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Because retroviruses are dependent on ubiquitous cellular processes, they provide a tractable microcosm to elucidate principles and mechanisms underlying infectious disease and cancer. Our team uses the retrovirus model system to define fundamental mechanisms of posttranscriptional gene expression in viruses and their host cells.
Our goal is comprehensive understanding of RNA expression mechanisms in healthy cells and fixing the deficiencies that produce disease. We have uncovered a fundamental paradigm controlling the growth of viruses and are dissecting this interface with cell biology.
The ability of human retrovirus to downregulate the cell's protein synthesis machinery presented us a prism to view the interworking of the virus-host cell machinery. Henceforth, a newly appreciated mechanism was uncovered that explains how the virus overcomes the to continue synthesis of viral proteins.
Viral countermeasures also overcome host microRNA activity. Ongoing studies show viral replication perturbs host microRNA activity and the defeat of antiviral response is disrupting cellular homeostasis.
Studies at the virus-host interface continue to demonstrate intriguing fundamental mechanisms and offer novel ways to abrogate the severity of viral infections and consequences of neoplasms.
Scholarship at the virus-host interface is the outcome of funded research and experimental contributions of graduate students and post-PhD trainees. The Boris-Lawrie lab members have earned awards for their research, prestigious fellowships and are well-prepared to become leaders in their chosen career. Our new fundamental understanding of posttranscriptional gene expression has broad significance across microbiology, cell biology and disease pathogenesis.
Please visit PubMed to view all of our publications.