A new map of the entire sky, as seen in X-rays, looks deeper into space than any other of its kind.

The map, released June 19, is based on data from the first full scan of the sky made by the eROSITA X-ray telescope onboard the Russian-German SRG spacecraft, which launched in July 2019. The six-month, all-sky survey, which began in December and wrapped up in June, is only the first of eight total sky surveys that eROSITA will perform over the next few years. But this sweep alone cataloged some 1.1 million X-ray sources across the cosmos — just about doubling the number of known X-ray emitters in the universe.

These hot and energetic objects include Milky Way stars and supermassive black holes at the centers of other galaxies, some of which are billions of light-years away and date back to when the universe was just one-tenth of its current age.

eROSITA’s new map reveals objects about four times as faint as could be seen in the last survey of the whole X-ray sky, conducted by the ROSAT space telescope in the 1990s (SN: 6/29/91). The new images “are just spectacular to look at,” says Harvey Tananbaum, an astrophysicist at the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass., not involved in the mission. “You have this tremendous capability of looking at the near and the far … and then, of course, delving in detail to the parts of the images that you’re most interested in.”

 eROSITA can flag potentially interesting X-ray phenomena, such as flares from stars getting shredded by black holes, which other telescopes with narrower fields of view but better vision can then investigate in detail, Tananbaum says. The new map also allows astronomers to probe enigmatic X-ray features, such as a giant arc of radiation above the plane of the Milky Way called the North Polar Spur.

This X-ray feature may be left over from a nearby supernova explosion, or it might be related to the huge blobs of gas on either side of the Milky Way disk, known as Fermi Bubbles, says eROSITA team member Peter Predehl, an X-ray astronomer at the Max Planck Institute for Extraterrestrial Physics in Garching, Germany (SN:6/8/20). eROSITA observations could help the Russian and German teams involved in the mission figure out what the spur is.

About 20 percent of the marks on eROSITA’s map are stars in the Milky Way with intense magnetic fields and hot coronae. Scattered among these are star systems containing neutron stars, black holes and white dwarfs, and remnants of supernova explosions. eROSITA also caught several fleeting bursts from events like stellar collisions.

Beyond the Milky Way, most of the X-ray emitters that eROSITA found are supermassive black holes gobbling up matter at the centers of other galaxies (SN: 6/18/20). Such active galactic nuclei comprise 77 percent of the catalog.

Distant clusters of galaxies made up another 2 percent of eROSITA’s haul. These clusters were visible to the telescope thanks to the piping hot gas that fills the space between galaxies in each cluster, which emits an X-ray glow.

“At present, we probably know about a little less than 8,000 clusters of galaxies,” says Craig Sarazin, an astronomer at the University of Virginia in Charlottesville not involved in the work. But over its four-year mission, eROSITA is expected to find a total of 50,000 to 100,000 clusters. In the first sweep alone, it picked up about 20,000.

That census could give astronomers a much better sense of the sizes and distributions of galaxy clusters over cosmic history, Sarazin says. And this, in turn, may give new insight into features of the universe that govern cluster formation and evolution. That includes the precise amount of invisible, gravitationally binding dark matter out there, and how fast the universe is expanding.

Closer to home, observations of supernova remnants could help clear up some confusion about the life cycles of big stars, says eROSITA team member Andrea Merloni, an astronomer also at the Max Planck Institute for Extraterrestrial Physics. Past X-ray surveys have found fewer supernova remnants than theorists expect to see, based on how many massive stars they think have blown up over the course of the galaxy’s history. But eROSITA observations are now revealing plumes of debris that could be previously overlooked stellar graves. “Maybe we’ll start balancing this budget between the expected number of supernovae and the ones that we are detecting,” Merloni says.

eROSITA is now beginning its second six-month, all-sky survey. When combined, the telescope’s eight total maps will be able to reveal objects one-fifth as bright as those that could be seen on a single map. That not only allows astronomers to see more X-ray sources in more detail, but track how objects in the X-ray sky are changing over time.

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To estimate your dog’s age in human years, multiply the dog’s age by seven, right? Wrong.

A more accurate conversion isn’t so easy to do in your head: Multiply the natural logarithm of the dog’s age by 16, then add 31. Researchers report this new canine age formula online July 2 in Cell Systems.

As animals get older, tiny chemical tags called methyl groups get added and removed from DNA. These changes track with different stages of growth and can be used to determine biological age. Scientists can even compare changes across species. In this case, the researchers compared the methylation states of 320 humans, ages 1 to 103 years, with those of 104 Labrador retrievers, ages 5 weeks to 16 years.

