In 2011, Dr. Jennifer Doudna began studying an enzyme called Cas9. Little did she know, in 2020 she would go on to win the Nobel Prize in Chemistry along with Emmanuelle Charpentier for discovering the powerful gene-editing tool, CRISPR-Cas9. Today, Doudna is a decorated researcher, the Li Ka Shing Chancellors Chair, a Professor in the Department of Chemistry and Molecular as well as Cell Biology at the University of California Berkeley, and the founder of the Innovative Genomics Institute.
How RNA technology may tip the balance in our favour when it comes to anti-COVID therapeutics as well as vaccines.
As the world has learned to its cost, the Delta variant of the pandemic coronavirus is more than twice as infectious as previous strains. Just what drives Delta’s ability to spread so rapidly hasn’t been clear, however. Now, a new lab strategy that makes it possible to quickly and safely study the effects of mutations in SARS-CoV-2 variants has delivered one answer: a little-noticed mutation in Delta that allows the virus to stuff more of its genetic code into host cells, thus boosting the chances that each infected cell will spread the virus to another cell.
In a new paper published today in the journal Science, researchers at the Innovative Genomics Institute (IGI) at UC Berkeley and Gladstone Institutes used a new method to explore why some variants of SARS-CoV-2, like the Delta variant, are more transmissible and infectious than others.
The new study, a collaboration between the labs of Jennifer Doudna at the IGI and Melanie Ott at Gladstone Institutes, uses virus-like particles instead of live virus, a safer and faster way to explore the effect of different mutations in the virus’s genome. Initial explorations with this method found a surprising result: while most research has focused on mutations in the virus’s spike protein that allows the virus to penetrate human cells, mutations in a different protein, the nucleocapsid protein, appear to be more important for enhancing infectivity.
The Quantitative Biosciences Institute (QBI) at UCSF presents “Scientific Collaborations Across Borders: QBI/Institut Pasteur: Epigenetic Modifications and Human Pathogenic Viruses,” a QBI Fireside Chat on October 20, 2021 at 10AM PT, co-organized by the Office for Science and Technology of the French Embassy in San Francisco.
This “fireside chat” featured Melanie Ott of Gladstone Institutes/UCSF and Melanie Hamon of Institut Pasteur, and was moderated by Héloïse Pajot of the Embassy of France in San Francisco. The conversation focused on the collaborative research between Institut Pasteur and QBI within the fields of epigenetics and virology, and highlighted the advantages of creating synergy in science across borders during a global pandemic and beyond.
Mélanie Hamon, Principle Investigator, Department of Cell Biology & Infection, Institut Pasteur
Melanie Ott, Principle Investigator, Virology, Gladstone Institutes | School of Medicine, UCSF
Héloïse Pajot, Deputy Attaché for Science and Technology, Embassy of France in the United States
To watch: http://https://youtu.be/j2z8oA3HVAs
Now, with a $26.5-million grant from the National Institutes of Health (NIH), a multi-disciplinary group of researchers from institutions around the world is trying a completely new strategy for curing HIV. The group, known as the HIV Obstruction by Programmed Epigenetics (HOPE) Collaboratory, will be led by researchers at Gladstone Institutes, Scripps Research Florida, and Weill Cornell Medicine. Their approach, which aims to both silence and permanently remove HIV from the body, takes advantage of knowledge about how other viruses have become naturally inactivated over time.