New Playbook for Covid-19 Protection Emerges After Year of Study, Missteps

Scientists are settling on a road map that can help critical sectors of the economy safely conduct business, from meatpacking plants to financial services, despite the pandemic’s continued spread.

After nearly a year of study, the lessons include: Mask-wearing, worker pods and good air flow are much more important than surface cleaning, temperature checks and plexiglass barriers in places like offices and restaurants. And more public-health experts now advocate wide use of cheap, rapid tests to detect cases quickly, in part because many scientists now think more than 50% of infections are transmitted by people without symptoms.

The playbook comes after months of investigations on how the coronavirus spreads and affects the body. Scientists combined that with knowledge gained from years of experience managing occupational-health hazards in high-risk workplaces, such as factories and chemical plants, where tiny airborne pollutants can build up and cause harm. They say different types of workplaces—taking into account the types of interactions workers have—need slightly different protocols.

The safety measures have taken on new urgency in recent weeks as new infections, hospitalizations and deaths rise across the U.S. and Europe, and potentially more-transmissible variants of the virus spread around the globe. This phase of the pandemic is prompting a new wave of stay-at-home orders, closures and travel restrictions, important first steps to curbing contagion. Infection-prevention specialists say known strategies for stemming spread should continue to work against the new variants, but that increased adherence is even more important.

Vaccines are rolling out, but slowly, and access will be limited mostly to high-priority groups for some time.

“We have to still deal with ‘the right now.’ We’ve zeroed in on this set of controls that we know work,” said Joseph Allen, director of the Healthy Buildings Program at the Harvard T.H. Chan School of Public Health.

Over the past year, the lack of consistent and cohesive messaging among scientists and lawmakers has seeded confusion over what makes up risky behavior, what activities should be avoided and why. That is beginning to change as consensus builds and scientists better understand the virus.

In the U.S., scientists at first advised people against wearing masks, in part because of shortages, while the idea of stay-at-home orders received severe pushback from some lawmakers. Early in the pandemic, testing was limited to people with symptoms, also partly due to shortages. That advice has shifted, but a year later, sufficient testing remains a critical issue.

Countries such as New Zealand and others in Asia adhered to a combination of basic mitigation strategies from the start—particularly masking, large-scale testing and lockdowns that broke transmission chains. They have tended to fare better than those that didn’t.

In one of his first moves, President Biden signed executive orders to require masks be worn on federal property and at airports and other transportation hubs. The administration said it is focusing on increasing the availability of vaccines, and also stressed the importance of widely available testing, which still lags in low-income and minority communities.

The current scientific playbook follows from two of the biggest research insights since the start of the pandemic. First, individuals who aren’t showing symptoms can transmit the virus. Infectious-disease experts worry most about this silent spread and say it is the reason the pandemic has been so hard to contain. While visibly sick people can pass on the virus, data cited by the Centers for Disease Control and Prevention estimate that 40% to 45% of those infected never develop symptoms at all. With the new viral variants that can transmit more readily, the potential for silent spread is even higher, infectious-disease experts said.

Secondly, researchers now know that tiny airborne particles known as aerosols play a role in the spread of Covid-19. These can linger in the air and travel beyond 6 feet.

An early hallmark of the pandemic response focused on the risk of transmission through large respiratory droplets that typically travel a few feet and then fall to the ground. Businesses rushed to buy plexiglass barriers, creating shortages.

The barriers can be good at preventing larger virus-containing droplets from landing on and infecting healthy individuals. They may offer some protection in shielding workers who have brief face-to-face interactions with many people throughout the workday, such as cashiers and receptionists, some occupational-health experts said.

Yet in settings like offices, restaurants or gyms, the role of the barriers is murkier, because activities like talking loudly and breathing deeply create aerosols that can waft on air currents and get around shields.

Also, installing such barriers could affect airflow throughout the space, environmental-health experts said. It is possible they could limit proper ventilation, making things worse, they said.

“There seems to be an assumption that particles are going to get stopped by the barriers, which is simply not true,” said Lisa Brosseau, an industrial hygienist and research consultant for the University of Minnesota’s Center for Infectious Disease Research and Policy. Airborne particles ferrying the virus “really distribute all over the place.”

The emphasis on intense surface cleaning has diminished as scientists have come to understand that indirect transmission through contaminated surfaces doesn’t play as critical a role in the spread of Covid-19 as they thought in the early days of the pandemic. In September, the CDC published sanitation guidelines for offices, workplaces, homes and schools that said that, for most surfaces, normal, routine cleaning should suffice, and that frequently touched objects, such as light switches and doorknobs, should be cleaned and disinfected.

“Sanitation is important in general always,” said Deborah Roy, president of the American Society of Safety Professionals. “The idea is we went overboard at the beginning because of the amount of unknowns. Now, we’re in a situation where we have more information.”

Temperature checks have become less popular among some employers because scientists now know that not all Covid-19 patients get fevers. One large study published online in November in the New England Journal of Medicine showed only 13% of Covid-19 patients reported a fever during the course of their illness.

Scientists now understand that brief encounters with an infected person can lead to spread, according to an October case study—an advance from earlier, when the rule of thumb was to avoid close contact for 15 consecutive minutes or longer. The report urged people to consider not just time and proximity in defining close contact with a Covid case, but also ventilation, crowding and a person’s likelihood of generating aerosols. Following the report, the CDC changed its definition of close contact to a total of 15 minutes or more over a 24-hour period.

Fresh air and effective filters indoors are important because they can remove virus particles before they have time to infect.

Masks offer a similar benefit, by lowering the amount of particles that infected individuals emit. Some scientists say there could be a benefit to doubling up on masks, as a second layer may improve both filtration and fit, so long as the masks are worn correctly.

A study published in October found that in countries where mask wearing was the norm or where governments put in place mask mandates, coronavirus mortality rates grew much more slowly than in countries without such measures. This fall, the CDC said that masks also offer some personal protection by reducing a wearer’s exposure to infected particles.

The combination of airborne particles and personal interactions, even among people who don’t feel ill, can turn wedding receptionsplane rides and choir practices into superspreading, potentially deadly events.

“For Covid, those two factors—asymptomatic spread and aerosolization—is what made mask-wearing so essential,” said Megan Ranney, emergency physician and assistant dean at Brown University.

Lessons can be gleaned from an outbreak at a Canadian spin studio last fall. The operators of the SPINCO studio in Hamilton, Ontario, had many public-health measures in place, including limiting the number of bikes in each class and screening staff and attendees with a questionnaire about topics including symptoms and travel. Rooms were sanitized within 30 minutes of a completed class, and towels were laundered, according to a statement provided last fall by Elizabeth Richardson, medical officer of health for the city of Hamilton.

Masks were also required before and after workout classes, Dr. Richardson said.

In total, 54 people who attended workouts over a span of several classes became infected. Another 31 cases were tied to the outbreak after spin-class attendees who contracted the virus then passed it on. The spin studio temporarily shut down following the outbreak and later reopened. It is currently not offering classes due to local regulations that mandated the closure of all gyms and fitness centers amid rising Covid-19 cases in the area.

In a November statement following the outbreak, Michelle August, founder of SPINCO, said that the company has “always put safety first and [has] exceeded all recommended guidelines from public health throughout” the pandemic. She said SPINCO has also strengthened and heightened its Covid-19 mitigation measures. SPINCO’s website currently says face masks are mandated throughout workouts in the company’s Hamilton location.

It also says that SPINCO is installing air purifiers in all of its studios that filter air in the rooms every 17 to 21 minutes. Airborne transmission experts recommend that building managers pump in clean, fresh air between three to six times an hour and that they install filters that are proven to effectively trap and remove a substantial number of virus-carrying particles.

To film a stage play of “A Christmas Carol” in November, the Guthrie Theater in Minneapolis upgraded its air filters and increased the rate at which the ventilation system pumps in outside air, said Brooke Hajinian, the Guthrie’s general manager. Management staggered arrival times, and a compliance officer made sure everyone socially distanced, wore their masks properly and washed their hands.

The theater divided staff into pods depending on how close they must get to the lone actor on stage, who portrayed Charles Dickens and didn’t wear a mask while performing, according to Ms. Hajinian. Those working nearest the stage underwent testing three times a week and wore N95 masks at all times, she said, while cleaning and security crews, who didn’t interact with the stage crews, wore cloth masks and didn’t undergo testing.