The relationship between human and dog years changes over time, the scientists found. Early in life, puppies develop much faster than humans, but as dogs get older, their aging curve begins to flatten. An 8-week-old puppy is roughly the same age as a 9-month-old human. A 1-year-old dog corresponds to around 31 human years, and a 4-year-old dog is closer to a 53-year-old human. The new equation also lines up the average life span of a Lab — 12 years — with the average 70-year human life span.

The study focused only on yellow Labrador retrievers. Since the life spans of other breeds vary, further studies are needed to find out the real age of every very good dog, the scientists say.

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Ethical concerns abound in the race to develop a COVID-19 vaccine. How do we ethically test it in people? Can people be forced to get the vaccine if they don’t want it? Who should get it first?

Tackling those questions demands that a vaccine exist. But a slew of other ethical questions arise long before anything is loaded into a syringe. In particular, some Catholic leaders in the United States and Canada are concerned about COVID-19 vaccine candidates made using cells derived from human fetuses aborted electively in the 1970s and 1980s. The group wrote a letter to the commissioner of the U.S. Food and Drug Administration in April, expressing concern that several vaccines involving these cell lines were selected for Operation Warp Speed — a multibillion-dollar U.S. government partnership aimed at delivering a COVID-19 vaccine by January 2021.

The group urged the FDA to instead provide incentives for COVID-19 vaccines that do not use fetal cell lines. But, as virologist Angela Rasmussen of Columbia University pointed out on Twitter, those other vaccines are being developed with scientific input from research using HeLA cells — which come with their own thorny ethical issues of consent.

Here’s how scientists and bioethicists are thinking about the cell lines they use as they develop COVID-19 vaccines.

What are cell lines, and what is their connection to vaccine research and development?

Cell lines are cultures of human or other animal cells that can be grown for long periods of time in the lab. Some of these cultures are known as immortalized cell lines because the cells never stop dividing. Most cells can’t perform this trick — they eventually stop splitting and die. Immortal cell lines have cheated death. Some are more than 50 years old.

Cell lines can be manipulated to become immortal. Or sometimes, immortality arises by chance. “Whenever people make primary cell cultures from different organs of different animals, every so often you just get … lucky, and some cultures just won’t die,” explains Matthew Koci, a viral immunologist at North Carolina State University in Raleigh. Such long-lasting cell lines go on to get studied, and studied some more. Some end up being used in labs around the world.

Immortalized cell lines are crucial for many different types of biomedical research, not just vaccines. They’ve been used to study diabetes, hypertension, Alzheimer’s and much more. Some are human cells, but many also come from animal models. For example, many COVID-19 studies — beyond just those related to vaccines — are using Vero cells, a cell line derived from the kidney of an African green monkey, Rasmussen says.

Two common immortalized cell lines go by the monikers HEK-293 and HeLa. HEK-293 is a cell line isolated from a human embryo that was electively aborted in the Netherlands in 1973. Catholic leaders and other antiabortion groups have objected to the use of HEK-293 in the development of some COVID-19 vaccine candidates. Cells derived from elective abortions, including HEK-293, have been used to develop vaccines, including rubella, hepatitis A, chickenpox and more. Other fetal cell lines, such as the proprietary cell line PER.C6, are also used in vaccine development, including for COVID-19.

HeLa cells are named after Henrietta Lacks, a Black tobacco farmer and mother of five from Virginia who was diagnosed with cervical cancer in 1951. That cell line comes from a sample taken from her cervix by researchers at Johns Hopkins University when she was undergoing treatment there. These cells have been used in development of vaccines including the polio and human papilloma virus, or HPV, vaccines. They’ve even contributed to our understanding of the human genome.

Are human immortalized cell lines necessary to make COVID-19 vaccines?

More than 125 candidate vaccines against COVID-19 are under development around the world. As of July 2, 14 were in human trials.

Those vaccines can be divided into a few different types. Some, such as RNA vaccines made by companies like Moderna (SN: 5/18/20), do not require a live cell, and thus, no cell line. But other types do require live cells during their production. That includes candidates that use the old-school method for developing vaccines: attenuation. This is “what Pasteur did” when he made the first vaccines against anthrax and rabies, explains Mark Davis, a virologist at Stanford University. “You grow a virus,” and over time the virus loses potency. “It’s still alive, but for some reason, it typically loses its more dramatic clinical effects.”

In another type of vaccine under development called viral-vector, the viral genes to produce immunity to the coronavirus are placed in another, harmless virus. That new combined virus is then grown in cells.

In vaccine development in general, “if we’ve got a virus that has to go through its life cycle, that happens in cell lines,” Koci says.

