Leor Weinberger, PhD
|Address||1650 Owens St|
San Francisco CA 94107
|Princeton University||Lewis-Thomas Fellow||Molecular Biology||2007|
|University of California, Berkeley||Ph.D.||Biophysics||2004|
|University of Maryland, College Park||B.Sc.||Biology, Physics||1998|
|2016||Senior Investigator, Gladstone Institutes|
|2013||NIH Director's Pioneer Award|
|2015||American Institute for Mechanical and Biological Engineering (AIMBE), College of Fellows|
|2013||NIH/NIDA Avant Garde Award for HIV Research (deferred)|
|2011||Alfred P. Sloan Research Fellow|
|2009||NIH Director's New Innovator Award|
|2009||Bill & Melinda Gates Foundation, Grand Challenges Award|
|2009||W.M. Keck Foundation, Research Excellence Award|
|2009||California HIV/AIDS Foundation, Young Investigator Innovative Development Award|
|2008||NIH K25 Career Development Award|
|2008||Pew Scholar in the Biomedical Sciences|
|2004||Lewis Thomas Fellowship, Princeton University|
|1999||E. Cota-Robles Fellowship, UC Berkeley|
|1999||Howard Hughes Medical Institute (HHMI) Pre-Doctoral Fellowship|
|1997||John Prost Award, University of Maryland|
|1997||HHMI Undergraduate Research Fellowship, 2nd Award|
|1996||Maryland Distinguished Scholar|
|1995||HHMI Undergraduate Research Fellowship|
|1993||NIH FAES Fellow|
Dr. Weinberger and colleagues pioneered the study of HIV’s decision circuit and demonstrated that stochastic ‘noise’ in gene expression—Brownian fluctuations arising from diffusion-limited reactions—can drive fate-selection decisions. The lab’s studies identified the molecular sources of noise in HIV, exposed the mechanisms regulating noise, and determined how feedback architectures tune noise for fate selection. The techniques developed for HIV also enabled the lab’s discovery of the first transcriptional accelerator circuit—a high-cooperativity feedback motif that enables signaling systems (e.g. inflammatory responses) to overcome a fundamental tradeoff wherein increased speed generates higher/toxic amplitude. These accelerator circuits in herpesviruses are being exploited for a new class of antiviral target.
Collectively, the lab’s studies overturned dogma that HIV latency was a deterministic cell-driven artifact and instead showed that HIV encodes a ‘hardwired’ latency program that is evolutionarily optimized to harness noise. Gene-expression noise is now acknowledged as a major clinical barrier to reversing HIV latency and curing HIV. These studies laid the foundation for new therapeutic strategies targeting the HIV-latency circuit, including the lab’s prediction and subsequent discovery of noise-enhancer molecules. Noise enhancers potentiate transcriptional activators, substantially increasing their efficacy and ability to activate persistent (i.e., latent) HIV.
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