Javidlab:research

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RESEARCH<br>
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OVERVIEW<br>
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INTEREST<br>
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The Javid lab principal interest is in mycobacterial pathophysiology. Tuberculosis causes more infectious disease deaths in China than any other pathogen, and the basic biology of its causative organism,Mycobacterium tuberculosis is still poorly understood.Our lab is interested in how fundamental physiological processes in mycobacteria can influence important clinical phenotypes such as antibiotic tolerance and immune evasion. We have shown that altering the protein translation error rate in mycobacteria can profoundly influence phenotypic resistance to first-line anti-mycobacterial drugs. We are now trying to understand the molecular mechanism and regulation of translational fidelity.Mycobacterium tuberculosis can reside within the host for decades without detection. We are trying to understand how this happens -- at the level of both innate and adaptive immunity.
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Tuberculosis causes more deaths globally, and in China, than any other single pathogen.  Some of the reasons for its success are the ability of the causative organism, Mycobacterium tuberculosis, to lie undetected in the host for decades (clinical latency), the very long treatment times for successful antibiotic treatment (phenotypic resistance) and emerging drug resistance to effective antibiotics. The Javid laboratory is interested in investigating  some of the fundamental physiological mycobacterial processes that may contribute to these phenotypes.
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Programme<br>
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Adaptive<br>
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Mistranslation<br>
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The Javid lab principal interest is in mycobacterial pathophysiology. Tuberculosis causes more infectious disease deaths in China than any other pathogen, and the basic biology of its causative organism,Mycobacterium tuberculosis is still poorly understood.Our lab is interested in how fundamental physiological processes in mycobacteria can influence important clinical phenotypes such as antibiotic tolerance and immune evasion. We have shown that altering the protein translation error rate in mycobacteria can profoundly influence phenotypic resistance to first-line anti-mycobacterial drugs. We are now trying to understand the molecular mechanism and regulation of translational fidelity.Mycobacterium tuberculosis can reside within the host for decades without detection. We are trying to understand how this happens -- at the level of both innate and adaptive immunity.
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We have previously shown that the protein translation error rate (mistranslation rate) in mycobacteria is unusually high.  Importantly, manipulation of the error rate, both up and down, appears to have profound effects on antibiotic phenotypic resistance. We have shown that mycobacterial strains with high error rates have remarkable phenotypic resistance to the antibiotic rifampicin, and the opposite is true for high fidelity mutants. We are interested in investigating the basic mechanism for these observations, and identifying other potentially adaptive phenotypes that arise from low translational fidelity.
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Programme<br>
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Mycobacteria<br>
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host-pathogen<br>
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2<br>
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interactions<br>
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The Javid lab principal interest is in mycobacterial pathophysiology. Tuberculosis causes more infectious disease deaths in China than any other pathogen, and the basic biology of its causative organism,Mycobacterium tuberculosis is still poorly understood.Our lab is interested in how fundamental physiological processes in mycobacteria can influence important clinical phenotypes such as antibiotic tolerance and immune evasion. We have shown that altering the protein translation error rate in mycobacteria can profoundly influence phenotypic resistance to first-line anti-mycobacterial drugs. We are now trying to understand the molecular mechanism and regulation of translational fidelity.Mycobacterium tuberculosis can reside within the host for decades without detection. We are trying to understand how this happens -- at the level of both innate and adaptive immunity.
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The majority of people infected with M. tuberculosis – almost a third of the world’s population – do not become ill unless their immune system weakens. This suggests that mycobacteria have evolved to evade host immune responses, much like other chronic infections. We are interested in investigating the mechanisms by which mycobacteria manipulate the host environment to their own ends. We use a variety of approaches – including proteomic profiling of mycobacteria-infected cells, flow cytometry and forward genetics to address these questions.
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Revision as of 09:22, 4 July 2013



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OVERVIEW

Tuberculosis causes more deaths globally, and in China, than any other single pathogen. Some of the reasons for its success are the ability of the causative organism, Mycobacterium tuberculosis, to lie undetected in the host for decades (clinical latency), the very long treatment times for successful antibiotic treatment (phenotypic resistance) and emerging drug resistance to effective antibiotics. The Javid laboratory is interested in investigating some of the fundamental physiological mycobacterial processes that may contribute to these phenotypes.



Adaptive
Mistranslation

We have previously shown that the protein translation error rate (mistranslation rate) in mycobacteria is unusually high. Importantly, manipulation of the error rate, both up and down, appears to have profound effects on antibiotic phenotypic resistance. We have shown that mycobacterial strains with high error rates have remarkable phenotypic resistance to the antibiotic rifampicin, and the opposite is true for high fidelity mutants. We are interested in investigating the basic mechanism for these observations, and identifying other potentially adaptive phenotypes that arise from low translational fidelity.



Mycobacteria
host-pathogen
interactions

The majority of people infected with M. tuberculosis – almost a third of the world’s population – do not become ill unless their immune system weakens. This suggests that mycobacteria have evolved to evade host immune responses, much like other chronic infections. We are interested in investigating the mechanisms by which mycobacteria manipulate the host environment to their own ends. We use a variety of approaches – including proteomic profiling of mycobacteria-infected cells, flow cytometry and forward genetics to address these questions.




Room 4-302 Biotech Building
School of Medicine
Tsinghua University

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