Actor Nathaniel Fuller performed in ‘A Christmas Carol’ at the Guthrie Theater in Minneapolis, where staff underwent tests often and workers disinfected the space. PHOTOS: KAITLIN SCHLICK(3)

Ms. Hajinian said she monitored the staff’s testing results and symptoms. “Any symptom is not a failure of this plan,” she said. Catching a case “and isolating it—that’s what success looks like for us,” she said. There were no cases, she said.

Scientists say multilayered safety efforts are needed because no single prevention method is 100% effective.

One of the largest studies of asymptomatic transmission to date showed that frequent testing was essential in identifying infections among a group of nearly 2,000 Marine recruits required to socially distance and wear masks except while eating and sleeping.

The study looked at cases identified with lab-based tests that search out and amplify the genetic material of the virus, but those tests aren’t as easily scaled as so-called rapid antigen tests, which search for viral proteins.

Results from lab-based tests can sometimes take days, while results from rapid tests are usually available in less than an hour. As a result, some epidemiologists have been advocating for widespread use of antigen tests to prevent outbreaks, because they are cheaper and don’t require high-tech laboratory equipment to run, meaning they can be deployed in a broader range of settings.

The shift toward using frequent, inexpensive and rapid tests on the same people multiple times a week to screen entire populations—instead of one-time tests on individuals who have symptoms—will be important to efficiently break transmission chains, epidemiologists said.

“Unless we’re doing really broad, frequent screening of the people at large, we’re completely missing the vast majority” of infections, said Michael Mina, an assistant professor of epidemiology at the Harvard T.H. Chan School of Public Health. “We have to change how we’re doing this.”

While rapid tests tend to be less sensitive than lab-based tests, Dr. Mina said the data suggest they have high sensitivity when people are most likely to be infectious.

Other infectious-disease experts have touted contact tracing to identify and bust clusters of infection. But they say the strategy works best when cases aren’t surging, as they are now. When transmission rates are too high, limiting gatherings, travel and crowding are more effective at denting spread, said Abraar Karan, a global-health physician at Brigham and Women’s Hospital and Harvard Medical School.

In places without big surges, a high-tech approach is becoming increasingly useful: genetic epidemiology, or tracking tiny changes in viral genomes to map out transmission chains. As the coronavirus replicates and moves from person to person, its genes change slightly. Sometimes, those tiny changes are unusual, and they can be particularly useful in mapping transmission events, according to Justin O’Grady, an infectious disease expert at the Quadram Institute in the U.K.

By sifting through the differences among more than 1,000 viral genomes, Dr. O’Grady and his collaborators found that a particular viral variant was moving through multiple nursing homes in the U.K., among patients and staff, but not among the wider community. The unpublished data suggested that transmission was facilitated by the movement of staff from one facility to another, Dr. O’Grady said. The team relayed the findings to government authorities and advised them to restrict staff moving among facilities during the pandemic.

“Sometimes genomic epidemiology is able to find hidden transmission links that traditional epidemiology would struggle to find,” Dr. O’Grady said. “We can’t stop transmission, but when we find a superspreader event…we can bring in the right prevention methods to stop it from spreading further.”

What Happens When COVID-19 Collides With Flu Season?


Many questions remain about how flu season might affect the pandemic, and vice versa. For example, would coinfection with influenza worsen the course of COVID-19? Experts also aren’t certain whether influenza vaccination could help protect against COVID-19 or whether steps taken to mitigate COVID-19 will reduce the burden of the coming flu season.

Some hints have come from preliminary research conducted in China, where influenza was still widely circulating when the first novel coronavirus infections emerged, and in the southern hemisphere, which is currently in the midst of its flu season.

At least 2 things are clear: Quicker and more widely available testing is needed to distinguish between COVID-19 and influenza, which have similar symptoms, at least at first, but require different treatments. On top of that, a severe influenza season—the result of more virulent strains, inadequate vaccination rates, or a combination of both—coupled with a COVID-19 pandemic that shows no signs of abating, could overwhelm already taxed emergency departments and intensive care units.

As pulmonary and critical care specialist Benjamin Singer, MD, wrote in a recent editorial, influenza and other causes of pneumonia represent the eighth leading cause of US deaths in nonpandemic years.

“We can expect that the new reality of COVID-19 will only complicate the next influenza season,” Singer, of the Northwestern University Feinberg School of Medicine, concluded in his editorial.

Flu-Like but Not Alike

Distinguishing between influenza and COVID-19 “has important prognostic implications,” Singer said in an interview. “In many ways it matters that you find out quickly.”

While the course of influenza is rapid, COVID-19 “kind of limps along a little bit,” he said. Knowing the reason for a patient’s respiratory symptoms “helps inform what you can expect.”

Identifying the cause, of course, helps determine how best to treat respiratory symptoms, Singer noted. Although supportive care for influenza and COVID-19 is similar, drug treatments don’t overlap, he said.

“We have things that we can do for COVID if we know someone’s infected,” he said. “If they have influenza, we can give antivirals targeted against influenza.”

But mistakenly treating patients with influenza as though they have COVID-19 is wasteful and potentially harmful, Singer said.

For example, he noted, randomized controlled trials have found that intravenous remdesivir, a broad-spectrum antiviral that is not approved anywhere in the world for any use, was more effective than a placebo in treating severe and moderate COVID-19. Remdesivir has received Emergency Use Authorization to treat COVID-19 from the US Food and Drug Administration and regulatory agencies in a few other countries, but, as an unapproved drug, it has been in short supply. Meanwhile, although earlier studies found that remdesivir had antiviral activity against influenza A, the drug has not been tested in patients with the flu, so there’s no evidence it’s effective in treating that disease.

Another drug, the corticosteroid dexamethasone, appears to be effective in some patients hospitalized with COVID-19, but it could harm those who instead have influenza. A recent preliminary report found that dexamethasone resulted in a lower 28-day mortality rate among patients hospitalized with COVID-19 who were receiving respiratory support. However, in 2019 clinical practice guidelines, the Infectious Diseases Society of America (IDSA) specifically advised against using corticosteroids to treat seasonal influenza unless clinically indicated for other reasons, such as asthma. Data from randomized controlled trials of corticosteroid treatment of influenza aren’t available, but 2 meta-analyses of observational studies suggested that corticosteroid treatment of patients hospitalized with influenza was associated with increased mortality, according to IDSA.

A retrospective study from Wuhan, China, suggested that lopinavir-ritonavir combination therapy led to faster resolution of pneumonia than standard care alone among patients with both COVID-19 and influenza. However, the World Health Organization (WHO) on July 4 discontinued the lopinavir-ritonavir arm of its Solidarity trial because interim results found the treatment, which is approved for HIV, produced little or no mortality reduction in patients hospitalized with COVID-19.

“Although we need more data to confirm the conclusion, we prefer to use the lopinavir-ritonavir to treat all COVID-19 patients with influenza,” coauthor Rui Zeng, MD, PhD, a kidney specialist on the faculty of Wuhan’s Tongji Medical College at Huazhong University of Science and Technology, said in an email.

Another reason it’s important to determine whether respiratory symptoms are due to influenza or to COVID-19 (or both) is that mitigation efforts for the former aren’t as strict as for the latter. “We’ve never told people with influenza to isolate themselves from everyone else,” Osterholm, founder and director of the Center for Infectious Disease Research and Policy at the University of Minnesota, said in an interview.

Without quickly learning which virus they have, some people with COVID-19 during flu season might mistakenly attribute their symptoms to influenza and not take the necessary precautions to prevent spreading severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is more easily transmitted, he said.

In addition, distinguishing between COVID-19 and influenza will be vital for disease surveillance, the authors of a recently published letter noted. Given the overlap of symptoms, systematic testing for SARS-CoV-2 and influenza will be needed during the upcoming flu season to determine the contributions of each viral illness to the burden of respiratory disease, the authors wrote.

Considering Coinfection

Physicians in several countries have reported patients who tested positive for both COVID-19 and seasonal influenza. “We have seen patients with both viruses,” Singer said. “It was early on, in March.”

But such patients have represented a small minority.

“The chances are more likely that they have one or the other,” Osterholm said, noting that only 3% or 4% of the population have SARS-CoV-2 infection, while 10% to 20% might become infected with influenza virus, so the odds of being infected with both are small.

