ARUP/U of U Health find self-collected saliva, deep nasal swabs are equally effective for diagnosing COVID-19

Self-collected saliva and deep nasal swabs collected by healthcare providers are equally effective for detecting SARS-CoV-2, the virus that causes COVID-19, according to a new study conducted by ARUP Laboratories and University of Utah (U of U) Health.

The study, published in the Journal of Clinical Microbiology, represents one of the largest prospective specimen type comparisons to date, said Julio Delgado, ARUP chief medical officer. Other studies, including one from the Yale School of Public Health, have reached similar conclusions but with markedly fewer patients and specimens.

Researchers also found that specimens self-collected from the front of the nose are less effective than deep nasal swabs for virus detection. This finding prompted a subsequent study that has not yet been published in which researchers learned they could improve the sensitivity of anterior nasal swab testing to 98% by combining an anterior nasal swab with a swab collected from the back of the throat.

The results have important implications for patients and providers. The collection process for saliva and anterior nasal specimens is less invasive than the deep nasal, or nasopharyngeal, swab. In addition, both specimen types can be self-collected, reducing the risk of exposure for healthcare workers who collect nasopharyngeal specimens, said Kimberly Hanson, section chief of clinical microbiology at ARUP and the primary author of the study.

“Saliva and nasal swab self-collection can resolve many of the resource and safety issues involved in SARS-CoV-2 diagnostic testing,” Delgado said.

ARUP and U of U Health anticipate being able to start offering testing on saliva in some U of U Health clinical settings in early September. They already are using anterior nasal swabs in combination with throat swabs to test some asymptomatic individuals.

COVID-19 testing on these alternatives to nasopharyngeal swabs will increase with time, Delgado said. “From the start of the COVID-19 pandemic, ARUP has worked to build capacity for high-quality COVID-19 testing,” he said. “Our goal is to make this testing available to hospitals and healthcare systems nationwide.”

Hanson and her colleagues analyzed more than 1,100 specimens from 368 volunteers at the U of U Health Redwood Health Center drive-through testing site from late May through June. Volunteers self-collected saliva that they spit into a tube and swabbed from the front of both nostrils to produce specimens for testing. The researchers compared test results from these specimen types with test results from nasopharyngeal swabs healthcare providers collected from the volunteers. Discrepant results across specimens collected from the same patient triggered repeat testing using a second polymerase chain reaction (PCR)-based platform.

The study showed that SARS-CoV-2 was detected in at least two specimen types in 90% of the patients who tested positive for the virus.

As a standalone alternative specimen to nasopharyngeal swabs, saliva proved to be an excellent option, Hanson said. Positivity rates for saliva specimens were nearly the same as those for nasopharyngeal specimens.

The research showed that self-collected nasal swabs, when used alone, can miss nearly 15% of infections, which prompted researchers’ further study combining them with oropharyngeal, or throat swabs.

The research is an example of how ARUP and U of U Health continue to explore new methods to serve patients and the community as well as keep healthcare workers safe, said Richard Orlandi, chief medical officer for ambulatory health at U of U Health. “We appreciate the researchers at ARUP, as well as the staff and patients at our Redwood testing center who have participated in this discovery,” he said. “This exciting advance reflects ARUP’s and U of U Health’s innovative spirit and the benefits of our partnership.”

About ARUP Laboratories

Founded in 1984, ARUP Laboratories is a leading national reference laboratory and a nonprofit enterprise of the University of Utah and its Department of Pathology. ARUP offers more than 3,000 tests and test combinations, ranging from routine screening tests to esoteric molecular and genetic assays. ARUP serves clients across the United States, including many of the nation’s top university teaching hospitals and children’s hospitals, as well as multihospital groups, major commercial laboratories, group purchasing organizations, military and other government facilities, and major clinics. In addition, ARUP is a worldwide leader in innovative laboratory research and development, led by the efforts of the ARUP Institute for Clinical and Experimental Pathology®. ARUP is ISO 15189 CAP accredited.

See original post here.

