Pew Biomed Scholar Shifts Her Focus to COVID-19

Scientist Pamela Bjorkman takes lessons from her HIV research and applies them to the coronavirus

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Pew Biomed Scholar Shifts Her Focus to COVID-19
Pamela Bjorkman
Courtesy of Pamela Bjorkman

Biochemist Pamela Bjorkman, a 1989 Pew biomedical scholar, runs a lab at the California Institute of Technology. In response to the global pandemic, she has shifted her work from the study of HIV to SARS-CoV-2, the virus that can result in COVID-19. During a recent interview with Pew’s “After the Fact” podcast, which this season features a series of “Conversations on Science,” Bjorkman discussed efforts to find a vaccine for COVID-19, as well as recent research on the novel coronavirus, to help us better understand the science behind the pandemic.

Q: You run a lab at Caltech that explores viruses, and your primary research relates to HIV, which is what causes AIDS. Can you help us understand how these types of viruses differ from the common cold and other infections?

A: HIV is an example of a virus that is highly evolved, so much so that everything our immune system does to counteract this virus, it has another trick up its sleeve to use against our immune system. HIV is not very transmissible—in fact it’s estimated that it’s transmitted in 1 out of 200 sexual encounters.

Unfortunately, HIV keeps evolving in the host, creating many different strains, which makes it impossible for the body to eliminate it. By the time antibodies are created to rid the body of the dominant strain of HIV, the virus has already mutated, and this new subset of the virus is resistant to those antibodies—and the cycle continues. It has been estimated that there are 10 to the power of 16 different strains of HIV in the world today. For context, there are far more strains of HIV in a single person than there are strains of influenza in the world. That’s a strategy for a very long-lived virus to evade our immune system.

Q: HIV remains a horrendous problem in the world, but now the world’s been gripped by a new virus— SARS-CoV-2. When did alarm bells go off that this type of virus may be a huge issue?

A: I used to read some of the coronavirus literature prior to the COVID-19 outbreak; it was interesting to me, as coronaviruses have some structural similarities to HIV. And every single paper said the virus was going to be a problem. In the past several decades, we experienced two major outbreaks of these zoonotic infections—meaning they came from animals—with SARS [severe acute respiratory syndrome] in the early part of the 2000s and then MERS [Middle East respiratory syndrome] in 2012. And while viruses that cause SARS-CoV and MERS-CoV are not easily transmissible, they actually have a higher mortality rate than the one that causes COVID-19. However, SARS-CoV-2 is a more dangerous form of virus because it has a perfect way to transmit through asymptomatic people. You’re young, you’re out there, you don’t know you’re sick, and you’re infecting all kinds of people.

So, coronaviruses have always been on my radar, but it was around February, when the news coming out of China indicated that this could be very, very bad, that my collaborator—Michel Nussenzweig at The Rockefeller University—and I decided to submit a supplement to one of our existing National Institutes of Health grants to request funding to look at SARS-CoV-2  antibodies.

Q: What has the scientific community learned about the coronavirus since it entered our consciousness in February?

A: At the beginning, the coronavirus strain circulating most commonly in China was sequenced in laboratories there almost immediately, and those findings were shared with the world. As the virus spread, scientists around the world also began examining the variants in their own cities. There’s a resource called run out of the University of Washington, and through this website you can trace the virus as it travels from one part of the world to another, and you can see how it has mutated. And while the coronavirus has mutated, the most important question is: Would the variations in the part of the virus that is recognized by antibodies matter for a vaccine? Research is still underway regarding this, but my preliminary conclusion is no, it should not matter. I think one vaccine could work, even with different variants and different isolates of the virus in different parts of the world.

Q: Can you break down the difficulties surrounding the development of a COVID-19 vaccine?

A: The average amount of change every time the virus makes a new copy of itself, or the variability, of the flu virus is higher than it is in SARS or any other coronavirus, and it’s even higher in HIV. Each year when you get a flu vaccine, it is the result of researchers going around the world, collecting samples of all the flu isolates they find in animal reservoirs or in people, and deciding what the most likely strains are going to be circulating that year. They then mix either three or four of these strains and give them to patients as either a trivalent [three components] or a quadrivalent [four components] vaccine. If their estimate about what’s going to be the most common strain circulating is correct, the flu shot works well. If it’s off, the flu shot doesn’t work as well. You can’t do that for HIV because you have far too many strains. For coronavirus, we mostly know what the variant strains are from, so we should be able to create a vaccine based on this information.

Q: What are unique aspects about this new virus?

A: One area of interest is our immunological memory—that’s how well the body remembers a virus from a prior infection (or vaccine). For instance, most people are vaccinated as children against measles, which prevents infection if [you’re] exposed to the measles virus. That’s incredible durable immunological memory. Coronaviruses appear to not induce very good immunological memory. The work that’s been done on immunological memory, especially B cells, meaning the cells that make antibodies, and how our bodies create memory B cells to respond to viruses that the body knows don’t belong based on colds and vaccines, will be especially important work. This type of research will be relevant to understanding how to make the best type of vaccine for COVID-19.

Q: Are scientists working together in different ways to come up with a vaccine much faster?

A: Yes, it’s been an exciting time for collaboration. Typically, when scientists complete their research, they would submit a paper to a peer-reviewed journal, which could take months to appear and be shared with the scientific community. Now, scientists can share their work quickly through preprint servers—which means the work is not yet reviewed, but it’s accessible to scientists to view, comment on, and consider. The speed of the vaccine development has been happening at a phenomenal pace, though it doesn’t feel fast enough with the whole world waiting for it.

It’s also been a time of ingenuity and creativity that’s encouraging more people to embrace science. For instance, I’ve heard of individuals developing new materials for personal protective equipment and city planners working with epidemiologists to come up with safer ways to be outside in the community. I’m hopeful that people will be more supportive of basic science, especially research that would prevent another pandemic, which I think is inevitable—but hopefully we can prevent the next one.


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