Early reports from China suggested that coinfection with other respiratory diseases was extremely rare in patients with COVID-19. For example, in a study of 99 patients with COVID-19 admitted to Wuhan Jinyintan Hospital from January 1 to January 20, none tested positive for any of 9 other respiratory pathogens, including influenza A and influenza B.

However, Zeng’s study, conducted at Wuhan’s Tongji Hospital, which the government had designated for treating patients with severe COVID-19, produced a much different finding. Of 544 patients with polymerase chain reaction–confirmed COVID-19 who were admitted from January 28 to February 18, 11.8% were coinfected with influenza A or influenza B. Zeng noted that the influenza infection rate in his study was similar to that reported in the US during the 2018-2019 influenza season.

“Coinfection was a significant risk factor for prolonged hospital stay,” Zeng said. In addition, his study found that COVID-19 patients who were coinfected with influenza shed SARS-CoV-2 longer than other COVID-19 patients (17 days vs 12 days on average). “We don’t know the reason.”

Studies about coinfection in the US have found rates more in line with those at Jinyintan Hospital than at Tongji Hospital.

A recent study in JAMA found that out of 1996 patients hospitalized with COVID-19 in metropolitan New York City who were tested for other respiratory viruses, only 42 (2.1%) were coinfected, and only 1 was coinfected with influenza. The patients were hospitalized between March 1 and April 4.

In Northern California, laboratories that simultaneously tested for SARS-CoV-2 and other respiratory pathogens found a 10-fold higher coinfection rate (20.7%) than the New York study, but only 0.9% of specimens were coinfected with influenza. The authors, who reported their findings in a JAMA research letter, studied 1217 specimens, 116 of which had tested positive for SARS-CoV-2 and 318 for other respiratory pathogens. Of the 116 that were positive for SARS-CoV-2, 24 were positive for at least 1 other respiratory pathogen. However, only 1 of the 116 was positive for influenza.

During the pandemic, “the possibility of COVID-19 should be considered regardless of positive findings for other pathogens,” Japanese researchers recommended in a recent case report about a 57-year-old restaurant worker.

COVID-19 Protection From Flu Shots?

study conducted at Ohio’s Wright-Patterson Air Force Base during the 2017-2018 flu season recently caught the attention of Luigi Marchionni, MD, PhD, an oncologist and computational biologist at Johns Hopkins University. The study compared the influenza vaccination status of approximately 6000 Department of Defense personnel with their respiratory virus status.

“That paper didn’t find vaccination was making people more likely or less likely to get another infection from another virus,” Marchionni explained. However, it did find that influenza vaccination was associated with a higher risk of non-SARS coronavirus infection, offset by a lower risk of influenza, parainfluenza, respiratory syncytial virus, and some other respiratory infections.

Marchionni wondered whether the finding of an association between flu shots and coronavirus infections might bode ill for influenza vaccination in the middle of a coronavirus pandemic. So he and his coauthors explored a possible county-level association between influenza vaccination coverage in people aged 65 years or older and the number of COVID-19 deaths.

Their findings, which have not yet been peer-reviewed, suggest that influenza vaccination in that age group is negatively associated with COVID-19 mortality. Marchionni said he and his coauthors have submitted an expanded version of their paper to a peer-reviewed journal.

“I’m quite confident in the fact that influenza vaccination in the population is associated with less [COVID-19] mortality,” Marchionni said. “There are many plausible biological explanations.”

Another study that has not yet undergone peer review also found that patients with COVID-19 who were immunized against influenza fared better than those who had not. The authors analyzed data from 92 664 confirmed COVID-19 cases in Brazil and found that recently vaccinated patients had, on average, an 8% lower chance of needing intensive care, an 18% lower chance of requiring invasive respiratory support, and a 17% lower chance of dying.

Can We Curb Flu Along With COVID-19?

Intuitively, it makes sense that wearing masks, social distancing, working from home, closing schools, and other strategies to minimize the spread of COVID-19 would lessen transmission of other respiratory infectious diseases as well.

That appeared to be the case in Taiwan, researchers concluded in a recent brief report. They compared 25 weeks of case data for severe influenza, invasive Streptococcus pneumoniae disease, and pneumonia deaths from 2016 to 2020. All 3 trended downward in 2020 compared with the same weeks in previous years, especially after Taiwan implemented COVID-19 prevention strategies. The downward trend does not appear to be a result of negligence in reporting cases, the authors noted, because there were still substantial cases of severe influenza-like illness reported. However, they tested negative for influenza.

Japanese researchers also observed less influenza activity week by week in 2020 compared with the previous 5 seasons. They speculated that high awareness among the Japanese public of measures to reduce COVID-19 transmission early in the year might explain their finding, according to a recent research letter in JAMA.

And researchers in Qatar recently reported a “dramatic decrease” of laboratory-confirmed influenza A after the state closed schools on March 10, although laboratory-confirmed cases of other respiratory pathogens, including influenza B, barely budged. Seasonal variations likely do not explain the 30-fold drop in laboratory-confirmed influenza A cases between February 13 to March 14 and March 15 to April 11, because a similar decline was not seen between the same periods in 2019, the authors wrote.

The situation in the southern hemisphere might provide more clues as to what the northern hemisphere can expect in the upcoming flu season. Or, as Osterholm cautioned, it might not.

“We’re seeing an incredibly mild flu season in the southern hemisphere,” he said. “To date, we’ve seen virtually little, little activity…We don’t know what’s going on right now.” And that’s throughout the southern hemisphere, including COVID-19 hotspots such as Brazil, Osterholm noted. “We have to be careful not to assume that’s what’s going to happen in the northern hemisphere.”

The best-case explanation for the southern hemisphere’s mild flu season is that COVID-19 mitigation strategies are tamping down the spread of other respiratory viruses, said Brendan Flannery, PhD, coauthor of the letter calling for systematic testing for both influenza and COVID-19. But the worst-case scenario is that COVID-19 has overwhelmed health care systems, so people with the flu are staying home and not being counted or seeking care but getting lost in the crowd of COVID-19 patients, said Flannery, lead investigator from the US Centers for Disease Control and for the US Flu Vaccine Effectiveness Network.

“We’re all going to learn a lot,” Osterholm said of the upcoming flu season. “We can speculate until we’re blue in the face, and I don’t think we know yet what’s going to happen.”

What if ‘Herd Immunity’ Is Closer Than Scientists Thought?


We’ve known from the beginning how the end will arrive. Eventually, the coronavirus will be unable to find enough susceptible hosts to survive, fading out wherever it briefly emerges.

To achieve so-called herd immunity — the point at which the virus can no longer spread widely because there are not enough vulnerable humans — scientists have suggested that perhaps 70 percent of a given population must be immune, through vaccination or because they survived the infection.

Now some researchers are wrestling with a hopeful possibility. In interviews with The New York Times, more than a dozen scientists said that the threshold is likely to be much lower: just 50 percent, perhaps even less. If that’s true, then it may be possible to turn back the coronavirus more quickly than once thought.

The new estimates result from complicated statistical modeling of the pandemic, and the models have all taken divergent approaches, yielding inconsistent estimates. It is not certain that any community in the world has enough residents now immune to the virus to resist a second wave.

But in parts of New York, London and Mumbai, for example, it is not inconceivable that there is already substantial immunity to the coronavirus, scientists said.

“I’m quite prepared to believe that there are pockets in New York City and London which have substantial immunity,” said Bill Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health. “What happens this winter will reflect that.”

“The question of what it means for the population as a whole, however, is much more fraught,” he added.

Herd immunity is calculated from the epidemic’s so-called reproductive number, R0, an indicator of how many people each infected person spreads the virus to.

The initial calculations for the herd immunity threshold assumed that each community member had the same susceptibility to the virus and mixed randomly with everyone else in the community.

“That doesn’t happen in real life,” said Dr. Saad Omer, director of the Yale Institute for Global Health. “Herd immunity could vary from group to group, and subpopulation to subpopulation,” and even by postal codes, he said.

For example, a neighborhood of older people may have little contact with others but succumb to the virus quickly when they encounter it, whereas teenagers may bequeath the virus to dozens of contacts and yet stay healthy themselves. The virus moves slowly in suburban and rural areas, where people live far apart, but zips through cities and households thick with people.

Once such real-world variations in density and demographics are accounted for, the estimates for herd immunity fall. Some researchers even suggested the figure may be in the range of 10 to 20 percent, but they were in the minority.

