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Human microbiome variation associated with race and ethnicity emerges as early as 3 months of age. 与种族和民族相关的人类微生物组变异最早在3个月大时出现。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002230
Elizabeth K Mallott, Alexandra R Sitarik, Leslie D Leve, Camille Cioffi, Carlos A Camargo, Kohei Hasegawa, Seth R Bordenstein

Human microbiome variation is linked to the incidence, prevalence, and mortality of many diseases and associates with race and ethnicity in the United States. However, the age at which microbiome variability emerges between these groups remains a central gap in knowledge. Here, we identify that gut microbiome variation associated with race and ethnicity arises after 3 months of age and persists through childhood. One-third of the bacterial taxa that vary across caregiver-identified racial categories in children are taxa reported to also vary between adults. Machine learning modeling of childhood microbiomes from 8 cohort studies (2,756 samples from 729 children) distinguishes racial and ethnic categories with 87% accuracy. Importantly, predictive genera are also among the top 30 most important taxa when childhood microbiomes are used to predict adult self-identified race and ethnicity. Our results highlight a critical developmental window at or shortly after 3 months of age when social and environmental factors drive race and ethnicity-associated microbiome variation and may contribute to adult health and health disparities.

在美国,人类微生物组变异与许多疾病的发病率、流行率和死亡率有关,并与种族和民族有关。然而,这些群体之间出现微生物组变异的年龄仍然是知识的核心差距。在这里,我们发现与种族和民族相关的肠道微生物组变异在3个月大后出现,并持续到儿童时期。三分之一的细菌分类群因照顾者确定的儿童种族类别而异,据报道,成年人之间的分类群也有所不同。来自8项队列研究的儿童微生物组的机器学习建模(来自729名儿童的2756个样本)以87%的准确率区分了种族和民族类别。重要的是,当儿童微生物群用于预测成年人自我识别的种族和民族时,预测属也是前30个最重要的分类群之一。我们的研究结果强调了一个关键的发育窗口,即在3个月大时或3个月后不久,社会和环境因素会导致种族和族裔相关的微生物组变异,并可能导致成人健康和健康差异。
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引用次数: 0
Paracrine regulation of neural crest EMT by placodal MMP28. MMP28对神经嵴EMT的旁分泌调节。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002261
Nadège Gouignard, Anne Bibonne, João F Mata, Fernanda Bajanca, Bianka Berki, Elias H Barriga, Jean-Pierre Saint-Jeannet, Eric Theveneau

Epithelial-mesenchymal transition (EMT) is an early event in cell dissemination from epithelial tissues. EMT endows cells with migratory, and sometimes invasive, capabilities and is thus a key process in embryo morphogenesis and cancer progression. So far, matrix metalloproteinases (MMPs) have not been considered as key players in EMT but rather studied for their role in matrix remodelling in later events such as cell migration per se. Here, we used Xenopus neural crest cells to assess the role of MMP28 in EMT and migration in vivo. We show that a catalytically active MMP28, expressed by neighbouring placodal cells, is required for neural crest EMT and cell migration. We provide strong evidence indicating that MMP28 is imported in the nucleus of neural crest cells where it is required for normal Twist expression. Our data demonstrate that MMP28 can act as an upstream regulator of EMT in vivo raising the possibility that other MMPs might have similar early roles in various EMT-related contexts such as cancer, fibrosis, and wound healing.

上皮-间充质转化(EMT)是上皮组织细胞扩散的早期事件。EMT赋予细胞迁移,有时是侵袭的能力,因此是胚胎形态发生和癌症进展的关键过程。到目前为止,基质金属蛋白酶(MMPs)还没有被认为是EMT的关键参与者,而是研究了它们在后期事件(如细胞迁移本身)中的基质重塑作用。在这里,我们使用非洲爪蟾神经嵴细胞来评估MMP28在EMT和体内迁移中的作用。我们发现,由邻近的板尾细胞表达的具有催化活性的MMP28是神经嵴EMT和细胞迁移所必需的。我们提供了强有力的证据,表明MMP28是在神经嵴细胞的细胞核中输入的,在那里它是正常Twist表达所必需的。我们的数据表明,MMP28可以在体内作为EMT的上游调节因子,这增加了其他MMP在各种EMT相关背景下(如癌症、纤维化和伤口愈合)可能具有类似早期作用的可能性。
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引用次数: 0
Optogenetic cleavage of the Miro GTPase reveals the direct consequences of real-time loss of function in Drosophila. Miro-GTPase的光遗传学切割揭示了果蝇实时功能丧失的直接后果。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002273
Francesca Mattedi, Ethlyn Lloyd-Morris, Frank Hirth, Alessio Vagnoni

