Victor J. Torres 微生物学家｜

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Victor J. Torres
Microbiologist | Class of 2021
Investigating how bacterial pathogens overcome the immune system and identifying potential therapies.


Portrait of Victor J. Torres

Title
Microbiologist
Affiliation
Department of Microbiology, New York University Grossman School of Medicine
Location
New York, New York
Age
44 at time of award
Area of Focus
Microbiology, Virology, and Immunology
Website
Torres Lab
New York University: Victor J. Torres
Social
Twitter
Published September 28, 2021
ABOUT VICTOR'S WORK
Victor J. Torres is a microbiologist investigating how multidrug-resistant bacteria cause disease and identifying new therapies to fight and prevent infection. Torres uses a diverse range of techniques spanning genetics, molecular biology, immunology, and bioinformatics to study the bacteria Staphylococcus aureus (S. aureus). S. aureus causes a wide range of diseases, from mild skin infections to life-threatening blood infections. Highly virulent and, in some instances, resistant to antibiotics (known as methicillin-resistant S. aureus, or MRSA), S. aureus is responsible for millions of illnesses and tens of thousands of deaths each year.

Torres’s work is elucidating the interactions between host cells and the toxins secreted by S. aureus. S. aureus produces toxins known as leukocidins, which attack immune cells by forming pores on the cell membranes, resulting in cell death. Torres and colleagues have discovered the specific receptors (binding agents) on host cells that leukocidins exploit to gain access to and attack the immune system. He found that CCR5, a protein receptor on the surface of T cells and other immune cells, is a receptor for leukocidin ED (LukED). T cells are a vital component of the immune system that recognize and attack foreign particles. LukED uses CCR5 to bind to T cells and kill them, thus preventing an immune response. Torres went on to show that mice deficient in CCR5 are largely resistant to lethal S. aureus infection—without CCR5, the LukED could not disable T cells and weaken the mice’s immune systems. This study suggests that pharmacologic approaches to block toxin-receptor interactions could be used to treat infections in humans. In recent work, he and colleagues demonstrated an innate immune mechanism that exploits toxin-receptor interactions to provide protection against MRSA infection. Autophagy, the removal of unnecessary or damaged cellular components, stimulates the release of extracellular vesicles known as exosomes. Torres and colleagues found that exosomes containing toxin-receptors lured toxins away from cells, acting as a sort of sponge to neutralize the toxin’s threat. Adding exosomes to mice infected with MRSA improved their survival rate, establishing the role of exosomes as a host anti-toxin response.

Torres’s finding that S. aureus toxins overwhelm the immune system by targeting specific cells—rather than indiscriminately attacking the host—upends previous models of host-cell interactions and has important implications for vaccine development. Vaccine candidates targeting the bacteria directly have been ineffective. Torres’s work suggests blocking leukocidins that are destroying immune system cells could be key to vaccine success. He and colleagues recently created a class of centyrins (engineered proteins) that neutralize leukocidins. In studies with animal models, the centyrins allowed the animals’ immune systems to clear the infection. Torres has greatly advanced our understanding of S. aureus pathogenesis, and his development of several potential treatment strategies will be critical in our heated battle with this increasingly acute threat to human health worldwide.

BIOGRAPHY
Victor J. Torres received a BS (2000) from the University of Puerto Rico at Mayagüez and a PhD (2004) from Vanderbilt University School of Medicine. After completing postdoctoral training in the Division of Infectious Diseases and Department of Microbiology and Immunology at Vanderbilt, Torres joined the faculty of New York University Grossman School of Medicine in 2008, where he is currently the C. V. Starr Professor of Microbiology. His articles have been published in Nature, Cell Host and Microbe, PNAS, and Science Translational Medicine, among other scientific journals.

IN VICTOR'S WORDS
Smiling Latino man wearing a light blue button down shirt stands in urban landscape with buildings behind and highway in background. Quote text below photo reads: Imagine a scenario where clinical procedures that we take for granted are no longer possible because we don't have effective antibiotics to prevent infections. If this sounds like a nightmare, you're correct.


Imagine a scenario where clinical procedures that we take for granted are no longer possible because we don't have effective antibiotics to prevent infections. If this sounds like a nightmare, you're correct. This huge threat to human health is likely to occur in the not-too-distant future. The occurrence of antimicrobial-resistant pathogens has outpaced the development and approval of new antibiotics and vaccines. In our laboratory, we are tackling this problem by deploying a collaborative and highly multidisciplinary approach to uncover secrets about how pathogens cause disease that will hopefully lead to novel preventives and treatments.