Many current vaccines, such as those for influenza, hepatitis B and HPV, are grown in nonhuman cell lines and even chicken eggs, bacteria or yeast. But human cell lines are especially useful when working with a new virus, Koci explains. “We don’t know what’s really important” yet in how the coronavirus replicates, he says. There’s no guarantee that a nonhuman cell line will work immediately. Over a few years of work, Koci says, a COVID-19 vaccine might be developed that could be grown in yeast or chicken eggs. But we don’t have years. “We want to make [the system] look as [much like] a human cell as we can.”

This is where immortal cell lines come in.

HEK-293 cells, for example, are especially useful for vaccine work, Rasmussen explains. It’s easy to put new viral genes in them, she says, and once they have the genes inside, HEK-293 cells can pump out large amounts of viral protein — exactly what’s needed to help people develop an immune response.

HeLa are also relatively easy to work with. They can be used to analyze how the coronavirus enters cells to hijack their machinery, for example. “It’s great to have them in the arsenal,” Rasmussen says. But, she says, it’s important to “think about their origins.”

What are some of the moral or ethical issues associated with cell lines such as HEK-293 and HeLa?

No matter what cell line is used, ethical questions will need to be answered. Cell lines derived from animals have all the ethical complications associated with animal research. But in the case of fetal cells, some anti-abortion groups are opposed to using anything that involves fetal cell lines anywhere in its development. The basis for the objection comes down to the idea that if you use anything derived from an abortion, you are in some small way complicit in the abortion itself.

Fetal cell lines have been widely used in basic science and clinical medicine for decades, says Nicholas Evans, a bioethicist at the University of Massachusetts Lowell. “Chances are if you have had a medical intervention in this country or pretty much any other country, you have benefited from the use of these cell lines in some way.”

Catholics got permission in 2005 and 2017 from the Vatican’s Pontifical Academy for Life to get vaccines that use historical fetal cell lines, if no alternatives are available. “The reason is that the risk to public health, if one chooses not to vaccinate, outweighs the legitimate concerns about the origins of the vaccine,” Evans explains. Of course, many people who are anti-abortion are not Catholic, and not all Catholics agree.

In the case of HeLa cells, the ethical problems began the day the cells were taken from Lacks, who was never told that her cells might be used for experimentation. “There was no informed consent. She wasn’t aware, and her family wasn’t aware,” says Yolonda Wilson, a bioethicist at Howard University in Washington, D.C. “The use of this Black woman’s body has I think contributed to a kind of cultural memory of mistrusting health institutions among Black folks,” she says. “It’s not this one-off … it’s a larger narrative of disrespecting Black patients, using Black people and Black bodies in experiments.”

In 2010, science writer Rebecca Skloot wrote a book about Lacks’ story. Since then, Wilson says, “Johns Hopkins University, at least, seems to recognize the ethical issues involved and [is] taking steps to repair some of the damage that has been done.” The university has worked closely with members of Lacks’ family to create scholarships, awards and symposiums about medical ethics. The university will also be constructing a building to be named in Lacks’ honor. But Wilson notes that damage still remains in the broader Black community.

How should those ethical issues be taken into account in COVID-19 vaccine development?

There’s no avoiding immortal cell lines. “Certainly I would expect they would be involved in some of the work, directly or not” in any vaccine that comes out, Rasmussen says. Even though HeLa cells or HEK-293 cells might not be used in the production of a particular COVID-19 vaccine, they are being used as scientists work to understand the virus. Some knowledge gained from those cell lines will go into a vaccine, at the very least.    

But for HeLa cells in particular, Wilson says, there’s an opportunity for restorative justice. Given the disproportionate effects of the virus among Black people in the United States due to underlying health conditions and jobs that may expose them more to the virus (SN: 4/10/20), “special effort should be made to ensure that Black people are vaccinated once we know that this is safe,” she says. Latino people have been similarly hard-hit by COVID-19.

Wilson also notes that it’s an opportunity to help researchers think more about the history and context of their work. “It’s important not to act as though the science that happens is divorced from the communities in which it happens.”

The world is waiting anxiously for a COVID-19 vaccine. But as work to make a vaccine goes on, scientists need to think about the materials they use and why, Rasmussen says. “I think probably more [scientists] think about HeLa cells in this way,” she explains. “Many of us have read Skloot’s excellent book.” But that doesn’t mean that scientists could, or should, stop using HeLa cells entirely. In the end, she says, “you’re going to use the cell type that’s right for the experiment.”