Assuming the virus ferrets out the most outgoing and most susceptible in the first wave, immunity following a wave of infection is distributed more efficiently than with a vaccination campaign that seeks to protect everyone, said Tom Britton, a mathematician at Stockholm University.

His model puts the threshold for herd immunity at 43 percent — that is, the virus cannot hang on in a community after that percentage of residents has been infected and recovered.

Still, that means many residents of the community will have been sickened or have died, a high price to pay for herd immunity. And experts like Dr. Hanage cautioned that even a community that may have reached herd immunity cannot afford to be complacent.

The virus may still flare up here and there, even if its overall spread is stymied. It’s also unclear how long someone who has recovered may be immune, and for how long.

The coronavirus crashed this year’s Purim celebrations in the Orthodox Jewish neighborhoods of New York City, tearing through the parades and masquerades in Brooklyn on March 9 and 10.

Schools and synagogues soon shut down to quell the spread, but it was too late. By April, thousands in the Brooklyn communities were infected, and hundreds had died.

“It’s like a black hole in my memory because of how traumatic it was,” said Blimi Marcus, a nurse practitioner who lives in Borough Park, which was hit hard by the virus.

But all that has changed now, Ms. Marcus added: “The general feeling is one of complacency, that somehow we’ve all had it and we’re safe.”CORONAVIRUS SCHOOLS BRIEFING: The pandemic is upending education. Get the latest news and tips as students go back to school.Sign Up

Is it possible that some of these communities have herd immunity? In some clinics, up to 80 percent of people tested had antibodies to the virus. The highest prevalence was found among teenage boys.

But people at clinics are more likely to be showing symptoms and therefore more likely to be infected, said Wan Yang, an epidemiologist at Columbia University’s Mailman School of Public Health in New York. Random household surveys would probably find lower rates — but still well above the 21 percent average reported for New York City, she said.

Researchers in Mumbai conducted just such a random household survey, knocking on every fourth door — or, if it was locked, the fifth — and took blood for antibody testing. They found a startling disparity between the city’s poorest neighborhoods and its more affluent enclaves. Between 51 and 58 percent of residents in poor areas had antibodies, versus 11 to 17 percent elsewhere in the city.

The lowest-income residents are packed tightly together, share toilets, and have little access to masks. “These factors contributed to a silent infection spread,” said Dr. Jayanthi Shastri, a microbiologist at Kasturba Hospital in Mumbai who led the work.

Most researchers are wary of concluding that the hardest-hit neighborhoods of Brooklyn, or even those in blighted areas of Mumbai, have reached herd immunity or will be spared future outbreaks.

But models like Dr. Britton’s hint that it’s not impossible. Other researchers have suggested, controversially, that herd immunity can be achieved at rates of immunity as low as 10 or 20 percent — and that entire countries may already have achieved that goal.

Criticism trailed Sunetra Gupta, a theoretical epidemiologist at Oxford University, after a widely circulated interview in which she said that London and New York may already have reached herd immunity because of variability among people, combined with a theoretical immunity to common cold coronaviruses that may protect against the new one.

“That could be the explanation for why you don’t see a resurgence in places like New York,” she said.

Most experts reject that notion. Several studies have shown that certain immune cells produced following infection with seasonal coronaviruses may also recognize the new coronavirus.

But “where is the evidence that it’s protective?” asked Natalie Dean, a biostatistician at the University of Florida.The Coronavirus Outbreak ›

These cities have not returned to pre-pandemic levels of activity, other experts noted.

“We are still nowhere near back to normal in our daily behavior,” said Virginia Pitzer, a mathematical epidemiologist at the Yale School of Public Health. “To think that we can just stop doing all that and go back to normal and not see a rise in cases I think is wrong, is incorrect.”

A second wave might also hit groups or neighborhoods that were spared by the first, and still wreak havoc, she said. Immunity is a patchwork quilt in New York, for instance: Antibodies were present in 68 percent of people visiting a clinic in the Corona neighborhood of Queens, for instance, but in just 13 percent of those tested at a clinic in the Cobble Hill section of Brooklyn.

But another group, led by the mathematician Gabriela Gomes of the University of Strathclyde in Britain, accounted for variations within a society in its model and found that Belgium, England, Portugal and Spain have herd immunity thresholds in the range of 10 to 20 percent.

“At least in countries we applied it to, we could never get any signal that herd immunity thresholds are higher,” Dr. Gomes said. “I think it’s good to have this horizon that it may be just a few more months of pandemic.”

Other experts urged caution, saying these models are flawed, as all models are, and that they oversimplify conditions on the ground.

Jeffrey Shaman, an epidemiologist at Columbia University, said it wasn’t clear to him that Dr. Gomes’s model offered only one possible solution. And he was suspicious of the big ranges among the four countries.

“I think we’d be playing with fire if we pretended we’re done with this,” Dr. Shaman said.

The new models offer food for thought, he and other experts said, but should not be used to set policy.

“Mathematically, it’s certainly possible to have herd immunity at these very, very low levels,” said Carl Bergstrom, an infectious disease expert at the University of Washington in Seattle. “Those are just our best guesses for what the numbers should look like.”

“But,” he added, “they’re just exactly that, guesses.”

But what about immunity at levels lower than those needed for herd immunity?

“Definitely the disease would not spread as well if it gets back into New York,” said Joel Miller, a mathematical modeler at La Trobe University in Australia. “The same level of behavior change will have more effect on the disease now than it did four months ago.”

Thinking of a city or country as composed of subgroups, demarcated by age, race and level of social activity, might also help governments protect those with the least immunity.

That perspective also might help put a renewed focus on groups who require the higher levels of immunity, because of greater exposure levels and other inequities, including Black and Latino residents, said Dr. Manoj Jain, an infectious disease expert at Emory University. “That’s where this info is very useful,” he said.

The models also suggest a vaccination strategy: Rather than uniformly vaccinate all groups, governments could identify and immunize those most likely to be exposed in “superspreader” events.

“Getting those people vaccinated first can lead to the greatest benefit,” said Dr. Michael Mina, an immunologist at Harvard University. “That alone could lead to herd immunity.”

Vaccination schemes for other pathogens have successfully exploited this approach. For example, when children were given the pneumococcal vaccine in the early 2000s, rates of bacterial pneumonia in the elderly rapidly dropped because of a “herd effect.”

Vaccines that offer just 50 percent protection are considered to be moderately effective, but at that efficiency, even a low herd immunity target would require that a large proportion of the population be immunized, Dr. Bergstrom noted.

If there are early reports of side effects that may scare away some people, he said, “we’d do well to start thinking about all that now.”

Back in Brooklyn, fewer than 1 percent of people tested at neighborhood clinics over the past eight weeks were infected with the virus. But there are still handfuls of cases, Ms. Marcus said, adding that her 10-year-old niece was in quarantine because a counselor at her day camp had tested positive.

“Sometimes that’s all you need, right?” she said. “I’m still hoping we don’t see what we had in March and April, but I’m not so sure that we’ve seen the end of it.”

Is It Healthy to Study in Bed?

With extracurriculars, academics and a social life to maintain, goal-oriented students have to squeeze time from their hectic schedules to get homework done. The result? Lots of studying, writing and reading happens while lying or lounging in bed. Though many parents insist children study only at a desk, they may be surprised to hear what experts think about where and when it’s best to review and learn. We gathered informed opinions from experts in education psychology, sleep medicine and ergonomics.

Doing the Homework

As a debate about homework escalates nationwide, a perhaps less-discussed issue is where this home-studying takes place. Among those who recognize that much of it happens in bed are industrial engineers and furniture designers. Over the years they have come up with across-the-bed tables that angle laptops for proper typing, reading pillows that cradle the neck, back and arms, even hard-sided lap pillows for resting a laptop on.

These can all help bed-studiers be more comfortable. However, Atul Malhotra, a physician and professor of medicine at the University of California, San Diego, with a focus on sleep medicine, notes: “Lying down or sitting upright doesn’t impact your brain function—your posture doesn’t matter.”

The only widely known study specifically on students doing homework in bed versus at a desk was published in May 1968. Of the 100 or so college students they surveyed—admittedly at a time when studying was quite different than the screen-based work now—the researchers at the University of California, Davis, found no difference in grade-point average between those who worked at their desk and those who studied in bed.

“The assumption that there is a single type of study environment optimal for all students appears unwarranted,” the authors concluded.

