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Science-trained journalist gives advice on simplifying the genetic details around COVID-19 Date: 02/04/21

Marla Broadfoot


By Bara Vaida

With news emerging that genetic variants of the SARS-CoV-2 virus have emerged globally, journalists with a deep background in genetics are in more demand.

Independent journalist Marla Broadfoot has a doctorate in genetics and molecular biology and is one of those writers well-positioned to be writing about this topic. In a recent interview for AHCJ, she talks about her coverage of COVID-19 over the past year for Scientific American and gives advice to reporters who write about the complicated topic of genetics.

Q: You’ve written many in-depth stories this year about the COVID-19 pandemic. What were some of the biggest obstacles you dealt with and how did you overcome them?

A: I would say that it wasn’t an obstacle per se, but rather a challenge, which has been keeping up with the relentless pace of scientific research coming out about the virus. Today, I went to PubMed — which is where I always start my research — and, just for fun, searched for “COVID-19.” More than 94,000 papers came up. That was obviously all in one year because it didn’t exist a little over a year ago. Trying to distill even a fraction of that information into something meaningful to our readers is a monumental challenge. I’ve heard some say journalism is the first draft of history, and I think science is similar in that it provides a first draft of what we know about the natural world. Then it provides a second draft and third draft, etc., through this iterative, self-correcting process. So I try to convey a bit of that process, that uncertainty, in my writing. Our understanding of the natural world always changes over time, and COVID-19 is no different. If conclusions shift, it isn’t necessarily that science is wrong, but rather that our understanding was incomplete.

Q: How have you used your background in genetics to help you cover this pandemic?

A: One of my first stories about the pandemic was trying to figure out why some people with COVID-19 get sicker than others and the role of genetics. It is still an open question, but there has been some progress as scientists have uncovered a handful of genes that could put some people at higher risk. The more digging I’ve done, the more I’ve been surprised to find that there have been decades of research focusing on this very question in other infectious diseases. A surprisingly large number of infections are asymptomatic — hepatitis C, flu, colds — and our genes may explain why. It’s pretty exciting research because it may be possible someday to do a genetic test and then be able to say: this is someone who is more likely to have a severe response to COVID-19 or some other infectious disease.

Q: On that point, I was really interested in a story you did recently about why many people, even those adhering to pretty strict social distancing measures, still came down with colds or other infectious diseases. I actually hear this a lot myself from family and friends. Tell us how you approached this story?

A: I approached that story almost like a detective story, thinking of every possible explanation for how someone could have caught a cold despite being so careful and then asking experts about those possibilities. So questions like: Are there simply more of other kinds of viruses out there? Are these other viruses more contagious? Can they stay on surfaces longer than SARS-CoV-2? Is asymptomatic spread a thing for other viruses too? Are there latent infections that reactivate after months? And then I thought about all the different access points that a pathogen might take to come into our (quarantine) world. Was it on our take-out boxes? Or on our pets? So I tried to find answers to each of those questions to see what might explain it. In the end, what I learned was that there are other viruses out there that are more numerous, hardy and contagious than the one that caused this pandemic. And that a lot of people weren’t being as careful as they thought.

Q: You’re in a great position with your background in genetics to report on what is happening with these genetic variants to SARS-CoV-2. Can you talk a little about what you are seeing?

A: It sounds like a super scary thing: “The virus is mutating!” And I see people (on Twitter) with the Nextstrain Project (like geneticist) Emma Hodcraft saying: “Hey! This is what viruses do. They mutate.” So this is something we want to monitor. Just because the virus is mutating doesn’t mean the vaccines won’t work, so a bit of a caution is in order, otherwise, every time we see a mutation in a virus, we will have to sound another alarm and it will be like the boy that cried wolf. That being said, I have seen some studies about the new variants that are a little concerning. Even if we find that the virus has evolved resistance to our vaccines, that doesn’t mean we have to go back to the drawing board. Our current vaccines are based on mRNA, strips of genetic code that can easily be swapped out to accommodate any consequential mutations in the virus. So genetics may solve it.

Q: Who would be your favorite experts to follow on Twitter to get the best information and stay on top of genetics and the emerging variants of the COVID-19 virus?

A: I have to admit that I wasn’t a big Twitter person before the pandemic. But it has become one of the best ways to find people to talk to. Among my favorite experts I follow are: Megan Srinivas, M.D., an infectious disease physician in Iowa; Caitlin Rivers, an epidemiologist with Johns Hopkins Center for Health Security; Mark Lipsitch, an epidemiologist at Harvard T.H. Chan School of Public Health; Trever Bedford, associate professor of vaccine and infectious disease division at the Fred Hutcherson Cancer Research Center; Emma Hodcroft, post-doctoral researcher at the University of Bern and a co-developer of Nextstrain tracking the COVID-19 virus; Eric Topol, founder and director of the Scripps Research Transitional Institute; Leana Wen, visiting professor of health policy and planning at George Washington University; Jesse Bloom, associate professor at the basic sciences division at Fred Hutcherson Cancer Research Center; Priya Dugal, an epidemiologist with the Johns Hopkins Bloomberg School of Public Health; Tara Smith, an epidemiologist at Kent State University College of Public Health; and Kizzy Corbett, a virologist at the NIH.

Q: What advice do you have for journalists trying to explain the complicated topic of genetics?

A: My go-to is to use metaphors whenever possible. You don’t have to explain the nitty-gritty details for people to understand genetics. If you can give people something to relate to, then they can more easily grasp complex concepts. Ask researchers if they have their own favorite analogies to describe their work because sometimes, they can work.

Q: What is your favorite analogy for explaining how the messenger RNA (mRNA) used in the Pfizer and Moderna COVID-19 vaccines works?

A: Everyone is familiar with this metaphor of DNA being the blueprint of life. mRNA is a kind of molecular scratch paper that carries these instructions around the cell where they can be used to construct proteins. In the case of the COVID-19 vaccines, the mRNA is giving our cells instructions for making the spike protein, a harmless bit of the coronavirus. Our cells recognize the protein as foreign and make antibodies against it and against the virus. In the meantime, the mRNA scratch paper disintegrates.

Marla Broadfoot (@mvbroadfoot) is a freelance science journalist with a doctorate in genetics and molecular biology. Her work has appeared in Scientific American, Science, Stat, The Scientist, Discover, Nature News, and Science News, among others. She is president of the Science Communicators of North Carolina, a contributing editor at American Scientist, and an adjunct professor at the University of North Carolina at Chapel Hill.