TestBoston, a large-scale research study that will facilitate at-home testing for both the SARS-CoV-2 virus and antibodies against it, is accepting applications from 10,000 current and former Brigham and Women’s Hospital patients.

Researchers from Harvard-affiliated Brigham, the Broad Institute of MIT and Harvard, and the MGB Center for COVID Innovation said the test will detect active COVID-19 cases, evidence of previous infection, and changes in the rates of both.

Over the course of six months, participants will be sent monthly at-home test kits for viral and antibody testing. They will also complete routine symptom surveys and be able to request additional testing if they develop symptoms during the study period. Ongoing study results may reveal critical clues and additional warning signs about how COVID-19 cases are changing in the Greater Boston area, while also helping investigators establish a model for at-home sample collection that is integrated with a medical and public health system. Those interested in participating in the trial can enroll here.

TestBoston will invite participation of patients who have been seen at any Brigham site within the past year and live within a 45-mile radius of Boston. The study will involve individuals enrolling online and then receiving a kit in the mail with instructions on how to collect the samples.

Samples collected by participants at home will be picked up and returned overnight to the Broad Institute for analysis. Samples taken using a swab of the front of the nose will be tested for active viral infection with all results being returned to the participant. Samples taken from a dried blood spot obtained by a small finger prick will be tested for antibodies to determine whether the participant has had a previous infection. Antibody results will be aggregated — so that individuals are not identified — and reported at the community level. Together, Broad and the Brigham investigators will analyze all findings in real-time and share them with key stakeholders at the state level, including the Massachusetts Department of Public Health, to enable public health responses to cases of new infection.

The program will be led by Ann Woolley and Lisa Cosimi, both infectious disease physicians at the Brigham, and Deborah Hung, a core faculty member and co-director of the Infectious Disease and Microbiome Program of the Broad Institute as well as an infectious disease and critical care physician at the Brigham.

“With ongoing limits on testing availability, we still face serious challenges to our understanding of how many people in Massachusetts have been infected and to our ability to detect new outbreaks, which is made all the more challenging because we know that asymptomatic people can transmit this virus to others,” said Woolley.

“The objective of our study is to provide at-home testing that pairs viral testing for active virus with antibody testing to give us a clearer picture of COVID-19 rates now and over time in different communities, as well as an understanding of who is getting infected,” said Cosimi. “We believe that this strategy of reaching patients at home is critical to being able to reach meaningful numbers of patients in order to have real impact.”

One of the team’s goals is to create a platform for home-based sample collection that can be scaled, if needed, should the Boston area experience a second surge of COVID-19 infections. It can also be modeled in other cities impacted by COVID-19 and future respiratory viruses. The investigators hope TestBoston will empower communities to better understand and end COVID-19 by providing an opportunity for patients to partner in research and public health interventions.

“While it is impossible to fully understand a pandemic when one is in the midst of it, integrating clinical, research and public health efforts, as is the goal of TestBoston, is critical for learning in real- time how we can offer patients the best possible care and informing how we can overcome some of the inequities that currently exist, such as access to testing,” said Hung.

Adapted from a Brigham and Women’s news release.

A worldwide forum convened to share insights gleaned from the fight against the novel coronavirus highlighted the importance of a strong, coordinated government response as crucial to stopping its spread, both within a country and internationally.

“It has never been more important for us than it is now to shoulder the responsibility to respond quickly and effectively to the threat posed to human lives and to the health of our communities, local, regional, national, and global,” said Mark Elliott, vice provost for international affairs and the Mark Schwartz Professor of Chinese and Inner Asian History. Introducing “Global Perspectives on COVID-19,” which brought together medical and scientific participants from China, Italy, South Africa, and the U.S. on Wednesday, Elliott characterized the pandemic as a “monumental public health crisis.”

There is strong evidence, however, that it is a crisis that responds to lockdown. Zhong Nanshan, professor of respiratory medicine at Guangzhou Medical University, discussed the speed of containment in Wuhan, China, where COVID-19 was first documented on Dec. 7, its severity apparent by Jan. 20, and the city locked down by Jan. 23. The containment appeared to work, said Zhong, who is also director of the National Clinical Research Center for Respiratory Disease, as cases in China leveled out at approximately 80,000 by March 1. To date, they have increased by only about 10,000, which he attributed to imported cases.

