Ott Lab News

About 70,000 people in the United States are diagnosed with COVID-19 each and every day. It’s clear that these new cases are being driven by the more-infectious Delta variant of SARS-CoV-2, the novel coronavirus that causes COVID-19. But why does the Delta variant spread more easily than other viral variants from one person to the next?

Now, an NIH-funded team has discovered at least part of Delta’s secret, and it’s not all attributable to those widely studied mutations in the spike protein that links up to human cells through the ACE2 receptor. It turns out that a specific mutation found within the N protein coding region of the Delta genome also enables the virus to pack more of its RNA code into the infected host cell. As a result, there is increased production of fully functional new viral particles, which can go on to infect someone else.

This finding, published in the journal Science [1], comes from the lab of Nobel laureate Jennifer Doudna at the Howard Hughes Medical Institute, the Gladstone Institutes, San Francisco, and the Innovative Genomics Institute at the University of California, Berkeley. Co-leading the team was Melanie Ott, Gladstone Institutes.

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.

SAN FRANCISCO (KGO) — The battle against COVID-19 has thrown a lot of heroes from the Bay Area medical community into the spotlight. And increasingly, the faces we see informing us about the fight are women. For some of them, it’s been a lifelong journey through a world once dominated by men.