One concern is that being cozy in bed typically brings on sleepiness, which may compromise a student’s ability to retain information, says Harris Cooper, a social psychologist with a specialty in education at Duke University. But he adds that figuring out how you learn and study most effectively at a young age isn’t a bad thing.

“If they are getting their work done and it is of quality, then knowing what environments work for them will prepare them to be lifelong learners in various locations,” Dr. Cooper says. The professor of psychology and neuroscience suggests parents and students track progress over time to see if they are, indeed, producing as good work in bed as at a desk.

Losing the Last Page

When someone reads a book just before falling asleep, and puts the bookmark on page 89, it’s common not to recall in the morning what happened on page 88, Dr. Malhotra says.

“That which happened right before you sleep doesn’t register, so many people have to re-read page 88—but they will remember page 87,” he says. He doesn’t take issue with one of his daughters who studies in bed with music on. But he suggests that anyone who does homework on the comforter at night go back a few pages or at least 10 minutes’ worth of work in the morning and redo and review it. Also, if you have to read and retain something important, don’t read it just before sleeping, as the few minutes just before sleep aren’t optimal for memory retention.

“Read it, then brush your teeth, then go to sleep,” he says. He also doesn’t mind a little morning lie-in coupled with studying. “You’re often free from distractions in bed in the morning, before the day’s chaos begins,” he says. If you find comfort in bed when the sun comes up, that might be a good opportunity to learn and retain new information.

Getting to Neutral

Standing with arms relaxed at your side is considered the “neutral” posture, with no stress put on any particular part of your body, says ergonomics specialist Janice Fletcher at UC San Diego Health, an academic medical center.

She makes sure people get close to neutral while working at their desks, adjusting keyboards so that the elbows are slightly wider than at right angles, and wrists are either straight or slightly bent downward, “never flexed in the ‘tell it to the hand’ position,” she says. She also places monitors so the neck is neither flexed nor extended. Perhaps surprisingly, the second-most neutral posture is lying in bed flat on your back, though not much studying can be accomplished in that position, she admits.

Ms. Fletcher is fine with people studying in bed, though she suggests that rather than just plopping onto a mattress to do homework, students should plan a little.

The best posture for reading in bed, she says, is sitting up with your back against the headboard and pillows under your arms to raise the reading material to eye level.

“That way you don’t have to bend your neck to view the book or device,” she says. Find a flat surface for writing or supporting a computer on your lap, and use a soft light to prevent a glare that may harm the eyes. For homework involving lots of paper and books, a desk might be a better choice, but bed-studying can be done effectively. “Make yourself as neutral as possible” by sitting similarly to the way you would if you were at a desk, with the help of cushioning, she says.

“If you’re at neutral, you’re more comfortable,” Ms. Fletcher says, “and I would guess you’d be less distracted because you wouldn’t be thinking about your discomfort.”



This article was originally published in The Wall Street Journal. Read the original article.

Gut bacteria may offer a treatment for autism

Autism affects people’s social behaviour and communication, and may impair their ability to learn things. All this is well known. Less familiar to most, though, are the gastrointestinal problems associated with the condition. The intestines of children with autism often harbour bacteria different from those in the guts of the neurotypical. As a consequence, such people are more than three times as likely as others are to develop serious alimentary-canal disorders at some point in their lives.

Unfortunate though this is, the upset gut floras of autistic people are seen by some investigators as the key to the condition—and to treating it. Recent research has shown that altering animals’ intestinal bacteria can have dramatic effects on their nervous systems. Ameliorating autism by tinkering with the ecology of the gut might thus be a fruitful line of inquiry.

A study just published in Neuron suggests that it is. In it, Mauro Costa-Mattioli of Baylor College of Medicine, in Texas, and his colleagues demonstrate that introducing a particular bacterium into the guts of mice that display autistic symptoms can abolish some of those symptoms. The bug in question is Lactobacillus reuteri. It is commonly found in healthy digestive systems and helps regulate acidity levels. And it is also easily obtainable for use as a probiotic from health-food shops.

Mens sana in corpore sano

Dr Costa-Mattioli and his team first reported L. reuteri’s effects on autism in 2016, after conducting experiments with obese female mice. These animals have a tendency to give birth to offspring with autistic traits familiar from people—unwillingness to socialise, repetitive behaviour and unwillingness to communicate (in the case of mice, via ultrasonic squeaking). The researchers noted that the guts of both the obese mothers and their young were bereft of L. reuteri. They wondered what effect transplanting these bugs into the animals might have. They found, when they did so to the offspring, that the youngsters’ autism-like traits vanished.

That led to the latest experiments, on mice that have autistic symptoms induced in four other, different ways. Some were genetically edited to be autistic. Some were exposed to valproic acid, a drug used to treat bipolar disorder and migraines that is known to induce autism in fetuses. Some had their guts cleared of all bacteria. And some belonged to a strain called btbr, individuals of which display autism-like traits that have no known cause.

Martina Sgritta, one of Dr Costa-Mattioli’s colleagues, analysed the bacteria in the guts of all of these animals. She found that, while the genetically engineered mice and the btbr mice had, as expected, reduced levels of L. reuteri, and those with bacteria-free guts were (obviously) free of the bug altogether, the valproic-acid mice had normal amounts of the bacterium.

This last result was unexpected, but the team carried on regardless. They arranged for between seven and 15 mice of each of the four types to have, starting at the age of three weeks, their drinking water laced with L. reuteri. Equivalent numbers of each type continued to be given ordinary water as a control. During the course of the experiment the mice had their faeces collected regularly, so that their bacteria could be tracked. And, at the age of seven weeks, they were given two sorts of social tests.

The first test involved putting each experimental mouse into a perspex container from which it could go either into a chamber where there was an empty wire cup or into one where there was a similar cup containing an unfamiliar mouse. Subject mice were left in the container for ten minutes and were monitored to see how long they spent with the empty cup and with the other mouse.

The second test placed a mouse in an arena where another, unfamiliar mouse was already present. An observer, who did not know which mice were controls and which had been given L. reuteri in their water, then noted how often over the course of ten minutes the two mice touched, sniffed, groomed and crawled on one another.

In both tests, all the mice that had had their water laced with L. reuteri, regardless of how their autism had been induced, were more sociable than equivalents that had been drinking unlaced water. In the first, they spent twice as much time with the mouse under the wire cup. In the second, they engaged in many more social interactions with the unfamiliar mouse.

The team’s initial hypothesis had been that the supplementary L. reuteri were somehow changing the gut flora of the mice exposed to them into something more normal. But they weren’t. Indeed, L. reuteriproved able to abolish autistic behaviour even in those mice which had guts otherwise devoid of microbes—as well as in those with valproic-acid-induced autism, which already had normal levels of the bug. That suggests boosting levels of this bacterial species is shaping behaviour all by itself.

Their next hypothesis was that the bacterium was doing this by interacting somehow with oxytocin, a hormone that shapes behaviour and plays a part in the ways in which people and other mammals form social bonds. Dr Costa-Mattioli knew from work published in 2013 that spraying oxytocin into the noses of mice with autistic symptoms helps to ameliorate some of those symptoms. Dr Sgritta therefore ran the experiments again, but this time on autistic mice that had had the oxytocin receptors on the relevant neurons disabled by genetic engineering. In these new experiments, the presence of L. reuteri in drinking water had no effect.

Follow-up examinations of the mice in all these experiments looked at the strengths of connections between nerve cells within part of the brain called the ventral tegmental region. This region regulates, among other things, motivation and reward-related social behaviour. Nerve signals are carried by the movement of ions (electrically charged atoms), so the team were able to measure connection-strength by monitoring the flow of ions at the junctions between nerve cells in this region. Strong connections, with lots of ion flow, indicated that social experiences were rewarding. These were normal in the mice exposed to L. reuteri, which makes sense since animals treated with the bacterium sought out more social experiences. Conversely, weak connections (those with little ion flow) indicated that social experiences were not triggering a reward. Such weak connections were found in animals that had not been exposed to the bacterium.

The researchers suspected that such effects were controlled by signals from the gut that are being transmitted by the vagus nerve, which connects gut and brain. To test this idea they cut that nerve in selected animals. In these animals, subsequent treatment with L. reuteri failed to abolish their autistic symptoms.

The crucial aspect of this work is L. reuteri’s wide availability—an availability approved by regulators such as America’s Food and Drug Administration. This existing approval, which means L. reuteri poses no known health hazard, simplifies the process of organising clinical trials.