SCALE-UP Utah awarded $5 million to improve COVID-19 testing among underserved and vulnerable populations

Across the US, COVID-19 is hitting some communities harder than others, and Utah is no exception. In our state, Latinos make up 14 percent of the population but represent 40 percent of cases. Similarly, there are disproportionately high case and death rates among Pacific Islanders, African-Americans, Native Americans, and Utahns living in low-income neighborhoods.

With a goal of reducing health disparities in Utah, the National Institutes of Health (NIH) has awarded $5 million to Rachel Hess, and Guilherme Del Fiol of University of Utah Health, and David Wetter of Huntsman Cancer Institute and U of U Health. The team leads SCALE-UP Utah, an initiative that aims to increase the acceptance, reach, uptake, and long-term sustainability of COVID-19 screening and testing. The initiative will be carried out in partnership with 12 community health center systems across the state that run 39 primary care clinics serving more than 115,000 patients—most of whom live in rural and underserved communities.

“SCALE-UP Utah brings together partners from across Utah to ensure that there is adequate screening and testing for all population groups with a specific emphasis on those experiencing higher rates of COVID-19 infection,” Wetter says. “No one should be left behind in being protected from COVID-19.”

U of U Health is one of 32 institutions that received an NIH award through the Rapid Acceleration of Diagnostics-Underserved Populations (RADx-UP) initiative. The program supports both projects designed to rapidly implement COVID-19 testing strategies in populations disproportionately affected by the pandemic and research that aims to better understand COVID-19 testing patterns among these populations.

“It is critical that all Americans have access to rapid, accurate diagnostics for COVID-19, especially underserved and vulnerable populations who are bearing the brunt of this disease,” says Francis S. Collins, director of NIH. “The RADx-UP program will help us better understand and alleviate the barriers to testing for those most vulnerable and reduce the burden of this disease.”

SCALE-UP Utah takes advantage of pre-existing, evidence-based interventions developed by the team at the Center for Health Outcomes and Population Equity (HOPE), led by Wetter at Huntsman Cancer Institute and the Center for Clinical and Translational Science at U of U Health. These include:

  • Initiating text messaging dialogues about testing and testing logistics between health care providers and patients who are at high risk for infection or severe disease.
  • Designing information technology tools that prompt health care providers to ask, advise, and connect patients to COVID-19 screening and testing.
  • Engaging patient navigators to motivate patients and address logistics and barriers that could otherwise prevent them from being tested for COVID-19.

The program is designed to roll out quickly and adapt as needed in order to reduce COVID-19-related health inequities. Wetter says an important goal of SCALE-UP Utah is to serve as a model for other health care systems that serve vulnerable and underserved populations.

Long-standing partnerships between the Center for Clinical and Translational Science, Huntsman Cancer Institute, Association for Utah Community Health, statewide community health centers, and the Utah Department of Health provide additional infrastructure and resources that will improve the reach of COVID-19 screening and testing.

In the future, the program can be readily adjusted and redeployed to meet additional health needs that arise during the pandemic. “SCALE-UP Utah will build an infrastructure that can be used for equitable dissemination of a COVID-19 vaccine once it becomes available,” Wetter says.

See original post here.

# # #

About Huntsman Cancer Institute at the University of Utah

Huntsman Cancer Institute (HCI) at the University of Utah is the official cancer center of Utah. The cancer campus includes a state-of-the-art cancer specialty hospital as well as two buildings dedicated to cancer research. HCI treats patients with all forms of cancer and is recognized among the best cancer hospitals in the country by U.S. News and World Report. As the only National Cancer Institute (NCI)-Designated Comprehensive Cancer Center in the Mountain West, HCI serves the largest geographic region in the country, drawing patients from Utah, Nevada, Idaho, Wyoming, and Montana. More genes for inherited cancers have been discovered at HCI than at any other cancer center in the world, including genes responsible for hereditary breast, ovarian, colon, head, and neck cancers, along with melanoma. HCI manages the Utah Population Database, the largest genetic database in the world, with information on more than 11 million people linked to genealogies, health records, and vital statistics. HCI was founded by Jon M. and Karen Huntsman.