“Strong action by the central government is still the most effective way to block transmission,” Zhong said. The next step, however, is the development of vaccines, he said, citing the “urgent need for international collaboration.”

Fabio Ciceri, scientific director of the San Raffaele Scientific Institute, said “earlier interventions and the introduction of some important treatments” in Northern Italy helped bring down mortality rates in the San Rafaelle hospital from 24 percent to less than 1 percent. As the country prepares for a possible second wave, perhaps as soon as December, he stressed the importance of early testing and tracing, networking between hospitals, and referrals to COVID-19 care hubs. “These centers have new clinical trials with investigational treatments,” as well as “post-COVID-19 clinics,” which follow up on long-term care and management of late and lingering symptoms, he said.

Salim Abdool Karim, director of the Centre for the AIDS Programme of Research in South Africa (CAPRISA) and member of the African Task Force on Coronavirus, Africa Centres for Disease Control and Prevention (Africa CDC), said that in Africa the coronavirus has infected approximately 1.5 million people and killed more than 36,000, a fatality rate of approximately 2.4 percent. COVID-19 now appears to be in decline on the continent, though that could be from underreporting or under-testing in some of its countries, or the facts that Africa’s population skews significantly younger than Europe or North America’s, and fewer of its citizens travel internationally.

However, he too credited a coordinated government response with saving lives. Citing a “strong and consistent political commitment” by the African Union, he noted that Africa CDC quickly set up a platform for a coordinated response for supplies. “We were not competing against each other for, say, test kits,” he said. This coordinated response also engaged the public. Karim pointed to a tradition of working for the collective good, which Karim called the principle of ubuntu, translated as “I am, because you are.”

“You are safe because I am safe,” Karim said. “Our collective interdependence is how we’ll protect ourselves going forward.

George Q. Daley, Harvard Medical School’s dean of the faculty of medicine, noted how in its 10th month, the pandemic has passed a “grim milestone” of 1 million deaths. “Vanquishing COVID-19 will depend critically on how we learn from each other and how we collaborate as a global biomedical community united against this common threat,” he said. Meanwhile, Megan Murray, the Ronda Stryker and William Johnston Professor of Global Health at HMS, discussed the possibility of zoonosis, the leap of pathogens from animals to humans and how it has been enabled by climate change and magnified by climate migration and the mass displacement of marginalized people. “As the natural environment is destroyed, we can expect to see more such disease,” she said, which will disproportionately affect the poor. “Epidemics expose the fault lines of our society.”

Paul Farmer, Kolokotrones University Professor of Global Health and Social Medicine and chair of Harvard Medical School’s Department of Global Health and Social Medicine, wrapped up the conference with a look at what doesn’t work: contact nihilism, in which governments give up tracing contacts, and clinical nihilism, in which they focus solely on containment and almost give up on treatment.

“When you see claims that the treatment of a pathology in a pandemic is impossible, unfeasible, not cost effective, make sure you’re not seeing clinical nihilism,” he said. “There’s always a gap between the development of a new therapeutic and its widespread distribution.”

The forum was co-sponsored by Harvard Medical School and the Massachusetts Consortium on Pathogen Readiness (MassCPR) as part of Worldwide Week at Harvard.

Last week, the Centers for Disease Control and Prevention confirmed what Harvard-affiliated physicians had reported from anecdotal and laboratory evidence: the delta variant of COVID-19 not only spreads more rapidly than other versions of the virus, it can sicken vaccinated individuals who can then spread the virus to others.

In its “Morbidity and Mortality Weekly Report,” the CDC on Friday revealed that 75 percent of patients in a cluster of 469 cases in Provincetown, Massachusetts, were vaccinated, a sobering statistic for Americans who only weeks ago were optimistic that the pandemic’s end was in sight.

“New scientific data shows that delta behaves differently than other variants,” CDC Director Rochelle Walensky said in a briefing last Wednesday. “On rare occasions, some vaccinated people may be contagious and spread the virus to others.”

Mark Poznansky, director of Massachusetts General Hospital’s Vaccine and Immunotherapy Center and an associate professor of medicine at Harvard Medical School, has seen up-close the situation Walensky discussed, including “breakthrough” cases of COVID-19 in vaccinated individuals.