Clearly, autism in people is more complicated than a mere willingness to associate with others. And getting too excited about a mouse trial is usually a mistake. But in Dr Costa-Mattioli’s view his results, which have been replicated in part by Evan Elliot’s laboratory in Bar-Ilan University, Israel, would justify embarking on at least preliminary trials intended to determine whether L. reuteri has positive effects on people with autism, and might thus be worth pursuing.

Others agree. Sarkis Mazmanian of the California Institute of Technology works in the same area. He says of these results: “I think the bar is now very low for getting this research moved on to human trials since most people already have these bacteria inside them and we know there are few, if any, safety or toxicity issues.”

The general availability of L. reuteri does, however, bring with it another possibility—that people will conduct their own, “off label” trials, either on themselves or on their children. Dr Mazmanian is cautious about that idea. “I don’t know if there is a barrier to people buying and using this stuff now. It may be strain-specific and the paper does not state which strain or strains were used,” he says.

At the moment, Dr Costa-Mattioli is unwilling to divulge that information. He is expecting to publish another paper soon, though, with more details. In practice, it may be hard to discourage people from testing L. reuteri’s effects themselves. All the more reason to do properly conducted trials quickly.




This article was originally published in The Economist. Read the original article.

The Results of Your Genetic Test Are Reassuring. But That Can Change.

The results of a genetic test may seem final — after all, a gene mutation is present or it is not. That mutation increases the risk of a disease, or it does not.

In fact, those findings are not as straightforward as they might seem, and the consequences may have grave implications for patients.

While a person’s genome doesn’t change, the research linking particular bits of DNA to disease is very much in flux. Geneticists and testing labs constantly receive new information that leads them to reassess genetic mutations.

As a result, a mutation seen as benign today may be found dangerous tomorrow. And vice versa. But there is no good way to get the new information to doctors and patients.

The result: The gene test you had a few years ago might yield a startlingly different result now.

The problem affects a minority of patients, mostly people with unusual mutations. The more common disease-causing mutations — like those that predispose you to breast or colon cancer — are so well studied that their meaning is not in doubt.

In a recent study, researchers at Myriad Genetics, a diagnostic company, reviewed data on 1.45 million patients who had genetic tests from 2006 to 2016 to see if the results originally reported still held true.

The lab issued new reports for nearly 60,000 of them, meaning the old results had been superseded by new data.

But many patients who carry mutations that have been reclassified remain in the dark. “The system is completely chaotic,” said Dr. Sharon E. Plon, a clinical geneticist at Baylor College of Medicine.

There is no systematic way, she said, to tell patients and doctors that a mutation once thought harmless has been shown to be a health hazard or one thought dangerous is actually benign.

“Some labs report out only one-time results,” said Dr. Theodora Ross, director of the cancer genetics program at the University of Texas Southwestern Medical Center. “They are not going back to reassess test interpretations from ten years ago unless doctors ask.”

But doctors seldom ask, she added.

Normally, a doctor orders genetic testing for a person with a strong family history of, say, heart attacks, strokes or cancer. A sample of a patient’s blood or saliva is sent to a lab, where the patient’s DNA is scanned for unusual alterations.

Not all of these are harmful. The lab compares the mutations to those shown in scientific studies to cause disease.

Some patients are told they have a mutation that is meaningless. Others learn they have “a variation of unknown significance” in a suspect gene — meaning no one knows quite what to make of it.

Still other patients have a mutation deemed dangerous, meaning there is a very high risk of developing cancer, heart disease or another condition. For those patients, such a result can mean regular monitoring and can alter a number of life decisions, including whether to have children.

Reclassification is a particular problem for members of racial and ethnic minorities —- populations whose genes have not been as well studied as those of white people. It can be difficult to know what a variation in DNA means for these patients.

A federally-supported database, ClinVar, allows laboratories to publicly share data on genetic mutations and what they are thought to mean. But some companies, like Myriad, which host huge databases on genetic mutations, do not contribute to ClinVar.

Even the terminology for DNA variants may not be widely shared. Different labs have different naming schemes.

For example, ClinVar renders one DNA variant this way:

NM_004004.5(GJB2):c.101T>C (p.Met34Thr).

But another lab does it like this:

c.101T>C, p.Met34Thr, GJB2.

Patients searching for information on their own “would not be sure what to type into ClinVar,” said Dr. Heidi Rehm, a clinical geneticist at Massachusetts General Hospital and the Broad Institute.

In addition to the terminology problem, Dr. Ross said, there is a problem of discordance among labs.

When one big lab “reports a reclassification and the other labs do not, and you have family members who get tested at different labs, we have different interpretations of the same patient data,” Dr. Ross said. “How do we deal with that? What do we tell our patients?”

Labs like Myriad often notify a doctor who ordered a genetic test when the results were reclassified. But even when they do, doctors may not be able to reach and inform their patients.

“I’ve changed my practice location over the years, and my patients have moved,” Dr. Plon said. “I have received updated reports for patients who no longer live in Houston, and we have no idea where they live.”

Some geneticists say the burden for getting updated results will fall on patients whose genetic alterations are rare ones. They will have to contact their doctors or genetic counselors annually to ask if there was a reclassification.

A reclassification is not always good news.

Dr. Jason Park, clinical director of the advanced diagnostics laboratory at Children’s Medical Center in Dallas, said he has told parents of children with severe epilepsy that a genetic mutation thought to be the cause of the disease actually is a benign change.

The reclassification may not alter treatment, since there often is no specific treatment for a mutation thought to be causing severe epilepsy. But now parents who thought they had found the cause of their child’s illness learn instead that the cause is unknown.

“For families this can be a major social issue,” Dr. Park said. “There are support groups centered around certain genes. Now they are no longer part of that group.”

But for some, like Ricky Garrison, a 61-year-old firefighter who lives in Denton, Tex., reclassification can be a lifesaver.

He went to a doctor a couple of years ago because a warty growth on his nose, but a pathology lab examining the tissue noticed some unusual changes in proteins linked to Lynch syndrome, a condition that greatly increases the risk for a variety of cancers

He was referred to Dr. Ross and her genetics team, who sent his blood to Invitae to test for mutations in Lynch genes.


Rick Garrison, who lives outside Dallas, went to a doctor because of a growth on his nose. The initial results of genetic testing: “Lynch-like syndrome.”CreditLaura Buckman for The New York Times

The results: Mr. Garrison had a “variant of unknown significance.” And his diagnosis was confusing: “Lynch-like syndrome.” It meant maybe he had Lynch syndrome — and maybe he did not.

Doctors said he should have annual colonoscopies, endoscopies and whole skin exams. But since his was not a mutation definitely linked to Lynch syndrome, his family members — he has five children — were not tested to see if they had inherited it.

“No lab that is reasonable would clinically test a family for a variation of unknown significance,” Dr. Ross said. Instead, family members were told to assume they might have Lynch syndrome and to go ahead with the intense cancer surveillance.

In June, though, the testing lab contacted Dr. Ross with news. Mr. Garrison’s mutation was no longer of “unknown significance.” Research in other patients had shown it to be linked to Lynch syndrome.

Everything changed. His children and direct relatives must be tested for the mutation. He must be monitored constantly for signs of cancer.

He will change his plans to retire next year because he worries about the cost of health insurance for someone with Lynch syndrome. Instead he will keep his firefighter job, which comes with insurance, and wait until he is 65 to retire and get Medicare.

“Cancer will probably get me in the end,” he said. “But because of this, I probably will have a few more good years.”



This article was originally published in The New York Times.  Read the original article.

Genetic Tests Can Hurt Your Chances Of Getting Some Types Of Insurance

Taking a genetic test in your 20s or 30s could, indeed, affect your ability to get long-term-care insurance later — or at least the price you’ll pay. And people who are considering enrolling in Medicare after age 65 would do well to read the fine print of the sign-up rules. Readers have insurance questions on these topics this month, and we have answers:

Q: Can getting a genetic test interfere with being able to buy long-term-care insurance in the future? If you do get a plan, can the insurer drop you after you find out the results of a genetic test?

In general, long-term-care insurers can indeed use genetic test results when they decide whether to offer you coverage. The federal Genetic Information Nondiscrimination Act does prohibit insurers from asking for or using your genetic information to make decisions about whether to sell you health insurance or how much to charge you. But those privacy protections don’t apply to long-term-care policies, life insurance or disability insurance.

