My research area involves the study of the mechanisms of resistance to the first-line antituberculosis drugs such as isoniazid and pyrazinamide, as well as the identification and testing of new inhibitors against M. tuberculosis. We have shown that the main target of isoniazid is the enoyl-ACP reductase InhA, an essential gene of the fatty acid synthase type II system, deciphered the mechanisms of resistance to isoniazid caused by mutations in ndh encoding the NADH dehydrogenase, and identified a novel mechanism of INH and ETH resistance in M. tuberculosis (mutations in the mycothiol biosynthesis pathway). Screening of a commercially available chemical library led to the identification of 2 new compounds that are cidal against drug-susceptible and drug-resistant M. tuberculosis.
Research Associate | email@example.com |
I am interested in environmentally-dependent regulation of bacterial gene expression and survival mechanisms of tuberculosis bacilli. I am specifically focused on the problem of persistence, the ability of small populations of tuberculosis bacilli to survive antibiotic treatment despite lacking alleles that code for genotypic drug resistance. The phenomenon of persistence may be the basis of the need for lengthy treatment regimens to cure tuberculosis and could also contribute the ability of the bacteria to establish a latent infection. I have characterized the transcriptome of tuberculosis persister cells to identify genes that may be involved in the phenomenon, and have created mutant strains defective for persistence. I am in the process of characterizing these mutants using mouse models and various -omics technologies and work collaboratively on other projects which require systems biological approaches.
Research Fellow | firstname.lastname@example.org |
Tuberculosis is a dreadful disease. Success of M.tb lies in its survival in macrophages by evasion of host immune responses. Only available vaccine till now is BCG, and its efficacy varies with age and geographical distribution. Therefore, my overall goal is to develop better understanding of the host-pathogen interactions and utilize that to identify potential new drug targets or vaccine candidates. My focus is (1) Identification of novel mycobacterial factors involved in virulence and evasion of host immune responses (2) Understanding of metabolic pathways required for survival and persistence of mycobacteria in the host. I am using multiple techniques involving combination of molecular biology, biochemistry, genetics, metabolomics, cell biology and Immunology to answer these queries.
Research Assistant Professor | email@example.com
Genetic tools are the integral part of research and are required to revolutionize the study of an organism. I am involved in the development of new tools to ease mycobacterial research, including the development of a mycobacterial expression system, generation of precise deletion mutants by high throughput specialized transduction and to efficiently excise the drug resistance marker (unmarking) from the deletion-substitution mutants. I amalso involved in the development of a rapid, sensitive and inexpensive TB detection/drug susceptibility test to be used in poor resource settings. We are at a junction of taking this test from bench to field testing.
Research Associate Professor | firstname.lastname@example.org
I am using genetic and biochemical tools to define novel regulators of mycobacterial growth and virulence with the goals of better understanding mycobacterial pathogenesis and developing improved therapies. My recent work has revealed the mechanisms by which the ESX-3 secretion system of M. tuberculosis promotes iron uptake by the organism and demonstrates that the importance of M. tuberculosis iron acquisition pathways in vivo depends on the genotype of the host. The same studies show that ESX-3 also modulates virulence though iron-independent mechanisms. We have also extended these studies to the emerging opportunistic pathogen Mycobacteriumhaemophilum, a mycobacterial species with unique requirements for iron supplementation to support its in vitro growth. These studies explain why M. haemophilum growth is iron-dependent and uncover striking similarities to Mycobacterium leprae, the causative agent of leprosy. I am also developing methods to genetically manipulate this organism to experimentally exploit these findings.
I have worked with Bill Jacobs for over 20 years, and currently act as the manager of his lab. I oversee and facilitate all the daily research-oriented activities of the Jacobs group. I am also responsible for coordinating the import/export of scientific materials that support our work. I run occasional targeted experiments for Dr. Jacobs. Acquiring and maintaining the supplies and equipment necessary for our studies is another key part of my role.
