La recherche sur le gain de fonction (GoFR) consiste à modifier de manière ciblée des agents biologiques afin d'altérer des caractéristiques phénotypiques spécifiques, telles que la transmissibilité, la virulence ou le spectre d'hôtes. Cette discipline utilise la génétique inverse, la mutagenèse dirigée et les passages en série pour étudier les mécanismes moléculaires de l'évolution virale et des zoonoses.
En identifiant les mutations qui permettent l'évasion immunitaire ou l'adaptation inter-espèces, les scientifiques prédisent les menaces pandémiques et accélèrent la conception de contre-mesures médicales.
L'index ci-dessous regroupe les publications récentes évaluées par des pairs et brevet Ces dossiers documentent les progrès techniques réalisés en génomique synthétique et en ingénierie virale. Ils précisent le statut des agents pathogènes potentiellement pandémiques améliorés (APPA) dans le cadre réglementaire de la surveillance de la recherche à double usage et des protocoles de biosécurité.
Voici notre dernière sélection de publications et de brevets internationaux en anglais sur le gain de fonction, issus de nombreuses revues scientifiques en ligne, classés et axés sur les passages en série, la recherche à double usage préoccupante, le gain de fonction, les agents pathogènes pandémiques potentiels améliorés, le P3CO, l'amélioration de la pathogénicité, l'amélioration de la transmissibilité, l'expansion de la gamme d'hôtes, le tropisme viral, la mutagenèse dirigée, la génétique inverse, la génomique synthétique, la pression de sélection, les mutants d'échappement, le squelette viral, la modification de la protéine Spike, l'affinité de liaison au récepteur, le potentiel de transmission zoonotique, le niveau de biosécurité 4, la surveillance de la biosécurité, la gestion des risques biologiques, l'infection acquise en laboratoire, les virus chimériques, le sauvetage viral, l'insertion du site de clivage de la furine, l'adaptation in vivo, le GoFR et le gain de fonction.
Muscle-Specific DNM2 Overexpression Improves Charcot–Marie–Tooth Disease In Vivo and Reveals a Narrow Therapeutic Window in Skeletal Muscle
Published on 2026-02-02 by Marie Goret, Gwenaelle Piccolo, Jocelyn Laporte @MDPI
Abstract: Charcot–Marie–Tooth disease (CMT), caused by dominant loss-of-function mutations in DNM2, encoding the GTPase dynamin-2, impairs motor and sensory function. However, the respective contributions of muscle and nerve pathology, and the therapeutic potential of increasing DNM2 expression, remain unresolved. We evaluated tissue-targeted and systemic approaches to increase DNM2 in a mouse model carrying the common K562E-CMT mutation. Muscle-specific DNM2 overexpression fro[...]
Our summary: Muscle-specific DNM2 overexpression improves symptoms in a mouse model of Charcot-Marie-Tooth disease. Systemic delivery of DNM2 worsens muscle pathology despite increased expression. Findings emphasize the importance of precise DNM2 dosage for effective treatment and highlight a narrow therapeutic window.
DNM2, Charcot-Marie-Tooth, muscle pathology, therapeutic window
Publication
Sublethal Antibiotic Exposure Induces Microevolution of Quinolone Resistance in Pathogenic Vibrio parahaemolyticus
Published on 2026-01-30 by Qian Wu, Han Yang, Tianming Xu, Pradeep K. Malakar, Huan Li, Yong Zhao @MDPI
Abstract: The microevolutionary pathways and molecular mechanisms by which the important pathogen Vibrio parahaemolyticus acquires resistance in the aquatic environment under continuous selective pressure from quinolone antibiotic residues are still unknown. Here, the study successfully simulated the long-term pressure of antibiotic residues in aquaculture by susceptible V. parahaemolyticus (VPD14) which was isolated from seafood, to a 30-day in vitro induction with sublethal concentrations of levofloxaci[...]
Our summary: Sublethal exposure to quinolone antibiotics induces microevolution in Vibrio parahaemolyticus. Mutants exhibit resistance to multiple antibiotics and adaptations such as decreased growth rates. Whole-genome sequencing reveals key mutations in resistance-determining regions associated with this resistance.
Microevolution, Quinolone Resistance, Vibrio parahaemolyticus, Antibiotic Exposure
Publication
Occurrence, Seasonal Variation, and Microbial Drivers of Antibiotic Resistance Genes in a Residential Secondary Water Supply System
Published on 2026-01-22 by Huaiyu Tian, Yu Zhou, Dawei Zhang, Weiying Li @MDPI
Abstract: The widespread use of antibiotics has led to the persistence of antibiotic-resistant bacteria (ARB) and antibiotic resistance genes (ARGs) in drinking water systems, posing potential public health risks at the point of use. In this study, a residential secondary water supply system (SWSS) in eastern China was investigated over one year to characterize microbial communities, ARB and ARG occurrence, and their associations with water quality in bulk water and biofilms. Culture-based methods, flow c[...]
Our summary: This study investigates the occurrence of antibiotic resistance genes (ARGs) in a residential secondary water supply system over one year. Significant microbial regrowth and higher ARG concentrations were observed, particularly in autumn and winter. The findings emphasize the influence of secondary distribution conditions and microbial interactions on resistance risks in drinking water systems.
Antibiotic Resistance, Microbial Communities, Water Quality, Seasonal Variation
Publication
Krüppel-like Factor 2 (KLF2) in the Regulation of Lipid Accumulation, ROS, and Mitochondrial Functions During Foam Cell Formation in RAW264.7 Cells
Published on 2026-01-06 by Md Sariful Islam Howlader, Manjusri Das, Surajit Hansda, Prathyusha Naidu, Hiranmoy Das @MDPI
Abstract: Foam cell formation, a hallmark of early atherosclerotic lesion development, is closely associated with mitochondrial dysfunction and excessive reactive oxygen species (ROS) production. Disruption in mitochondrial activity leads to electron leakage, elevated ROS generation, and collapse of mitochondrial membrane potential, contributing to vascular pathogenesis. In this study, we investigated the role of Krüppel-like factor 2 (KLF2), a transcription factor known for its vasculoprotec[...]
Our summary: KLF2 regulates lipid accumulation and mitochondrial functions during foam cell formation in RAW264.7 cells. Its loss promotes foam cell formation and increases ROS, while its gain reduces these effects. This study highlights KLF2 s potential as a therapeutic target for cardiovascular diseases.
KLF2, foam cells, mitochondrial dysfunction, reactive oxygen species
Publication
Methods of treatment of neurological disorders
Patent published on the 2025-12-18 in WO under Ref WO2025259553 by PRAXIS PREC MEDICINES INC [US] (Frizzo Silvana [us], Silva De Souza Marcio [us], Petrou Steven [us])
Abstract: The present disclosure is generally directed to methods of treating a disease, disorder, or condition, e.g., a neurological disorder, a disorder associated with excessive neuronal excitability, or a disorder associated with de novo gain-of-function or loss-of-function mutations in major central nervous system sodium channel genes, such as for example, SCN1A, SCN2A, and SCN8A, using Compound 1 represented by the following structural formula:or a pharmaceutically acceptable salt thereof.[...]
Our summary: The document discusses treatment methods for neurological disorders linked to sodium channel gene mutations. It focuses on using Compound 1 or its pharmaceutically acceptable salts. The target disorders involve excessive neuronal excitability due to specific genetic mutations.
neurological disorders, sodium channel genes, treatment methods, Compound 1
Patent