When you apply for a long-term-care policy, the insurer is permitted to review your medical records and ask you questions about your health history and that of your family. It’s all part of the underwriting process to determine whether to offer you a policy and how much to charge.

If the insurer asks you whether you’ve undergone genetic testing, you generally must disclose it, even if the testing was performed through a direct-to-consumer site like 23andMe, says Catherine Theroux, a spokeswoman for LIMRA, an insurance industry trade group.

You should release any medically relevant information, she says.

Some states provide extra consumer protections related to genetic testing and long-term-care insurance, says Sonia Mateu Suter, a law professor at George Washington University who specializes in genetics and the law. But most follow federal law.

If you get genetic testing after you have a policy, the results can’t affect your coverage.

“Once the policy has been underwritten and issued, the insurer doesn’t revoke the policy if new medical information comes to light,” Theroux says.



This article was originally published in NPR. Read the original article.

Anti-Vaccine Activists Have Taken Vaccine Science Hostage

Americans who don’t want to vaccinate are increasingly getting their way: A June study found that, over the past decade, the number of philosophical vaccine exemptions rose in two-thirds of the states that allow them.

What drives these wrongheaded decisions is fear — fear that vaccines are somehow dangerous, even though research shows the opposite. And these choices have consequences. The 2015 Disneyland measles outbreaksickened at least 125 people, many of them unvaccinated.

As a science journalist, I’ve written several articles to quell vaccine angst and encourage immunization. But lately, I’ve noticed that the cloud of fear surrounding vaccines is having another nefarious effect: It is eroding the integrity of vaccine science.

In February I was awarded a fellowship by the nonpartisan Alicia Patterson Foundation to report on vaccines. Soon after, I found myself hitting a wall. When I tried to report on unexpected or controversial aspects of vaccine efficacy or safety, scientists often didn’t want to talk with me. When I did get them on the phone, a worrying theme emerged: Scientists are so terrified of the public’s vaccine hesitancy that they are censoring themselves, playing down undesirable findings and perhaps even avoiding undertaking studies that could show unwanted effects. Those who break these unwritten rules are criticized.

The goal is to protect the public — to ensure that more people embrace vaccines — but in the long-term, the approach will backfire. Our arsenal of vaccines is exceptional, but it could always be better. Progress requires scientific candor and a willingness to ask inconvenient questions.

Here’s a case that typifies this problem and illustrates how beneficial it can be when critical findings get published. In 2005, Lone Simonsen, who was then with the National Institute of Allergy and Infectious Diseases, and her colleagues published a study in JAMA Internal Medicine showing that the flu vaccine prevented fewer deaths than expected in people over 65.

“I had interesting conversations with vaccine people. They said, ‘What are you doing, Lone? You are ruining everything,’” recalls Dr. Simonsen, who is now a global public health researcher at George Washington University. Her work helped lead to the development of a more effective flu vaccine for older people, yet she felt ostracized. “I felt it personally, because I wasn’t really invited to meetings,” she says. “It took a good decade before it was no longer controversial.”

It’s understandable for scientists to be nervous. The internet has made it easy for anti-vaccine activists to mislead. Dr. Simonsen’s study, for instance, inspired a story with the ridiculous headline “Flu Vaccines Are Killing Senior Citizens, Study Warns.”

But concerns over what these groups might do are starting to take precedence over scientific progress.

“Scientists’ perception of public irrationality is having an impact on our ability to rationally discuss things that deserve discussion,” says Andrew Read, the director of the Center for Infectious Disease Dynamics at Pennsylvania State University. Dr. Read studies how pathogens evolve in response to vaccines, and he is fiercely pro-vaccine — his goal is to keep the shots effective. He says he has had unpleasant encounters at scientific conferences; colleagues have warned him, for instance, not to talk too openly about his work. “I have felt the pressure — and for that matter the responsibility — acutely,” he says.

In 2009, Danuta Skowronski, the lead epidemiologist in the division of Influenza and Emerging Respiratory Pathogens at the British Columbia Center for Disease Control, and her colleagues stumbled across unexpected data that suggested a link between seasonal flu shots and an increased risk for pandemic flu. The findings could not prove a causal link — perhaps people who get seasonal flu shots differ from those who don’t in ways that make them more susceptible to pandemic strains. But one possible interpretation is that seasonal flu shots inhibit immunity to those strains. Dr. Skowronski’s team replicated the findings in five different studies and then shared the data with trusted colleagues. “There was tremendous pushback,” Dr. Skowronski recalls, and some questioned whether “the findings were appropriate for publication.”

“I believed I had no right to not publish those findings,” Dr. Skowronski says. “They were too important.” The findings were submitted to three journals and underwent at least eight lengthy reviews before the final study was published in PloS Medicine.

Last September, researchers with the Vaccine Safety Datalink, a collaborative project between the Centers for Disease Control and Prevention and various health care organizations, published a study in the journal Vaccine that found an association — not a causal link, the authors were careful to note — between a flu vaccine and miscarriage. Soon after, Paul Offit, the director of the Vaccine Education Center at the Children’s Hospital of Philadelphia and co-inventor of a lifesaving rotavirus vaccine, said in The Daily Beast that the paper shouldn’t have been published, in part because the study was small and conflicted with earlier research. He also suggested that the authors had cherry-picked their data — a charge they vehemently deny. One physician questioned in the popular blog Science-Based Medicine why the research had been funded in the first place.

Dr. Offit says that researchers should handle findings differently when there’s a chance they might frighten the public. He thinks that small, inconclusive, worrying studies should not be published because they could do more harm than good. “Knowing that you’re going to scare people, I think you have to have far more data,” he explains.

But even an inconclusive paper can be important, others say, as it can spur the larger, more definitive studies that are needed. It should be “put out there for the scientific community, to look at it, see it, know about it, refine study design and go and look again,” says Gregory Poland, a Mayo Clinic vaccinologist and the editor in chief of Vaccine. It is crucial, though, for researchers to carefully explain such results in their papers to prevent misinterpretation.

If a study scares parents away from vaccines, people could die. That’s a big risk to take to protect the sanctity of scientific discourse. I was warned several times that covering this issue could leave me with “blood on my hands,” too. But in the long run, isn’t stifling scientific inquiry even more dangerous?

“If we get to the point where we don’t want to look anymore because we don’t want to know the answer, then we’re in trouble,” says Dr. Edward Belongia, one of the authors of the Vaccine study and director of the Center for Clinical Epidemiology and Population Health at the Marshfield Clinic Research Institute.

This is not to say that anyone is covering up major safety problems, by the way; critical studies generally concern minor issues in specific contexts. But scientists could one day miss more important problems if they embrace a culture that suppresses research. And at the end of the day, by cherry-picking data, public health researchers are doing “exactly what the anti-vaccine people do,” Michael Osterholm, the director of the Center for Infectious Disease Research and Policy at the University of Minnesota, warns.

There’s no question that bad vaccine science does not deserve a forum — and much of the research cited by anti-vaccine activists is very bad indeed. But good science needs to be heard even if some people will twist its meaning. One thing vaccine scientists and vaccine-wary parents have in common is a desire for the safest and most effective vaccines possible — but vaccines can’t be refined if researchers ignore inconvenient data. Moreover, vaccine scientists will earn a lot more public trust, and overcome a lot more unfounded fear, if they choose transparency over censorship.

This article was originally published in The New York Times.  Read the original article.

Scientists See Promise in Resurrecting These Rhinos That Are Nearly Extinct

When the last male northern white rhinoceros died in March, people mourned the beloved mammal’s step toward extinction.

With no members of the subspecies left in the wild and just two females remaining in captivity, it felt like the last bit of sand was draining through the rhino’s hourglass.

But several teams of scientists are working to flip the hourglass back over.

One group, led by researchers at the San Diego Zoo Institute for Conservation Research, hopes to revive the northern white rhino using preserved cells. In a study published Thursday in Genome Research, the scientists sequenced the DNA of these cells and concluded that they hold a promising amount of genetic diversity for re-establishing a viable population of northern whites.

With the right advances in assisted reproduction or cloning, there could be a second chance for this “unique form of rhinoceros,” said Oliver Ryder, director of conservation genetics at San Diego Zoo Global.