Many of these patients shrug off initial symptoms, Poznansky said, attributing them to a cold or some other mild ailment. When the condition worsens, they get tested and ask for treatment advice, but the delay means that they might have been spreading the virus as they went about their lives. Poznansky, whose clinical practice at MGH is focused on immune-compromised patients who are potentially vulnerable even when vaccinated, said it’s important that vaccinated individuals get tested right away if they feel sick with COVID symptoms.

For vaccinated people who develop symptoms, “The stress should be on testing along with mask-wearing in public spaces and self-isolating where possible,” he said.

The delta variant has spread rapidly across the country, with the CDC reporting last week that it has been detected in eight in 10 samples nationally. In Massachusetts, the recent increase in cases — still at a far lower level than in U.S. hotspots — has been virtually all delta, according to Jacob Lemieux, an instructor in medicine at Harvard Medical School and an infectious disease expert at Mass General.

“We are sequencing all the cases from MGH and from the Brigham … and they’re all Delta,” said Lemieux, whose lab is conducting genetic testing on samples from COVID-19 cases. “It’s been present in the region for a couple of months, but really just over the last few weeks, just taken over.”

Paul Sax, an infectious disease expert at Brigham and Women’s Hospital, said evidence of Delta’s surge is apparent not just in lab data. The number of calls from primary care doctors seeking infectious-disease guidance has also signaled a rise in cases.

Simone Biles was flying over a vault at the Tokyo Olympics when she felt the “twisties” — a kind of mental block that disorients gymnasts midair. The four-time American gold medalist stumbled on the landing and promptly left the floor. She soon began to withdraw from team and individual events, citing mental health concerns. “I have to focus on my mental health and not jeopardize my health and well-being,” Biles told reporters.

She is not alone.

Earlier this year, tennis star Naomi Osaka withdrew from the French Open and Wimbledon, citing her struggles with anxiety and depression. Both athletes have been widely praised for speaking up about their efforts to cope with the pressures that come with high-level competition and for foregrounding an issue many have suffered with in silence. The Gazette spoke with Harvard psychologist Michael R. Hollander about the toll anxiety can take on athletic performance and what must change to ensure athletes get the support they need.

Q&A

Michael R. Hollander

GAZETTE: As a psychologist who has worked with high-level athletes, what is your response to Biles’ decision to withdraw from some Olympic events?

HOLLANDER: I think she did absolutely the right thing. These athletes are under so much stress. And while it’s true professional athletes and amateur athletes at this level are always under a lot of stress, the amount of stress and how pervasive it is at an event like the Olympics are just incomparable, and there is really no place they can go to get out of the limelight. You show a picture of Simone Biles in the supermarket and everybody’s going to know who she is. The expectations for her are beyond what we would really reasonably expect for a human being. So, while I appreciate some of the people who’ve been saying stress has always been part of the competition, and I think that’s true, I also think that’s incomplete. It doesn’t really account for the changing nature of social media. She could be on Facebook, Instagram, TikTok, all in the same hour. That makes it very difficult for someone like her to say: “I’m just going to do the best I can and I’m not going to worry about all the people who are watching me.” We also have to remember that this is a young person.

GAZETTE: For younger athletes in particular, what responsibility should fall on the shoulders of adults who are, in many cases, driving and pushing children to succeed?

HOLLANDER: You could write a few books on this, but my sense is that sometimes when it goes sour, it’s because the adults around these athletes have forgotten that this is a form of play. I love sports, and I am 73. I still play tennis. I box. I’m doing CrossFit. I really do try to stay in shape, but it’s fun. It’s serious fun. I take what I do seriously, but in my mind, it’s recreation. Somewhere along the line that gets lost, and it becomes more life and death. And I think that happens especially in the Olympic sports. As an Olympian, it’s not like you’re going to have a season. It’s once every four years and you’re training for a couple of hours in your life. And I think that adults need to be providing kids more contextual information about that. As in, “Put your heart and soul into this, and remember, this isn’t your career, this isn’t even your education.” These young athletes are not getting enough support from adults, coaches, and parents around keeping perspective about what this is all about because parents and coaches get vicariously caught up in the athlete’s accomplishments.

GAZETTE: What happens to the body when stress and anxiety overwhelm us?

HOLLANDER: Your cortisol levels go up and your entire body is now hypervigilant to the point where you’re actually making mistakes because you’re hyper-focused on things. Your body is saying “There’s danger.” In a way you can think of that as you now have two tasks. One is managing the danger that’s in your mind, and the other is doing your triple twist off the floor mat. And trying to do two things at once rarely, rarely works. Your focus is gone, and you stumble.