Miro GTPases control mitochondrial morphology, calcium homeostasis, and regulate mitochondrial distribution by mediating their attachment to the kinesin and dynein motor complex. It is not clear, however, how Miro proteins spatially and temporally integrate their function as acute disruption of protein function has not been performed. To address this issue, we have developed an optogenetic loss of function "Split-Miro" allele for precise control of Miro-dependent mitochondrial functions in Drosophila. Rapid optogenetic cleavage of Split-Miro leads to a striking rearrangement of the mitochondrial network, which is mediated by mitochondrial interaction with the microtubules. Unexpectedly, this treatment did not impact the ability of mitochondria to buffer calcium or their association with the endoplasmic reticulum. While Split-Miro overexpression is sufficient to augment mitochondrial motility, sustained photocleavage shows that Split-Miro is surprisingly dispensable to maintain elevated mitochondrial processivity. In adult fly neurons in vivo, Split-Miro photocleavage affects both mitochondrial trafficking and neuronal activity. Furthermore, functional replacement of endogenous Miro with Split-Miro identifies its essential role in the regulation of locomotor activity in adult flies, demonstrating the feasibility of tuning animal behaviour by real-time loss of protein function.

Miro GTP酶控制线粒体形态、钙稳态,并通过介导其与驱动蛋白和动力蛋白运动复合体的连接来调节线粒体分布。然而,目前尚不清楚Miro蛋白是如何在空间和时间上整合其功能的,因为尚未对蛋白功能进行急性破坏。为了解决这个问题,我们开发了一种光遗传学功能丧失的“分裂Miro”等位基因,用于精确控制果蝇的Miro依赖性线粒体功能。Split Miro的快速光遗传学切割导致线粒体网络的显著重排,这是由线粒体与微管的相互作用介导的。出乎意料的是,这种治疗并没有影响线粒体缓冲钙的能力或它们与内质网的结合。虽然Split-Miro过表达足以增强线粒体运动性,但持续的光切割表明,Split-Maro在维持线粒体加工能力方面是令人惊讶的可有可无。在体内成年果蝇神经元中,Split Miro光切割影响线粒体运输和神经元活动。此外,用Split Miro功能性取代内源性Miro确定了其在成年苍蝇运动活动调节中的重要作用,证明了通过蛋白质功能的实时丧失来调节动物行为的可行性。
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引用次数: 0
SMOC-1 interacts with both BMP and glypican to regulate BMP signaling in C. elegans. SMOC-1与BMP和glypian相互作用以调节秀丽隐杆线虫中的BMP信号传导。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002272
Melisa S DeGroot, Byron Williams, Timothy Y Chang, Maria L Maas Gamboa, Isabel M Larus, Garam Hong, J Christopher Fromme, Jun Liu

Secreted modular calcium-binding proteins (SMOCs) are conserved matricellular proteins found in organisms from Caenorhabditis elegans to humans. SMOC homologs characteristically contain 1 or 2 extracellular calcium-binding (EC) domain(s) and 1 or 2 thyroglobulin type-1 (TY) domain(s). SMOC proteins in Drosophila and Xenopus have been found to interact with cell surface heparan sulfate proteoglycans (HSPGs) to exert both positive and negative influences on the conserved bone morphogenetic protein (BMP) signaling pathway. In this study, we used a combination of biochemical, structural modeling, and molecular genetic approaches to dissect the functions of the sole SMOC protein in C. elegans. We showed that CeSMOC-1 binds to the heparin sulfate proteoglycan GPC3 homolog LON-2/glypican, as well as the mature domain of the BMP2/4 homolog DBL-1. Moreover, CeSMOC-1 can simultaneously bind LON-2/glypican and DBL-1/BMP. The interaction between CeSMOC-1 and LON-2/glypican is mediated specifically by the EC domain of CeSMOC-1, while the full interaction between CeSMOC-1 and DBL-1/BMP requires full-length CeSMOC-1. We provide both in vitro biochemical and in vivo functional evidence demonstrating that CeSMOC-1 functions both negatively in a LON-2/glypican-dependent manner and positively in a DBL-1/BMP-dependent manner to regulate BMP signaling. We further showed that in silico, Drosophila and vertebrate SMOC proteins can also bind to mature BMP dimers. Our work provides a mechanistic basis for how the evolutionarily conserved SMOC proteins regulate BMP signaling.

