Viruses are hijackers. When they infect a cell, they take over that cell’s protein-making machinery, causing it to produce the viral proteins that allow infection to successfully accelerate and spread. And as has been seen in the recent outbreak of coronavirus (COVID-19), just labeled a pandemic by the World Health Organization, a successful virus can be very dangerous indeed.

Dr. Noam Stern-Ginossar and her team in the Weizmann Institute’s Department of Molecular Genetics are using innovative methods to study how viruses come to dominate the infected cell’s protein production machinery. These methods, and the insights they provide, may help scientists and their clinical partners develop future anti-viral treatments.

Dr. Stern-Ginossar uses a deep-sequencing technique called ribosome profiling to provide a comprehensive view of genetic translation—the process by which a ribosome reads the genetic template that guides protein synthesis. Revealing the “what, when, where, and how” of protein production, ribosome profiling enables scientists to determine the identity and the relative levels of translation of each protein during the course of infection.

Dr. Noam Stern-Ginossar

Recent work in the Stern-Ginossar lab revealed how a common modification to RNA—a genetic messenger that delivers instructions from DNA and controls the synthesis of proteins—helps viruses successfully infect cells.
This modification, which occurs frequently in both viral and human RNA, “turns down” the production of interferon, a protein that is released when a virus invades a cell and instruct cells to prepare for a viral attack. But when produced in very high levels, interferon can kill the cell.

Dr. Stern-Ginossar’s research, which was performed in collaboration with departmental colleagues Prof. Jacob Hanna and Dr. Schraga Schwartz, and was recently published in Nature Immunology, reveals a novel target for the development of anti-viral medications. Such medications might be designed to target the RNA modification that lowers interferon production. This could potentially provide a drug-based mechanism for modulating host cells’ innate anti-viral response.

Dr. Noam Stern-Ginossar is supported by the Skirball Chair in New Scientists, the American Committee for the Weizmann Institute of Science 70^th Anniversary Lab, the Alan and Laraine Fischer Foundation, and the European Research Council.