Director of BSL-3 Lab | email@example.com
I focus on new TB vaccine research and novel
anti-tuberculosis agent development, use of animal models to investigate
infections and pathogen-host interactions. I am responsible for the safe
use of our HHMI Bio-Safety Level 3 facility at Einstein, including training and
testing post-docs and students according to their own research projects. I also
chair the regular meetings of the TB Research Group internal Biosafety
Committee for TB research projects and coordinate protocols and resources for
Research Technician | firstname.lastname@example.org |
I’m a technician in the lab, providing technical support for PhD students, post-docs, and other lab staff. I mainly work on molecular cloning, phage packaging and high-titer phage preparation for specific gene deletions. Also, I carry out some routine laboratory tasks such as preparing specific agar plates which are commonly and largely used in the lab.
Research Technician | email@example.com |
Research Fellow | firstname.lastname@example.org |
Persistence in Mycobacterium tuberculosis is a phenomenon of cells where a fraction is resistant to a killing assault as a consequence of a transient gene expression or protein modifications. While several genes were previously proposed as contributing to the emergence of persistence, the complete regulatory network is still unknown and it is clearly not attributed to one 'persister gene'. My goal is to define the genetic network causing the persistence phenotype in Mycobacterium tuberculosis. I plan to tackle this problem by exploring the roles of the transcription initiation sigma factors in persistence in the presence of bactericidal drugs. This will be done by combining precise null deletions of the sigma factor encoding genes, along with in vitro high throughput screens and in vivo experiments.
Post-Doctoral Fellow | kayla.weiss.yu.edu |
Pathogens have developed an arsenal of strategies to evade host immunity. My research interests lie in defining the mechanisms that either Mycobacterium tuberculosis or herpes simplex virus employ to circumvent detection and elimination by the host immune response. Additionally, I wish to define the immune components that provide the host with the best protection against these pathogens. By delineating both immune evasion strategies and the optimal immune response following either M.tb or HSV infection, I envision vaccines and therapeutic approaches can be developed to permit pathogen sterilization in the host.
Mycobacterium tuberculosis has been the most successful pathogen in human history and remains a considerable threat. In part, this is due to a compositionally unique cell wall structure laden with lipids, sugars and lipoglycans. My goal in the lab is to provide a better understanding of the cell wall and to use this knowledge to uncover new drug targets to combat the increasing rate of drug resistant bacteria. To better understand the interaction between the bacterial cell wall and the preferred host cell niche, the human macrophage, I will be using targeted gene deletions in human induced pluripotent stem cells.
My research interests are directed at the metabolism and energetics of Mycobacteriumtuberculosis (Mtb). These processes are fundamental to all living organisms and are correspondingly essential for successful infection and survival of Mtb in humans. In part, I have focused on the study of amino acid biosynthetic pathways and the electron transport chain to identify novel drug targets for the treatment of TB. For instance, disruption of certain biosynthetic pathways prevents infection, as well as abolishes persistent infections in mouse models of tuberculosis. My goal is to elucidate the mechanisms by which this bactericidal activity occurs. The electron transport chain is also an essential pathway that is integral in oxidative phosphorylation, the primary mechanism by which cells generate ATP (the main source of energy). My goal here is to investigate less well understood enzymes, such as alternative terminal oxidases, in order to understand their role in redox homeostasis. Such a function may be important in the ability of Mtb to evade host defenses and adapt to antibiotic exposure.
HHMI Medical Fellow | email@example.com
My research uses recombinant HSV viruses to study antibody-dependent cell-cytotoxicity (ADCC). I also create viruses that harness ADCC for broadly protective vaccines against Influenza, HIV, and other pathogens. ADCC occurs when our bodies make antibodies against pathogens which act like calling cards for immune cells. Immune cells recognize these antibodies and kill the infected cells. ADCC is an often-forgotten arm of the immune system, but I believe it holds the key to curing a broad array of disease.
Post- Doctoral Fellow | firstname.lastname@example.org
Mycobacterium tuberculosis (Mtb) represents one of the most persistent bacterial threats to human health. My aim is to find new drug candidate(s) which are needed to limit its impact. I am also involved in our lab's project on identification of improved BCG vaccine.