GAZETTE: What lessons can we take from the example set by Biles, Osaka, and the other athletes who are putting their mental health and safety above winning?

HOLLANDER:: There will be people who will say, “Me, too — this is not wrecking my mental health and I don’t want to live with this.” In the best of all possible worlds the coaches and parents will take this more seriously and build into the training regimens ways for athletes to recognize when their anxiety is getting to the point where it’s more than they can manage.

GAZETTE: Can you spell out some of the warning signs?

HOLLANDER: Is your sleep way off? Are you having trouble concentrating because you’re totally preoccupied, because this has become all-encompassing? Is your appetite disappearing in some way? Are you more irritable than you usually are before a competition? There are signs out there. My sense is that there are people examining and researching ways we can predict this and what can we do to avoid these really gifted athletes having these kinds of difficulties.

Interview was edited for clarity and length.

The COVID-19 pandemic has impacted virtually every aspect of cancer care and research– from introducing new risks for cancer patients to disrupting the delivery of cancer treatment and the continuity of cancer research, a review of scientific literature shows. The report, by researchers at Dana-Farber Cancer Institute and other institutions, suggests that while COVID-19 has complicated the treatment of cancer patients, it has also spurred creative solutions to challenges in clinical care, and research into the new disease is benefiting from insights gained over years of cancer research.

While much remains to be learned about the intersection of cancer and COVID-19, the new paper, published online by Cancer Cell, represents the most comprehensive survey to date about what physicians have learned, and what research is suggesting, about the interrelationship between the two diseases, the authors said.

“COVID-19 has been responsible for killing more than one million people worldwide. Among those most at risk of developing severe forms of the illness are patients with cancer,” said Ziad Bakouny of Dana-Farber, the co-lead author of the study with Jessica Hawley of Columbia University Medical Center. “Research into why patients with cancer are at heightened risk is moving very quickly. In this paper, we look at the state of the science in this area and others related to these two illnesses.”

The paper summarizes findings in four areas: the interconnected biology of cancer and COVID-19; changes in patient care prompted by the pandemic; effects on cancer research; and insights from cancer research applicable to the treatment of COVID-19.

COVID-19 and cancer biology

In patients with cancer, COVID-19 can be especially harsh. This is likely because many patients have a weakened immune system — either as a result of the cancer itself or the therapies used to treat it — and are therefore less able to fight off infection by the novel coronavirus. Several studies have examined whether systemic cancer therapies such as chemotherapy and targeted therapies increase patients’ vulnerability to COVID-19. The results so far are mixed, Bakouny said, possibly because such studies have focused on systemic therapies as a group rather than on specific agents. Future studies will attempt to tease out the effects of particular drugs.

One of the most dangerous consequences of COVID-19 is an overaggressive immune response known as a “cytokine storm,” which can damage lung and other tissues. Patients with cancer treated with immune-stimulating therapies such as immune checkpoint inhibitors, chimeric antigen receptor (CAR) T-cell therapies and bi-specific T-cell engagers (BiTEs) are at risk for complications if the immune response produced by these therapies results in an attack on normal, healthy tissue. Patients treated with CAR T-cell therapies and BiTEs, in particular, can develop a side effect known as cytokine release syndrome, which is similar to the cytokine storm in patients with COVID-19. Researchers have theorized that COVID-19 could exacerbate cytokine release syndrome in patients treated with certain immunotherapies, but studies have not definitely shown that this is happening, the new report states.

Although patients may be understandably concerned about facing an increased risk from COVID-19 as a result of cancer therapy, they shouldn’t let this deter them from seeking treatment for their cancer, Bakouny said. “Therapies for cancer can prolong life and even be curative in many cases,” he remarks. “It’s very important to be mindful of the goals of therapy and discuss with your doctor the risks and benefits of therapy in your own particular case.”

COVID-19 and cancer care

Around the world, efforts to thwart the spread of COVID-19 included steps to decrease in-person visits between patients and physicians. Among these was a jump in the use of telemedicine, which, some studies indicate, can be just as effective as in-person meetings. One study involving patients with breast cancer found that telehealth was associated with a higher quality of life and less depression and distress compared with usual care. While virtual visits offer a variety of benefits — less need to travel to physician appointments and incur the costs and inconvenience associated with travel — they’re valuable only insofar as they don’t take the place of in-person visits for exams, treatment, or diagnosis, research shows.