分泌模块化钙结合蛋白(SMOC)是从秀丽隐杆线虫到人类等生物体中发现的保守基质细胞蛋白。SMOC同源物特征性地包含1或2个细胞外钙结合(EC)结构域和1或2种甲状腺球蛋白1型(TY)结构域。果蝇和爪蟾中的SMOC蛋白已被发现与细胞表面硫酸乙酰肝素蛋白多糖(HSPGs)相互作用,对保守的骨形态发生蛋白(BMP)信号通路产生积极和消极的影响。在这项研究中,我们结合生物化学、结构建模和分子遗传学方法来剖析秀丽隐杆线虫中唯一SMOC蛋白的功能。我们发现CeSMOC-1与肝素硫酸盐蛋白聚糖GPC3同源物LON-2/glypian以及BMP2/4同源物DBL-1的成熟结构域结合。此外,CeSMOC-1可以同时结合LON-2/glypian和DBL-1/BMP。CeSMOC-1和LON-2/glypian之间的相互作用是由CeSMOC1的EC结构域特异性介导的,而CeSMOC-11和DBL-1/BMP之间的完全相互作用需要全长的CeSMOC.1。我们提供了体外生物化学和体内功能证据,证明CeSMOC-1在调节BMP信号传导方面既以LON-2/glypian依赖的方式负向发挥作用,又以DBL-1/BMP依赖的方式正向发挥作用。我们进一步证明,在计算机中,果蝇和脊椎动物的SMOC蛋白也可以与成熟的BMP二聚体结合。我们的工作为进化上保守的SMOC蛋白如何调节BMP信号提供了机制基础。
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引用次数: 0
Divergent combinations of cis-regulatory elements control the evolution of phenotypic plasticity. 顺式调控元件的不同组合控制表型可塑性的进化。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002270
Mohannad Dardiry, Gabi Eberhard, Hanh Witte, Christian Rödelsperger, James W Lightfoot, Ralf J Sommer

The widespread occurrence of phenotypic plasticity across all domains of life demonstrates its evolutionary significance. However, how plasticity itself evolves and how it contributes to evolution is poorly understood. Here, we investigate the predatory nematode Pristionchus pacificus with its feeding structure plasticity using recombinant-inbred-line and quantitative-trait-locus (QTL) analyses between natural isolates. We show that a single QTL at a core developmental gene controls the expression of the cannibalistic morph. This QTL is composed of several cis-regulatory elements. Through CRISPR/Cas-9 engineering, we identify copy number variation of potential transcription factor binding sites that interacts with a single intronic nucleotide polymorphism. Another intronic element eliminates gene expression altogether, mimicking knockouts of the locus. Comparisons of additional isolates further support the rapid evolution of these cis-regulatory elements. Finally, an independent QTL study reveals evidence for parallel evolution at the same locus. Thus, combinations of cis-regulatory elements shape plastic trait expression and control nematode cannibalism.

表型可塑性在生命各个领域的广泛存在证明了其进化意义。然而,可塑性本身是如何进化的,以及它是如何促进进化的,人们对此知之甚少。在此,我们利用重组自交系和天然分离株之间的数量性状位点(QTL)分析,研究了捕食性线虫和平原(Prisionchus pacificus)及其取食结构的可塑性。我们发现,核心发育基因上的单个QTL控制着同类相食变体的表达。该QTL由几个顺式调控元件组成。通过CRISPR/Cas-9工程,我们确定了与单个内含子核苷酸多态性相互作用的潜在转录因子结合位点的拷贝数变化。另一个内含子元素完全消除了基因表达,模仿基因座的敲除。额外分离物的比较进一步支持了这些顺式调节元件的快速进化。最后,一项独立的QTL研究揭示了在同一基因座平行进化的证据。因此,顺式调控元件的组合塑造了可塑性性状的表达并控制了线虫的自相残杀。
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引用次数: 1
Extensive topographic remapping and functional sharpening in the adult rat visual pathway upon first visual experience. 首次视觉体验后成年大鼠视觉通路的广泛地形重映射和功能锐化。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002229
Joana Carvalho, Francisca F Fernandes, Noam Shemesh

