Ott Lab News

To spread between cells in the body and hop from person to person, human immunodeficiency virus (HIV) must copy its genetic material, produce viral proteins, and assemble new virus particles. For this complex process to occur, a viral protein called Tat must bind to a section of the virus’s RNA—the molecules that carry instructions for making new proteins—which is called the HIV trans-activation response element (TAR).

The TAR RNA can assume many different shapes, known as conformations. However, the Tat protein can only bind to one of these conformations, and if TAR is in a conformation that does not bind to Tat, HIV won’t replicate. So, understanding how these molecules interact could help scientists design therapies that block HIV replication.

As we approach the height of the holiday season, some medical experts have warned of a potential “tripledemic”—a simultaneous surge in cases of COVID-19, the flu, and RSV (respiratory syncytial virus).

How concerned should you be, and what does this mean for your holiday plans?

We asked three Gladstone virologists—Senior Investigator Warner Greene, MD, PhD; Director of the Gladstone Institute of Virology Melanie Ott, MD, PhD; and Senior Investigator Nadia Roan, PhD—for their perspectives.

While the world continues to deal with the COVID-19 pandemic, MPXV has emerged as another global public health emergency. Commonly referred to as monkeypox, this viral disease has now spread to dozens of countries where it is not typically found.

As of August 29, 2022, over 18,000 cases have been reported in the US—the biggest outbreak of MPXV ever seen in the country. More than 700 cases have now occurred in San Francisco. Still, the general risk of MPXV remains very low.

As the Omicron variant of SARS-CoV-2 spread rapidly around the globe earlier this year, researchers at Gladstone Institutes, UC Berkeley, and the Innovative Genomics Institute used virus-like particles to identify which parts of the virus are responsible for its increased infectivity and spread.

A while ago, some researchers had suggested that blocking a set of proteins, known as bromodomain and extraterminal (BET) proteins, might be a way to fight COVID-19. However, in a surprising study, scientists at Gladstone Institutes and UC San Francisco (UCSF) discovered that BET proteins are actually crucial for the body to fight the infection. In fact, the SARS-CoV-2 virus itself blocks the proteins to try to gain an advantage and continue to spread.

In unvaccinated people, infection with the Omicron variant of SARS-CoV-2 provides little long-term immunity against other variants, according to a new study by researchers at Gladstone Institutes and UC San Francisco (UCSF), published today in the journal Nature.

Over the course of 2020, the world watched with bated breath as biotechnology companies—in less than one full year—developed, tested, and released vaccines against the SARS-CoV-2 virus that causes COVID-19.

In some ways, these vaccines upended the paradigm of vaccines that came before; they were deployed on a faster timeline and it was the first time mRNA vaccines were used and mass-produced. But the science behind all COVID-19 vaccines rests on decades of research on infectious diseases, the human immune system, and vaccination.

A vaccine for hepatitis C has eluded scientists for more than 30 years, for several reasons. For one, the virus that causes the disease comes in many genetic forms, complicating the creation of a widely effective vaccine. For another, studying hepatitis C has been difficult because options in animals are limited and lab methods using infected cells have not adequately reflected the real-life dynamics of infection.

As the Omicron variant of SARS-CoV-2 continues to sweep through Europe and moves into the Middle East and Latin America, a new variant of Omicron, known as BA.2, is running up case counts in several nations. Denmark has been particularly hard hit with BA.2, which now accounts for over half of all infections in the country. In the United States, hospitalizations remain at high levels even as COVID-19 cases are declining in many of the communities that were hardest-hit by the virus earlier in the pandemic, allowing the San Francisco Bay Area, for example, to relax certain mandates.

Where is this pandemic taking us next?

In late November 2021, scientists reported the emergence of a new variant of SARS-CoV-2, the virus that causes COVID-19. In a matter of weeks, the variant, dubbed Omicron, spread around the globe.

Today, the Omicron variant accounts for about 98 percent of all COVID-19 cases in the United States, and case counts and hospitalizations are spiking at all-time highs in many places. At the same time, recommendations are constantly shifting about how to prevent COVID-19, and when to isolate or quarantine. Across both social media and mainstream media outlets, conflicting opinions are being raised about what Omicron means for the future of the COVID-19 pandemic.

This week, three virologists at Gladstone Institutes—Warner Greene, MD, PhD, director of the Michael Hulton Center for HIV Cure Research; Melanie Ott, MD, PhD, director of the Gladstone Institute of Virology; and Nadia Roan, PhD, associate investigator—discussed what people should know about Omicron, home testing, and more.