“It is also important to consider the unintended consequences of widespread adoption of technology,” Bakouny said. “There is a serious potential risk of compounding health disparities between patients of different socioeconomic status, if telehealth services are mandated.”

On the negative side, studies have shown a sharp decline in cancer diagnoses and screening during the peak of the pandemic. One study found that routine screening dropped by 85-90 percent. Delays in diagnosing cancer are likely to have long-term ripple effects. A British study estimates that, because of diagnostic delays, deaths five years from now may be 4-17 percent higher, depending on tumor type, than they would have been had the pandemic not occurred.

COVID-19 and cancer research

To limit the opportunities for viral transmission, many research centers enacted policies limiting the number of lab workers allowed on-site, putting many studies on hold. For the most part, research projects funded by government appropriations have not been hobbled by the pandemic, but some projects supported by private philanthropy face a funding gap. COVID-19 has drastically decreased donations to cancer-focused philanthropic organizations. The American Cancer Society, for example, expects a $200 million decrease in donations this year and has not been able to accept applications for research grants for the Fall grant cycle.

Clinical cancer research, in which potential new therapies are tested in patients, has also experienced difficulties as a result of COVID-19. Some cancer centers halted enrollment on clinical trials entirely during the height of the pandemic. A survey of dozens of clinical investigators in March found that nearly 60 percent of respondents had halted screening and/or enrollment in certain trials, and that half of their institutions had ceased collection of blood and other tissue for research purposes.

Despite these challenges, investigators found a variety of ways to adapt to straitened circumstances so trials could continue. These included leveraging telehealth to limit in-person visits, use of e-signatures for trial documentation, shipping oral medications to trial participants rather than requiring them to be picked up at the clinic, and allowing laboratory tests to be done at outside labs.

“The relaxation of some of the regulatory requirements associated with clinical research has been accomplished without compromising patient safety,” Bakouny said. “Many investigators see this as a plus — something that could be part of clinical research going forward, to reduce the cost of trials and facilitate the arrival of new therapies for patients.”

COVID-19 and lessons from cancer

Some promising approaches to treating COVID-19 have come, perhaps surprisingly, from cancer research, the paper’s authors write. While cancer and COVID-19 are fundamentally different in their origin, development, and effect on the body, some of the insights gained in decades of research in cancer are showing relevance to fighting the new coronavirus.

A variety of drugs used to alleviate cytokine release syndrome in cancer patients are being evaluated for effectiveness against cytokine storm in patients with COVID-19. Other drugs in the anti-cancer arsenal are undergoing tests of their potential value against COVID-19. An example is acalabrutinib, which is used in the treatment of lymphoid cancers. In one trial, it resulted in rapid improvements in oxygen requirements and a sharp drop in inflammation in patients with COVID-19.

Another potential point of connection between cancer and COVID-19 involves a protein called TMPRSS2. When the coronavirus is breathed in, it binds to lung cells and is split by TMPRSS2, allowing it to enter and infect the cells. Research has shown that in prostate cancer, TMPRSS2 is regulated by the androgen receptor, a cell structure that signals the cell to grow in response to androgen. The androgen receptor is found not only on prostate cells but on cells of the lung as well. It isn’t clear yet whether the receptor regulates TMPRSS2 in lung tissue, but if it does, it could open the way to a new treatment for COVID-19.

Androgen-targeting therapies already used to treat prostate cancer could block TMPRSS2 from entering lung cells, preventing COVID-19 at its source.

“Since the start of the pandemic, we’ve accumulated a substantial amount of evidence about the dynamic between cancer and COVID-19,” Bakouny said. “This review gave us an opportunity to take a step back and take stock of what we’ve learned — to get a sense of the most promising directions for patients, as well as where more study is needed, what we need to dig deeper into.”

The senior author of the study is Corrie Painter of the Broad Institute of MIT and Harvard. Co-authors are Toni Choueiri of Dana-Farber; Solange Peters of the Centre Hospitalier Universitaire Vaudois, in Lausanne, Switzerland; and Brian Rini and Jeremy Warner of Vanderbilt University Medical Center.

The research was partly funded by VUMC CCSG grant P30 CA068485.

Hamburgers may not cause heart attacks, but we have long known that lifestyle choices —including diet, exercise, and sleep patterns — play a role in cardiovascular health. What we don’t know is exactly how these factors actually affect our various bodily functions.

