功能获得性研究（GoFR）是指对生物制剂进行靶向改造，以改变其特定的表型特征，例如传播能力、毒力或宿主范围。该学科运用反向遗传学、定点诱变和连续传代等方法，研究病毒进化和人畜共患病溢出的分子驱动因素。
通过识别能够逃避免疫或跨物种适应的突变，科学家可以预测大流行病的威胁，并加快医疗对策的设计。
以下索引汇总了近期经同行评审的出版物和 专利 这些文件记录了合成基因组学和病毒工程领域的技术进展。这些条目阐明了增强型潜在流行病原体（ePPP）在双用途研究监管和生物安全规程的约束下的状态。
这是我们最新精选的全球英文出版物和专利，涵盖众多科学在线期刊，并按以下主题进行分类和重点介绍：连续传代、关注的双用途研究、功能获得、增强的潜在流行病原体、P3CO、致病性增强、传播性增强、宿主范围扩展、病毒嗜性、定点诱变、反向遗传学、合成基因组学、选择压力、逃逸突变体、病毒骨架、刺突蛋白修饰、受体结合亲和力、人畜共患病溢出潜力、生物安全等级 4、生物安全监管、生物风险管理、实验室获得性感染、嵌合病毒、病毒拯救、弗林蛋白酶切割位点插入、体内适应、GoFR 和功能获得。
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
