Ott Lab News

In the span of just weeks, millions of Canadians became infected with SARS-CoV-2. Globally, more cases were reported in the first 10 weeks after the Omicron variant was identified than in all of 2020.

It was a mass infection event quite unlike anything we’d seen in the pandemic to date, hitting both the unvaccinated and vaccinated — but not in the same way.

While vaccinated and boosted individuals largely avoid dire outcomes from COVID-19, data continues to show that unvaccinated individuals remain at a far higher risk of serious illness, hospitalization, and death.

Two years into the pandemic, and two months into Omicron’s globe-crushing surge, our COVID-19 vaccines are finally on the cusp of a federally sanctioned update. To counter the new variant’s uncanny knack for slipping past antibodies roused by our first-generation shots, Moderna and Pfizer have both kick-started clinical trials to see how Omicron-specific vaccines fare in people. Results are expected within the next few months, and if all goes well, syringes around the world could be locked and loaded with Omicron’s wonky-looking spike protein by the summer.

Omicron-izing our COVID vaccines is a good, if unfortunately timed, move, experts told me. But the same strangeness that makes an Omicron-specific vaccine wise is also a warning against trashing our original-recipe shots too soon. We don’t know what the next major variant will look like. It could be an offshoot of Omicron, something that strongly mirrors the ancestral SARS-CoV-2, or something that resembles neither variant at all.

Finding the omicron coronavirus variant in San Francisco on Wednesday may have caused concern among the general public, but to the Bay Area scientists eager to study the highly mutated virus and understand the threat it may pose, having a sample in their backyard was a stroke of luck.

In the mad global dash to study omicron, getting copies of the variant to analyze in U.S. labs has been a challenge. Some Bay Area scientists said they’ve been on waiting lists for at least a week — since Thanksgiving, when the variant was first reported out of South Africa.

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.

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.