Filip K. Swirski, director of the Cardiovascular Research Institute at the Icahn School of Medicine at Mount Sinai, outlined what is already known about the interaction between lifestyle, the brain, and cardiovascular health, and what scientists are still working on. The former Harvard Medical School professor spoke late last month at a virtual event in the Topics in Bioengineering series presented by the Harvard John A. Paulson School of Engineering and Applied Sciences.

Swirski acknowledged that “there is no question” that genetics play a role in cardiovascular health, but in the last several years, four risk factors — stress, sleep interruption or fragmentation, diet, and sedentary lifestyle — have been clearly identified as contributing to atherosclerosis, commonly referred to as hardening of the arteries, which can lead to a variety of complications, including death.

Current and ongoing research is seeking to uncover the mechanism by which these factors “alter the tissue on the cellular and molecular level,” he said, focusing on “inter-organ communication.” The goal, he said, is to “discover pathways to design therapeutic approaches and also change health policy,” much as research around smoking shaped public policy.

Briefly summarizing the current findings on sleep — “on average, we’re not getting enough” — as well as the widely recognized roles of diet and lifestyle, Swirski then settled in for a deep dive into the role of stress. Citing not-yet-published research, he used slides to illustrate how neutrophils — a type of white blood cell — can be seen “swarming” in the ears of mice subjected to stress. This is not surprising, he said, referencing a Curt Richter Award-winning study 10 years ago that showed the redistribution of such immune cells due to stress.

Current research is taking these studies down to a cellular level, however, examining the movements of different blood components associated with the immune system both during induced acute stress and in the recovery following. For example, in response to stress the levels of neutrophils appear to increase in the lung, liver, and spleen — but decrease in bone marrow. “It may be the case that the source of the neutrophils is the bone marrow,” he said. “And that they’re mobilizing very quickly” to the other organs.

However, two other components — B and T cells — increase in bone marrow under acute stress. While emphasizing that this work is still ongoing, Swirski offered a hypothesis. “What we think is going on is that in response to acute stress, there’s a mass migration of B and T cells into the bone marrow,” he said. “They hide in the bone marrow, perhaps as a safe haven, and, after the storm passes, they start to return to the blood.”

Additional research is seeking to understand the mechanisms for these changes. Because these large-scale shifts are induced by stress, he pointed out, “Stress centers in the brain are the likely culprits.” Ongoing studies on mice are suggesting that the two primary stress centers seem to have different functions. The hypothalamic pituitary adrenal axis, for example, controls two of these blood components, lymphocytes and monocytes, but the sympathetic nervous system controls another, noradrenaline release.

Such a division was “unexpected,” said Swirski, and raises both further questions and avenues to explore. “We think that these processes have evolved for reasons that benefit the host, but they can also backfire,” he said.

Questioned after his presentation about the adaptive nature of these responses, Swirski discussed the evolutionary importance of stress. Not only does stress provoke the palpable “fight, flight, or freeze” reaction that can save us when threatened, on a molecular level these immune-related responses may have helped our bodies fight off antigens — such as the germs on the teeth of a predator after a bite.

However, these adaptive responses have a price. Not only is recovery — the time it takes to revert to pre-stress levels — slow, but ongoing research indicates that with repeated stress, levels react increasingly quickly, jumping into emergency mode. “Keep in mind, there are two systems in our body — the immune system and the nervous system — that learn,” said Swirski. “They require input and are very intertwined.”

This has implications in the current pandemic. “There’s a socio-economic component” to the health of our immune systems, he said, pointing out deleterious effect of “the stress of not being able to feed your family,” among other factors. “Stressed mice die of COVID at a much higher-rate than non-stressed mice,” he said.

“This permeates all of health and disease,” Swirski concluded. “Some parts of stress are beneficial. We need stress, but it’s that balance of positive and negative stress. It’s a complicated issue.”

People who survive serious COVID-19 infections have long-lasting immune responses against the virus, according to a new study led by researchers at Harvard-affiliated Massachusetts General Hospital (MGH).

The study, published in Science Immunology, offers hope that people infected with the virus will develop lasting protection against reinfection. The study also demonstrates that measuring antibodies can be an accurate tool for tracking the spread of the virus in the community.