Wilson agrees. Ethical considerations are not about weighing an ethical approach against the need to save lives. “That’s false framing,” she says. “It’s not: Be ethical or save lives. Ethics should guide us in thinking how to save lives.”

The Rules of Contagion
Adam Kucharski
Basic Books, $30

Epidemiologists like to say, “If you’ve seen one pandemic, you’ve seen … one pandemic.” But behind each outbreak lie core principles that help explain why the outbreak began, why it grew, why it peaked when it did and why it ended. In The Rules of Contagion, mathematician and epidemiologist Adam Kucharski of the London School of Hygiene & Tropical Medicine outlines those principles and shows how they apply beyond infectious disease, to the spread of ideas, financial crises, violence and more.

Kucharski hardly mentions the novel coronavirus sweeping the globe. He was just wrapping up final edits when the first cases of COVID-19 appeared in Wuhan, China. But the book still feels extraordinarily prescient. Kucharski provides context for readers to understand the current pandemic, as well as a framework for thinking about other types of contagious spread. Science News spoke with Kucharski about the principles of contagion, disease modeling and misinformation. The following conversation has been edited for length and clarity.

SN: Your book looks at the principles of contagion and how they apply beyond infectious diseases. Why is it useful to transport those ideas to other fields?

Kucharski: I’ve noticed that the same mistakes get made repeatedly across fields. For example, after the 2008 financial crisis, a lot of people realized that the network structure between banks and loans and exposure to risk was very similar to a lot of the network features that caused problems with sexually transmitted infections in the 1970s and ’80s. If there are a lot of “loops” in the network, with people connected to each other in multiple ways, it makes it harder to stop the spread. If the network is structured so that highly connected individuals are disproportionately linked to less-connected individuals, it can result in an outbreak that spreads slower at first, but eventually reaches more of the network. Pre-2008, the financial network had both of these features.

It’s also important to understand the underlying network. When looking at violence, it might be tempting to think the events are random, but there is often a series of connections that link them, and targeting these links with interventions can help prevent future incidents.

SN: You write that we need to separate the features that are specific to a particular outbreak from the underlying principles that drive contagion. What are those principles?

Kucharski: There are four factors that are worth bearing in mind. The first one is duration — how long people are infectious for. The second is what people do while they’re infectious: the opportunities for contagion. Another feature is what I call the transmission probability — the chance something actually gets across during an interaction. Then the final important one is susceptibility. If you have the virus or if you try to spread an idea, what is the chance that someone is susceptible?

SN: Modeling, which is the focus of your book, has played an important role in the coronavirus response. But models aren’t perfect. How do we prevent inaccurate predictions from eroding people’s confidence in modeling?

Kucharski: It helps to get away from the idea that all models are trying to make an exact forecast of what will happen in a month’s time or two months’ time. I see models as a way of clarifying our thinking about how the process works. Every time you see someone in the media claiming they have a solution to COVID, they are implicitly relying on a model. They might not outline what that model is, but they are making assumptions about how transmission functions, and they’re making assumptions about how their proposed measure will influence transmission. The advantage of a model is it lays out those steps very clearly, and it means that people can criticize them.

SN: After the 2016 U.S. presidential election, the spread of misinformation gained a lot of attention. How have social media platforms tried to combat this in response to COVID-19?

Kucharski: We’ve seen some quite dramatic changes in terms of what’s being limited. A few years ago, the focus was on attempting to remove all the harmful content. The problem with trying to reactively remove all harmful content is that online outbreaks spread so quickly — it’s difficult to keep up with transmission. A more effective approach may be to reduce susceptibility. We’re seeing a lot more focus on preemptive messaging. If you type COVID into a search bar on most tech platforms, you will have a huge amount of credible information before you find anything that might lead you down some sort of rabbit warren into unreliable information. This is one of the first times that we’ve really seen that level of blanket preempting across multiple platforms — Google, Instagram, Twitter, Facebook.

SN: Technologies like contact tracing apps could help curb the spread of coronavirus, but they also raise privacy concerns. How do we strike a balance?

Kucharski: If you look at countries in Asia that have been very good at contact tracing, often the surveillance data is far more detailed. In Korea, they have access to people’s credit card transactions, to their cell phone locations. We haven’t seen anything near that scale in Europe or the U.S. If we’re talking about learning from these countries, we have to look at what they’ve done and then decide what elements of that we do or don’t want to introduce. Do you want to give up more data in the possibility that disease control could work better and you could get back to elements of normality quicker, or do you want to protect privacy with the knowledge that it may mean that we’d need some additional physical distancing in place? We need to have a really frank public discussion about what we think of appropriate trade-offs.

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