Understanding the dynamics of stability/plasticity balances during adulthood is pivotal for learning, disease, and recovery from injury. However, the brain-wide topography of sensory remapping remains unknown. Here, using a first-of-its-kind setup for delivering patterned visual stimuli in a rodent magnetic resonance imaging (MRI) scanner, coupled with biologically inspired computational models, we noninvasively mapped brain-wide properties-receptive fields (RFs) and spatial frequency (SF) tuning curves-that were insofar only available from invasive electrophysiology or optical imaging. We then tracked the RF dynamics in the chronic visual deprivation model (VDM) of plasticity and found that light exposure progressively promoted a large-scale topographic remapping in adult rats. Upon light exposure, the initially unspecialized visual pathway progressively evidenced sharpened RFs (smaller and more spatially selective) and enhanced SF tuning curves. Our findings reveal that visual experience following VDM reshapes both structure and function of the visual system and shifts the stability/plasticity balance in adults.

了解成年期稳定性/可塑性平衡的动态对于学习、疾病和从损伤中恢复至关重要。然而,感觉重映射的全脑地形图仍然未知。在这里,我们使用第一种在啮齿类动物磁共振成像(MRI)扫描仪中提供模式化视觉刺激的装置,结合生物学启发的计算模型,无创地绘制了全脑特性感受野(RF)和空间频率(SF)调谐曲线,这些曲线目前只能从侵入性电生理学或光学成像中获得。然后,我们追踪了可塑性慢性视觉剥夺模型(VDM)中的RF动力学,发现光照逐渐促进了成年大鼠的大规模地形重映射。在光照下,最初未专门化的视觉通路逐渐证明RF变尖(更小且更具空间选择性)和SF调谐曲线增强。我们的研究结果表明,VDM后的视觉体验重塑了视觉系统的结构和功能,并改变了成年人的稳定性/可塑性平衡。
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引用次数: 0
NCoR1 controls Mycobacterium tuberculosis growth in myeloid cells by regulating the AMPK-mTOR-TFEB axis. NCoR1通过调节AMPK-mTOR TFEB轴来控制结核分枝杆菌在骨髓细胞中的生长。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002231
Viplov Kumar Biswas, Kaushik Sen, Abdul Ahad, Arup Ghosh, Surbhi Verma, Rashmirekha Pati, Subhasish Prusty, Sourya Prakash Nayak, Sreeparna Podder, Dhiraj Kumar, Bhawna Gupta, Sunil Kumar Raghav

Mycobacterium tuberculosis (Mtb) defends host-mediated killing by repressing the autophagolysosome machinery. For the first time, we report NCoR1 co-repressor as a crucial host factor, controlling Mtb growth in myeloid cells by regulating both autophagosome maturation and lysosome biogenesis. We found that the dynamic expression of NCoR1 is compromised in human peripheral blood mononuclear cells (PBMCs) during active Mtb infection, which is rescued upon prolonged anti-mycobacterial therapy. In addition, a loss of function in myeloid-specific NCoR1 considerably exacerbates the growth of M. tuberculosis in vitro in THP1 differentiated macrophages, ex vivo in bone marrow-derived macrophages (BMDMs), and in vivo in NCoR1MyeKO mice. We showed that NCoR1 depletion controls the AMPK-mTOR-TFEB signalling axis by fine-tuning cellular adenosine triphosphate (ATP) homeostasis, which in turn changes the expression of proteins involved in autophagy and lysosomal biogenesis. Moreover, we also showed that the treatment of NCoR1 depleted cells by Rapamycin, Antimycin-A, or Metformin rescued the TFEB activity and LC3 levels, resulting in enhanced Mtb clearance. Similarly, expressing NCoR1 exogenously rescued the AMPK-mTOR-TFEB signalling axis and Mtb killing. Overall, our data revealed a central role of NCoR1 in Mtb pathogenesis in myeloid cells.

