Ott Lab News

Earlier this year, the World Health Organization declared an end to the global health emergency for COVID-19. This announcement was quickly followed by the US federal government’s plan to end its own public health emergency declaration for the SARS-CoV-2 virus.

Of course, SARS-CoV-2 is still with us. It is also a matter of when, not if, the next pandemic will emerge. These realities mean that the research advances made by Gladstone scientists over the last three years will continue to impact efforts against existing and new viruses for years to come.

Melanie Ott, MD, PhD, director of the Gladstone Institute of Virology (GIV), reflects on the early days of the pandemic, her team’s biggest contributions to COVID-19 research, and the new directions they are taking to understand the underlying biology of viruses, including coronaviruses and HIV.

Here’s the future: a doctor takes a blood sample from her sick patient. In the lab down the hallway, scientists reset the patient’s blood cells into a developmental blank slate using a cocktail of chemicals. Then, they add a combination of tiny molecules that edit the cells’ DNA. Perhaps this editing process repairs a disease-causing mutation or gives the cells a new ability to ward off infection, inflammation, or cancer. Finally, the embryo-like cells are grown into healthy, adult cells—heart cells to quell heart disease, brain cells to treat Alzheimer’s, or immune cells to shrink a tumor—and infused back into the patient’s body. Or perhaps, the doctor infuses the specially designed molecules that edit cells’ DNA right into the patient, and corrections are made directly inside their body.

Born and raised in Bangladesh, Mir Khalid (he/him) is a scientist in Melanie Ott’s lab at Gladstone Institutes. He completed his bachelors and master’s in genetic engineering and biotechnology at the University of Dhaka, Bangladesh. He completed a master’s in infection and immunity at Erasmus University in Rotterdam, Netherlands. He performed his PhD research in the Ott lab studying molecular virology, and received his degree from Erasmus University.

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.