The immune system produces proteins called antibodies in response to SARS-CoV-2, the virus that causes COVID-19. “But there is a big knowledge gap in terms of how long these antibody responses last,” said Richelle Charles, an investigator in the Division of Infectious Diseases at MGH and a senior author of the paper. To find out, she and her colleagues obtained blood samples from 343 patients with COVID-19, most of whom had severe cases. The blood samples were taken up to four months after a patient’s symptoms emerged. The blood’s plasma was isolated and applied to laboratory plates coated with the receptor-binding domain (RBD) of the virus’ “spike” protein, which attaches to cells, leading to infection. The team studied how different types of antibodies in the plasma bound to RBD. The results were compared to blood samples obtained from more than 1,500 individuals prior to the pandemic.

The researchers found that levels of an antibody called immunoglobulin G (IgG) remained elevated in infected patients for four months and were associated with the presence of protective neutralizing antibodies, which also demonstrated little decrease in activity over time.

“That means that people are very likely protected for that period of time,” said Charles. “We showed that key antibody responses to COVID-19 do persist.”

They also found that measuring IgG was highly accurate in identifying infected patients who had symptoms for at least 14 days. Since the standard PCR (nasal swab) test for SARS-CoV-2 loses sensitivity over time, augmenting it with a test for antibodies in patients who have had symptoms for at least eight days (at which time 50 percent are producing antibodies) will help identify some positive cases that might otherwise be missed, said Charles, a professor of medicine at Harvard Medical School (HMS).

In another finding, Charles and her colleagues showed that people infected with SARS-CoV-2 had immunoglobulin A (IgA) and immunoglobulin M (IgM) responses that were relatively short-lived, declining to low levels within about two and a half months or less, on average.

“We can say now that if a patient has IgA and IgM responses, they were likely infected with the virus within the last two months,” said Charles.

Knowing the duration of the immune response by IgA and IgM will help scientists obtain more accurate data about the spread of SARS-CoV-2, explained co-senior author of the study Jason Harris, a pediatric infectious disease specialist at MGH, and an associate of pediatrics at HMS.

“There are a lot of infections in the community that we do not pick up through PCR testing during acute infection, and this is especially true in areas where access to testing is limited,” he said. “Knowing how long antibody responses last is essential before we can use antibody testing to track the spread of COVID-19 and identify ‘hot spots’ of the disease.”

Lead authors of the paper are Anita Iyer, a postdoctoral fellow at MGH, and Forrest K. Jones, a doctoral student in infectious disease epidemiology at the Johns Hopkins Bloomberg School of Public Health.

Funding was provided by Centers for Disease Control and Prevention, National Institutes of Health, and MassCPR.

Officials at the Centers for Disease Control and Prevention (CDC) are warning that “the war has changed” with the surge of the highly contagious delta variant. The New York Times reports that new cases in the U.S. have soared 139 percent in the past two weeks, and the CDC estimates that more than 82 percent of those are delta variant. Public health officials believe the strain — which appears to cause more serious illness than earlier variants — is now the predominant one in the nation.

William Hanage, associate professor of epidemiology at the Harvard T.H. Chan School for Public Health, offered a few pieces of advice on prevention during a Q&A on the variant hosted jointly by the Chan School and GBH’s “The World” on Tuesday.

Get vaccinated

The delta variant moves swiftly, so it is vital to be vaccinated against exposure, Hanage said.

“It’s reasonable to suggest that before terribly long, everyone in the country will either have been infected with delta or vaccinated,” he said.

The greater the proportion of the population vaccinated, the better, he said. The vaccines’ efficacy against severe or lethal infection will likely prevent the overload on the health care system that the Alpha variant caused last spring.

Redoubling efforts to get people vaccinated as soon as possible can prevent the worst of the surge, Hanage said, but in areas with low rates of vaccination, delta can be “nothing short of catastrophic.”

“We’re here with delta because the pandemic is a very long-term event, and it’s going to be with us for some time. But we’re in a much better position because we have vaccines,” he added. “The vaccine is the single best thing anyone can do to protect themselves and others.”

Mask up

The CDC has resumed its guidance for masking indoors, especially in areas with low vaccination and higher transmission. Even for people who are already vaccinated, masking offers another layer of protection, Hanage said.

Outdoor transmission remains relatively low, but wearing masks in large crowds — or avoiding them altogether — can provide more protection, especially for the unvaccinated.

“Even though we have vaccines, all these other weapons in our arsenal have not become useless,” Hanage said. “Masks are a pretty light lift.”