结核分枝杆菌(Mtb)通过抑制自噬溶酶体机制来防御宿主介导的杀伤。我们首次报道了NCoR1共阻遏物作为一种关键的宿主因子,通过调节自噬体成熟和溶酶体生物发生来控制骨髓细胞中Mtb的生长。我们发现,在活动性结核分枝杆菌感染期间,人类外周血单核细胞(PBMC)中NCoR1的动态表达受到损害,经过长期的抗分枝杆菌治疗后,这种情况得以挽救。此外,髓系特异性NCoR1的功能丧失显著加剧了结核分枝杆菌在体外THP1分化巨噬细胞、离体骨髓衍生巨噬细胞(BMDM)和体内NCoR1MyeKO小鼠中的生长。我们发现,NCoR1缺失通过微调细胞三磷酸腺苷(ATP)稳态来控制AMPK-mTOR TFEB信号轴,从而改变参与自噬和溶酶体生物发生的蛋白质的表达。此外,我们还表明,用雷帕霉素、抗霉素-A或二甲双胍处理NCoR1缺失的细胞可以挽救TFEB活性和LC3水平,从而提高Mtb清除率。类似地,外源性表达NCoR1挽救了AMPK-mTOR TFEB信号轴和Mtb杀伤。总体而言,我们的数据揭示了NCoR1在骨髓细胞Mtb发病机制中的核心作用。
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引用次数: 2
Target-selective vertebrate motor axon regeneration depends on interaction with glial cells at a peripheral nerve plexus. 脊椎动物运动轴突的靶向选择性再生取决于与周围神经丛神经胶质细胞的相互作用。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2023-08-17 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002223
Lauren J Walker, Camilo Guevara, Koichi Kawakami, Michael Granato

A critical step for functional recovery from peripheral nerve injury is for regenerating axons to connect with their pre-injury targets. Reestablishing pre-injury target specificity is particularly challenging for limb-innervating axons as they encounter a plexus, a network where peripheral nerves converge, axons from different nerves intermingle, and then re-sort into target-specific bundles. Here, we examine this process at a plexus located at the base of the zebrafish pectoral fin, equivalent to tetrapod forelimbs. Using live cell imaging and sparse axon labeling, we find that regenerating motor axons from 3 nerves coalesce into the plexus. There, they intermingle and sort into distinct branches, and then navigate to their original muscle domains with high fidelity that restores functionality. We demonstrate that this regeneration process includes selective retraction of mistargeted axons, suggesting active correction mechanisms. Moreover, we find that Schwann cells are enriched and associate with axons at the plexus, and that Schwann cell ablation during regeneration causes profound axonal mistargeting. Our data provide the first real-time account of regenerating vertebrate motor axons navigating a nerve plexus and reveal a previously unappreciated role for Schwann cells to promote axon sorting at a plexus during regeneration.

外周神经损伤后功能恢复的关键步骤是再生轴突,使其与损伤前的目标连接。重建损伤前目标特异性对肢体神经支配轴突来说尤其具有挑战性,因为它们遇到神经丛,即外周神经汇聚的网络,来自不同神经的轴突混合在一起,然后重新分类为目标特异性束。在这里,我们在位于斑马鱼胸鳍底部的神经丛中观察了这个过程,相当于四足前肢。利用活细胞成像和稀疏轴突标记,我们发现来自3条神经的再生运动轴突融合到神经丛中。在那里,它们混合并分类成不同的分支,然后以高保真度导航到它们的原始肌肉域,从而恢复功能。我们证明,这种再生过程包括选择性回缩错误的轴突,这表明了积极的纠正机制。此外,我们发现雪旺细胞富集并与神经丛的轴突结合,再生过程中的雪旺细胞消融会导致严重的轴突定位错误。我们的数据首次实时描述了脊椎动物运动轴突在神经丛中的再生,并揭示了施旺细胞在再生过程中促进神经丛轴突分类的先前未被重视的作用。
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引用次数: 0
Functional unknomics: Systematic screening of conserved genes of unknown function. 功能未知基因组学:对功能未知的保守基因进行系统筛选。
IF 7.8 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-08-08 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002222
João J Rocha, Satish Arcot Jayaram, Tim J Stevens, Nadine Muschalik, Rajen D Shah, Sahar Emran, Cristina Robles, Matthew Freeman, Sean Munro

