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Harvard Postdoctoral Fellow Position: Novel tech interface of HIV and Cell Biology

Employer
Tsibris Lab, Brigham and Women's Hospital, Harvard Medical School
Location
Cambridge and Boston, Massachusetts (US)
Salary
Salary will follow NIH and BWH guidelines - up to $70,000 per year with benefits.
Closing date
Nov 8, 2019

Job Details

An NIH-funded position is available for an exceptionally talented, motivated, and hardworking postdoctoral fellow to investigate the mechanisms of HIV reactivation from latency using molecular biology, genetics, high-throughput sequencing, and biochemical techniques. Experience with RNAseq, ChIP-qPCR, locus targeting via Cas9, and/or molecular cloning techniques will be viewed favorably. Prior virology-related work is not required. The successful candidate will join a vibrant research team exploring novel aspects of HIV-1 and HIV-2 pathogenesis and the mechanisms of virus latency and reactivation. The postdoctoral fellow will have appointments both at Brigham and Women’s Hospital and Harvard Medical School and will participate in the activities of the Division of Infectious Diseases at Brigham and Women’s Hospital. Recent graduates with less than three years of postdoctoral experience and a background in the biological sciences, a track-record of productivity, and excellent references are encouraged to apply. Salary will follow NIH and BWH guidelines. Candidates should send a statement of interest and future goals and a curriculum vitae to Dr. Athe Tsibris at the email address provided. While three letters of reference from mentors familiar with the applicant’s scientific abilities will ultimately be required, this is not needed for first contact. Additional information about the Tsibris lab may be found at http://tsibrislab.bwh.harvard.edu/.

Company

The Tsibris Lab studies the biology and dynamics of HIV reservoirs in blood and tissue. We use these insights to expand our understanding of HIV persistence and design and test novel strategies to eliminate latently HIV-infected cells.

Lentiviral integration into CD4+ T cells, and potentially other cell types, is the major barrier to HIV eradication. Efforts to reactivate virus transcription and clear the reservoir through immune-mediated approaches have identified an important problem: the reversal of HIV latency may not generate sufficient virus antigen to clear the reservoir. Our lab seeks to understand precisely what, mechanistically, is required to reactivate HIV translation while minimizing off-target effects on cell function; virtually any eradication approach based on the human immune system will require HIV translation. We use novel technologies to define the transcription factor requirements of robust latency reversal, quantify HIV translation efficiency, and map the cellular pathways that are essential to virus reactivation. Particular interests include HIV-1 reservoir dynamics in women, HIV-2 latency, the role of RNA structure in latency reversal, and the effects of opioid use on virus reactivation. This work leverages our HIV Eradication and Latency (HEAL) cohort and a network of collaborators in industry and academia to deliver on the promise that the use of the word “cure” implies.

Company info
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