BRIKEN LAB

Department of Cell Biology and Molecular Genetics

 

 

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Volker Briken

Associate Professor

Ph.D. - University of Paris (France), 1998
Telephone: (301) 405-0289
Fax: (301) 314-9489
E-mail: vbriken@umd.edu

Research Interests: Mycobacterium tuberculosis, Host-Pathogen Interactions, Apoptosis, Lipid and Protein Antigen Presentation, Virulence Genes.

 

Tuberculosis (TB) is an infectious disease of global importance. It is estimated that about one third of all humans are latently infected with its etiologic agent, Mycobacterium tuberculosis (Mtb) and 2.5 million people will die of TB annually. The currently used vaccine strain, Bacillus Calmette-Guérin (BCG) has proven to be very safe but its efficiency in protecting adults from TB has ranged from 0 to 80%. The chemotherapy of TB is inefficient since it takes 6-9 month to complete. In addition, multi-drug resistant (MDR) strains of Mtb have been detected in over 70 countries and more recently outbreaks of extreme-drug (XDR) resistant strains have raised growing concerns. The emergence of tuberculosis due to MDR/XDR-Mtb and the deadly synergy of the HIV/AIDS epidemic with TB killing millions of people every year, strongly underlines the need for an improved vaccine and/or better drugs to protect humans from TB.

In order for Mtb to survive and persist, bacteria need to manipulate infected cells at many levels. In my laboratory we recently executed an innovative “gain-of-function” genetic screen to identify anti-apoptosis genes in Mtb. We identified three independent genomic regions of Mtb that contain anti-apoptosis genes. Subsequently, we identified one of the genes (nuoG) within one of the regions as being important for the anti-apoptosis phenotype and virulence of Mtb (PLOS Pathogens 2007).These findings established that the capacity of Mtb to inhibit host cell apoptosis is a new virulence pathway. The research focus of my laboratory is to identify the anti-apoptosis genes in the Mtb genome, to investigate the molecular mechanism of their host cell apoptosis inhibition and to characterize their impact on bacterial virulence using the mouse model of TB.

 

 
     

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