The human genome encodes approximately 20,000 proteins, many still uncharacterised. It has become clear that scientific research tends to focus on well-studied proteins, leading to a concern that poorly understood genes are unjustifiably neglected. To address this, we have developed a publicly available and customisable "Unknome database" that ranks proteins based on how little is known about them. We applied RNA interference (RNAi) in Drosophila to 260 unknown genes that are conserved between flies and humans. Knockdown of some genes resulted in loss of viability, and functional screening of the rest revealed hits for fertility, development, locomotion, protein quality control, and resilience to stress. CRISPR/Cas9 gene disruption validated a component of Notch signalling and 2 genes contributing to male fertility. Our work illustrates the importance of poorly understood genes, provides a resource to accelerate future research, and highlights a need to support database curation to ensure that misannotation does not erode our awareness of our own ignorance.

人类基因组编码了约 20,000 种蛋白质,其中许多仍未定性。显而易见的是,科学研究往往集中在研究透彻的蛋白质上,导致人们担心了解不多的基因被无端忽视。为了解决这个问题,我们开发了一个公开的、可定制的 "Unknome 数据库",该数据库根据蛋白质的未知程度对其进行排序。我们在果蝇中应用 RNA 干扰(RNAi)技术,研究了 260 个在果蝇和人类之间保守的未知基因。敲除一些基因会导致果蝇丧失生存能力,而对其余基因进行功能筛选后,我们发现了一些与果蝇生育、发育、运动、蛋白质质量控制和抗压能力有关的基因。CRISPR/Cas9基因干扰验证了Notch信号的一个组成部分和两个有助于雄性生育能力的基因。我们的工作说明了不为人们所了解的基因的重要性,为加速未来的研究提供了资源,并强调了支持数据库整理的必要性,以确保错误注释不会侵蚀我们对自身无知的认识。
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引用次数: 0
Evolutionary safety of lethal mutagenesis driven by antiviral treatment. 抗病毒治疗驱动的致命突变的进化安全性。
IF 7.8 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-08-08 eCollection Date: 2023-08-01 DOI: 10.1371/journal.pbio.3002214
Gabriela Lobinska, Yitzhak Pilpel, Martin A Nowak

Nucleoside analogs are a major class of antiviral drugs. Some act by increasing the viral mutation rate causing lethal mutagenesis of the virus. Their mutagenic capacity, however, may lead to an evolutionary safety concern. We define evolutionary safety as a probabilistic assurance that the treatment will not generate an increased number of mutants. We develop a mathematical framework to estimate the total mutant load produced with and without mutagenic treatment. We predict rates of appearance of such virus mutants as a function of the timing of treatment and the immune competence of patients, employing realistic assumptions about the vulnerability of the viral genome and its potential to generate viable mutants. We focus on the case study of Molnupiravir, which is an FDA-approved treatment against Coronavirus Disease-2019 (COVID-19). We estimate that Molnupiravir is narrowly evolutionarily safe, subject to the current estimate of parameters. Evolutionary safety can be improved by restricting treatment with this drug to individuals with a low immunological clearance rate and, in future, by designing treatments that lead to a greater increase in mutation rate. We report a simple mathematical rule to determine the fold increase in mutation rate required to obtain evolutionary safety that is also applicable to other pathogen-treatment combinations.

核苷类似物是一类主要的抗病毒药物。其中一些类似物通过增加病毒突变率,对病毒产生致命的诱变作用。然而,它们的诱变能力可能会导致进化安全性问题。我们将进化安全性定义为一种概率保证,即治疗不会产生更多的突变体。我们建立了一个数学框架,用于估算在有诱变处理和没有诱变处理的情况下产生的突变体总量。我们预测这种病毒突变体的出现率是治疗时机和患者免疫能力的函数,并对病毒基因组的脆弱性及其产生可行突变体的潜力做出了现实的假设。我们将重点放在莫能吡韦的案例研究上,莫能吡韦是美国食品及药物管理局批准的一种针对冠状病毒病-2019(COVID-19)的治疗方法。我们估计,根据目前的参数估计,莫能吡韦在进化上具有一定的安全性。通过限制免疫清除率较低的个体使用这种药物进行治疗,以及在未来设计会导致突变率增加的治疗方法,可以提高进化安全性。我们报告了一个简单的数学规则,用于确定获得进化安全性所需的突变率增加倍数,该规则也适用于其他病原体-治疗组合。
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引用次数: 0
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