Victor J. Torres
微生物学家｜2021级
研究细菌病原体如何克服免疫系统并确定潜在的治疗方法。


维克多-J-托雷斯的肖像

标题
微生物学家
工作单位
纽约大学格罗斯曼医学院微生物学系
工作地点
纽约，纽约
年龄
获奖时44岁
重点领域
微生物学、病毒学和免疫学
网站
托雷斯实验室
纽约大学。Victor J. Torres
社会
推特
2021年9月28日发布
关于维克托的工作
维克多-J-托雷斯是一名微生物学家，研究耐多药细菌如何导致疾病，并确定对抗和预防感染的新疗法。托雷斯使用跨越遗传学、分子生物学、免疫学和生物信息学的各种技术来研究金黄色葡萄球菌（S. aureus）。金黄色葡萄球菌引起广泛的疾病，从温和的皮肤感染到危及生命的血液感染。金黄色葡萄球菌毒性很强，在某些情况下对抗生素有抗药性（被称为耐甲氧西林金黄色葡萄球菌，或MRSA），每年造成数百万人患病和数万人死亡。

托雷斯的工作是阐明宿主细胞与金黄色葡萄球菌分泌的毒素之间的相互作用。金黄色葡萄球菌产生的毒素被称为白蛋白，它通过在细胞膜上形成孔隙攻击免疫细胞，导致细胞死亡。托雷斯和他的同事已经发现了宿主细胞上的特定受体（结合剂），白细胞毒素利用这些受体进入并攻击免疫系统。他发现，CCR5是T细胞和其他免疫细胞表面的一种蛋白质受体，是白细胞介素ED（LukED）的受体。T细胞是免疫系统的一个重要组成部分，它识别并攻击外来颗粒。LukED利用CCR5与T细胞结合并杀死它们，从而阻止免疫反应。托雷斯继续表明，缺乏CCR5的小鼠在很大程度上对致命的金黄色葡萄球菌感染有抵抗力--没有CCR5，LukED不能使T细胞失灵，并削弱小鼠的免疫系统。这项研究表明，阻断毒素-受体相互作用的药理学方法可用于治疗人类的感染。在最近的工作中，他和同事证明了一种利用毒素-受体相互作用提供保护以抵御MRSA感染的先天免疫机制。自噬，即清除不必要的或受损的细胞成分，刺激了称为外泌体的细胞外囊泡的释放。托雷斯及其同事发现，含有毒素受体的外泌体将毒素引离细胞，作为一种海绵来中和毒素的威胁。给感染了MRSA的小鼠添加外泌体可以提高它们的存活率，从而确立了外泌体作为一种宿主抗毒素反应的作用。

托雷斯的发现是，金黄色葡萄球菌毒素通过针对特定细胞而不是不分青红皂白地攻击宿主来压倒免疫系统，这颠覆了以前的宿主-细胞互动模型，对疫苗开发具有重要意义。直接针对细菌的候选疫苗一直都是无效的。托雷斯的工作表明，阻断破坏免疫系统细胞的白细胞素可能是疫苗成功的关键。他和同事们最近创造了一类能中和白蛋白的centyrins（工程蛋白）。在对动物模型的研究中，仙人球蛋白使动物的免疫系统能够清除感染。托雷斯极大地促进了我们对金黄色葡萄球菌发病机制的理解，他开发的几种潜在的治疗策略将在我们与这种对全世界人类健康日益严重的威胁的激烈斗争中起到关键作用。

个人简历
Victor J. Torres在波多黎各大学马亚圭斯分校获得学士学位（2000年），在范德比尔特大学医学院获得博士学位（2004年）。在范德比尔特大学传染病科和微生物学与免疫学系完成博士后培训后，托雷斯于2008年加入纽约大学格罗斯曼医学院，目前是C. V. Starr微生物学教授。他的文章发表在《自然》、《细胞-宿主与微生物》、《PNAS》和《科学-转化医学》等科学杂志上。

胜利者的话
身穿浅蓝色纽扣衬衫的拉丁裔男子微笑着站在城市景观中，背后是建筑物，背景是高速公路。照片下面的引言文字是：。想象一下这样的情景：我们认为理所当然的临床程序不再可能，因为我们没有有效的抗生素来预防感染。如果这听起来像一场噩梦，你是对的。


想象一下这样的场景：我们认为理所当然的临床程序不再可能，因为我们没有有效的抗生素来预防感染。如果这听起来像一场噩梦，你是对的。这种对人类健康的巨大威胁有可能在不远的将来发生。耐抗生素病原体的发生速度已经超过了新抗生素和疫苗的开发和批准速度。在我们的实验室里，我们正在通过部署一个高度多学科的合作方法来解决这个问题，以发现关于病原体如何导致疾病的秘密，这将有望带来新的预防和治疗方法。