Socialize responsibly

We might not need to return to our insular social bubbles, but taking appropriate precautions is still beneficial. Vaccinated people interacting with other vaccinated people are likely relatively safe from infection, but activities such as eating indoors at restaurants or attending large events like sports games or concerts could still put people at risk of the delta variant.

“Because you’re vaccinated, you could be feeling overly confident and making contacts you wouldn’t have otherwise,” Hanage said. “Think about contacts who are unvaccinated, or immunocompromised people. Those are the ones for whom the delta surge will be a risk.”

The hospitalization rate for acute cardiovascular disease events in a large southern California health system was 1.62 times higher in the two days immediately after the 2016 presidential election when compared with the same two days in the week prior to the 2016 election, according to new research from Harvard T.H. Chan School of Public Health and Kaiser Permanente. The results were similar across sex, age, and race and ethnicity groups, and the findings suggest that sociopolitical stress may trigger similar responses.

“This is a wake-up call for every health professional that we need to pay greater attention to the ways in which stress linked to political campaigns, rhetoric and election outcomes can directly harm health,” says David Williams, Florence Sprague Norman and Laura Smart Norman Professor of Public Health at Harvard Chan School and corresponding author of the study, which was published in the Proceedings of National Academy of Sciences on Oct. 12..

Previous research has shown that there is an increased risk of acute cardiovascular events soon after significant stressful changes such as earthquakes, industrial accidents, terror attacks, and even sporting events. The American Psychological Association has recently noted that a large portion of adults consider the current political climate as a significant source of stress, though little is known about how that stress may affect health.

For this study, researchers analyzed data collected by Kaiser Permanente Southern California, an integrated health system that provides care to 4.6 million people in the region. The researchers focused on diagnoses of acute myocardial infarction and stroke among adults, as well as emergency department diagnoses for chest pain and unstable angina. In the two days after the 2016 presidential election, the rate of hospitalizations for such events was 573.14 per 100,000 person years (or 94 total hospitalizations), compared with a rate of 353.75 per 100,000 person years (or 58 total hospitalizations) in the same two days of the week in the week prior to the election.

“In our diverse patient population that is reflective of Southern California as a whole, we saw that the risk of heart attacks increased after the 2016 election irrespective of sex, age, and racial/ethnic groups,” said the study’s lead researcher, Matthew Mefford of the Kaiser Permanente Southern California Department of Research & Evaluation. “It is important that people are aware that stress can trigger changes in their health, and that health care providers help patients cope with stress by encouraging wellness strategies such as exercise, yoga, meditation, and deep breathing.”

Other Harvard Chan School authors include Murray Mittleman, Alan Geller, and Elizabeth Mostofsky.

Funding for this study came from W.K. Kellogg Foundation grant P0131281.

With the delta variant wreaking havoc on unvaccinated populations, the ability to quickly diagnose and track emerging variants of the virus is crucial. Researchers have now created a simple, inexpensive, CRISPR-based diagnostic test that allows users to test themselves for multiple variants of the SARS-CoV-2 virus at home, using just a sample of their saliva.

Developed by researchers at the Wyss Institute for Biologically Inspired Engineering at Harvard University, the Massachusetts Institute of Technology, and several Boston-area hospitals, the diagnostic device, called Minimally Instrumented SHERLOCK (miSHERLOCK), is easy to use and provides results that can be read and verified by an accompanying smartphone app within one hour.

miSHERLOCK successfully distinguished between three different variants of SARS-CoV-2 in experiments, and can be rapidly reconfigured to detect additional variants like delta. The device can be assembled using a 3D printer and commonly available components for about $15, and re-using the hardware brings the cost of individual assays down to $6 each.

“miSHERLOCK eliminates the need to transport patient samples to a centralized testing location and greatly simplifies the sample preparation steps, giving patients and doctors a faster, more accurate picture of individual and community health, which is critical during an evolving pandemic,” said co-first author Helena de Puig, a postdoctoral fellow at the Wyss Institute and MIT.

The diagnostic device is described in a paper published Friday in Science Advances.

From supply chain to SHERLOCK

As an instructor in pediatrics at Boston Children’s Hospital with a specialization in infectious diseases, co-first author Rose Lee has been working on the front lines of the COVID-19 pandemic for over a year. Her experiences in the clinic provided inspiration for the project that would ultimately become miSHERLOCK.