2586). Oxidative stress was assessed microscopically after two hours of exposure, and proteome changes were quantified after six hours, for each compound alone and in combination. Fluorescence microscopy showed that AAB C9 and β-escin interacted differently depending on the ROS compartment and strain: in the strain ATCC 90030, the combination antagonized β-escin-induced mitochondrial superoxide, whereas in the multidrug-resistant isolate 2586 it exceeded either agent alone for both cytosolic and mitochondrial superoxide, indicating a strain-dependent, additive interaction. Quantitative proteomics showed that strain genetic background, rather than treatment, was the dominant source of proteome variance. Preranked gene set enrichment analysis revealed that AAB C9 significantly suppressed accumulation of biofilm-formation-associated proteins specifically in isolate 2586, corroborating its phenotypic antibiofilm activity, while β-escin and the combination produced opposing transmembrane-transport signatures, pointing to compound-specific mechanisms underlying their differential antifungal and antibiofilm effects.