Dr. Oliver Ryder, of the San Diego Zoo Global’s Frozen Zoo, inspecting cell cultures from a store of tissue and genetic material.CreditSan Diego Zoo Global

Not everyone agrees that having the capacity to bring back the northern white rhino means it should be done. Critics question whether the buzz around resurrecting a functionally extinct creature takes attention and resources away from other animals with greater chances of survival.

They also point out that any resurrected northern white rhinos would likely remain in captivity, rather than roaming free in their former habitat in central and eastern Africa, where poaching for horns remains a serious threat.


Nola, a northern white rhino at the San Diego Zoo, died in 2015.CreditSan Diego Zoo Global

In their study, Dr. Ryder and his colleagues focused on the feasibility of recovering the northern white rhino using cells stored in the Frozen Zoo, a large collection of cryopreserved samples at the San Diego Zoo. These cell lines represent eight presumably unrelated northern whites, Dr. Ryder said.

The researchers sequenced these genomes and compared them to genomes from southern white rhinos, the northern white rhino’s closest kin, which underwent a spectacular recovery under protection over the last century, although it remains near-threatened.

They confirmed scientists’ long-held hypothesis that the two rhinos are subspecies, rather than distinct species. This close relationship might bode well for someday using southern white rhinos as surrogates for northern white embryos.

The scientists also discovered sufficient genetic diversity in their northern white rhino samples when compared with the southern white rhinos, Dr. Ryder said. “If it came down to the materials in the Frozen Zoo, we could turn those cells into animals.”


A sample from the Frozen Zoo at San Diego, which holds thousands of specimens from many species.CreditSan Diego Zoo Global

But Marty Kardos, an evolutionary biology researcher at the University of Montana, cautioned that the southern white rhino comparison is “not necessarily worth banking on.” Purely by chance, harmful mutations could exist at high frequency among the northern white rhinos, and have a detrimental effect, he said.

Jason Gilchrist, an ecologist at Edinburgh Napier University in Scotland, questioned the point of reviving an animal that can’t return to its native way of life. “As an ecologist, what I want is to see wild ecosystems functioning as close to naturally as they can,” he said.

Joseph Bennett, a conservation researcher at Carleton University in Ontario, feels the northern white rhino is a good candidate for resurrection because there’s a relatively high chance of success compared to more ambitious projects like the de-extinction of the woolly mammoth or passenger pigeon.

It could be a “really nice ‘good news story’ for people,” he said.

Cathy Dean, chief executive of the charity Save the Rhino, said that efforts to revive the northern white rhino likely attract different sources of funding than conserving remaining wild rhinos. Still, she wishes other rhinos, like the critically endangered SumatranJavan and black rhinos, received nearly as much airtime as the northern white, she said.

Dr. Ryder said his team’s efforts are not in lieu of, but in addition to, efforts to conserve wild animals, adding that “we are seeing species go extinct in spite of a global commitment” to protect them.

In light of that, he said, providing “more options for the existence of species into the future is an appropriate quest.”

This article was originally published in The New York Times.  Read the original article.

The Golden State Killer Is Tracked Through a Thicket of DNA, and Experts Shudder

Genetic testing services have become enormously popular with people looking for long-lost relatives or clues to hereditary diseases. Most never imagined that one day intimate pieces of their DNA could be mined to assist police detectives in criminal cases.

Even as scientific experts applauded this week’s arrest of the Golden State Killer suspect, Joseph James DeAngelo, 72, some expressed unease on Friday at reports that detectives in California had used a public genealogy database to identify him. Privacy and ethical issues glossed over in the public’s rush to embrace DNA databases are now glaringly apparent, they said.

“This is really tough,” said Malia Fullerton, an ethicist at the University of Washington who studies DNA forensics. “He was a horrible man and it is good that he was identified, but does the end justify the means?”

Coming so quickly on the heels of the Cambridge Analytica scandal, in which Facebook data on more than 70 million users was shared without their permission, it is beginning to dawn on consumers that even their most intimate digital data — their genetic profiles — may be passed around in ways they never intended.

“There is a whole generation that says, ‘I don’t really care about privacy,’” said Peter Neufeld, a co-founder of The Innocence Project, which uses DNA to exonerate people who were wrongly convicted. “And then they do, once there is a Cambridge Analytica. No one has thought about what are the possible consequences.”

The trail of the Golden State Killer had gone cold decades ago. The police had linked him to more than 50 rapes and 12 murders from 1976 to 1986, and he had eluded all attempts to find him.

In the years since, scientists have developed powerful tools to identify people by tiny variations in their DNA, as individual as fingerprints. At the same time, the F.B.I. and state law enforcement agencies have been cultivating growing databases of DNA not just from convicted criminals, but also in some cases from people accused of crimes.

The California police had the Golden State Killer’s DNA and recently found an unusually well-preserved sample from one of the crime scenes. The problem was finding a match.


Joseph James DeAngelo was arrested in Sacramento, Calif., and charged with several counts of murder.CreditAgence France-Presse — Getty Images

But these days DNA is stored in many places, and a near-match ultimately was found in a genealogy website beloved by hobbyists called GEDmatch, created by two volunteers in 2011.

Anyone can set up a free profile on GEDmatch. Many customers upload to the site DNA profiles they have already generated on larger commercial sites like 23andMe.

The detectives in the Golden State Killer case uploaded the suspect’s DNA sample. But they would have had to check a box online certifying that the DNA was their own or belonged to someone for whom they were legal guardians, or that they had “obtained authorization” to upload the sample.

“The purpose was to make these connections and to find these relatives,” said Blaine Bettinger, a lawyer affiliated with GEDmatch. “It was not intended to be used by law enforcement to identify suspects of crimes.”

But joining for that purpose does not technically violate site policy, he added.

Erin Murphy, a law professor at New York University and expert on DNA searches, said that using a fake identity might raise questions about the legality of the evidence.

The matches found in GEDmatch were to relatives of the suspect, not the suspect himself.

Since the site provides family trees, detectives also were able to look for relatives who might not have uploaded genetic data to the site themselves.

On GEDmatch, “it just happens they got lucky,” said Dr. Ashley Hall, a forensics science expert at the University of Illinois in Chicago.

23andMe has more than 5 million customers, and has 10 million. But the DNA in databases like these are relevant to tens of millions of others — sisters, parents, children. A lot can be learned about a family simply by accessing one member’s DNA.

“Suppose you are worried about genetic privacy,” Ms. Murphy said. “If your sibling or parent or child engaged in this activity online, they are compromising your family for generations.”


A screen shot of a message posted on the GEDmatch website to its users, addressing its role in the apprehension of Mr. DeAngelo.

DNA profiles can be held indefinitely, and the data can be handed over to police who have warrants or subpoenas. You may never commit a crime. But how should you feel if your DNA was used to locate a distant relative who did?

On a Facebook page dedicated to genealogy, hobbyists debated this new use of DNA data.

“I’ll volunteer to give my DNA and out any of my cousins who may be rapist/murderers. So much drama over nothing,” wrote Stu Pike, who said he had used GEDmatch to track down relatives.

But others expressed outrage. “My relatives consented for their data to be used for genealogy but not for criminal investigations,” wrote Leah LaPerle Larkin, who adjusted her settings to make sure her family’s data was private on the GEDmatch site.

“I’ve had many sleepless nights the last few years, realizing that it’s coming,” CeCe Moore, a genetic genealogist, said of the possibility that an online site might be used to identify a suspect.

The founder of DNA Detectives, a group that helps adoptees find their biological parents and reunite long-lost relatives, Ms. Moore said that she has been approached numerous times by law enforcement asking her help in solving murder and rape cases.

She declined, she said, “because I was still wrestling with the ethical questions of using genealogy databases for criminals.”

It’s not clear how often law enforcement turns to burgeoning DNA databases. Andy Kill, a spokesman for 23andMe, said the company has “had a handful of inquiries over the course of 11 years,” and that no data were “given out in any circumstance.”

It is unlikely that the apparent success of the method in the Golden State Killer case will spur a rush to use genealogy databases to solve crimes.

“Using a database of this kind will generate an extraordinary number of leads, and running them all down using both nongenetic and genetic information requires a lot of police power,” Ms. Murphy said. “So I doubt it will be run of the mill any time soon.”

But it clearly is time for a wider discussion about law-enforcement access to stored DNA, Mr. Neufeld said. “What really needs to happen is for ethicists, lawyers and minorities likely to be disproportionately affected to think of the unintended consequences of this genetic data.”