About University of Utah Health

University of Utah Health is the state’s only academic health care system, providing leading-edge and compassionate care for a referral area that encompasses 10 percent of the US, including Idaho, Wyoming, Montana, and much of Nevada. A hub for health sciences research and education in the region, U of U Health touts a $408 million research enterprise and trains the majority of Utah’s physicians, including more than 1,460 health care providers each year at its Colleges of Health, Nursing, and Pharmacy and Schools of Dentistry and Medicine. With more than 20,000 employees, the system includes 12 community clinics and five hospitals: University Hospital, Huntsman Mental Health Institute, Huntsman Cancer Hospital, University Orthopaedic Center, and the Craig H. Neilsen Rehabilitation Hospital. For 11 straight years, U of U Health has ranked among the top 10 US academic medical centers in the rigorous Vizient Quality and Accountability Study.

COVID-19 causes ‘hyperactivity’ in blood-clotting cells

Changes in blood platelets triggered by COVID-19 could contribute to the onset of heart attacks, strokes and other serious complications in some patients who have the disease, according to University of Utah Health scientists. The researchers found that inflammatory proteins produced during infection significantly alter the function of platelets, making them “hyperactive” and more prone to form dangerous and potentially deadly blood clots.

They say better understanding the underlying causes of these changes could possibly lead to treatments that prevent them from happening in COVID-19 patients. Their report appears in Blood, an American Society of Hematology journal.

“Our finding adds an important piece to the jigsaw puzzle that we call COVID-19,” says Robert A. Campbell, senior author of the study and an assistant professor in the Department of Internal Medicine. “We found that inflammation and systemic changes, due to the infection, are influencing how platelets function, leading them to aggregate faster, which could explain why we are seeing increased numbers of blood clots in COVID patients.”

Headshot of a man with blonde hair in white button shirt, yellow wearing glasses.

Depiction of a blood clot forming inside a blood vessel. 3D illustration

Emerging evidence suggests COVID-19 is associated with an increased risk of blood clotting, which can lead to cardiovascular problems and organ failure in some patients, particularly among those with underlying medical problems such as diabetes, obesity or high blood pressure.

To find out what might be going on, the researchers studied 41 COVID-19 patients hospitalized at University of Utah Hospital in Salt Lake City. Seventeen of these patients were in the ICU, including nine who were on ventilators. They compared blood from these patients with samples taken from healthy individuals who were matched for age and sex.

Using differential gene analysis, the researchers found that SARS-CoV-2, the virus that causes COVID-19, appears to trigger genetic changes in platelets. In laboratory studies, they studied platelet aggregation, an important component of blood clot formation, and observed COVID-19 platelets aggregated more readily. They also noted that these changes significantly altered how platelets interacted with the immune system, likely contributing to inflammation of the respiratory tract that may, in turn, result in more severe lung injury.

Surprisingly, Campbell and his colleagues didn’t detect evidence of the virus in the vast majority of platelets, suggesting that it could be promoting the genetic changes within these cells indirectly.

One possible mechanism is inflammation, according to Bhanu Kanth Manne, one of the study’s lead authors and a research associate with the University of Utah Molecular Medicine Program (U2M2). In theory, inflammation caused by COVID-19 could affect megakaryocytes, the cells that produce platelets. As a result, critical genetic alterations are passed down from megakaryocytes to the platelets, which, in turn, make them hyperactive.

In test-tube studies, the researchers found that pre-treating platelets from SARS-CoV-2 infected patients with aspirin did prevent this hyperactivity. These findings suggest aspirin may improve outcomes; however, this will need further study in clinical trials. For now, Campbell warns against using aspirin to treat COVID-19 unless recommended by your physician.

In the meantime, the researchers are beginning to look for other possible treatments.

“There are genetic processes that we can target that would prevent platelets from being changed,” Campbell says. “If we can figure out how COVID-19 is interacting with megakaryocytes or platelets, then we might be able to block that interaction and reduce someone’s risk of developing a blood clot.”

Find original post here.


This study titled, “Platelet Gene Expression and Function in COVID-19 Patients,” was funded by the National Institutes of Health, the University of Utah Health 3i Initiative and the American Heart Foundation.

SARS-CoV-2-like particles very sensitive to temperature

Winter is coming in the northern hemisphere and public health officials are asking how the seasonal shift will impact the spread of SARS-CoV-2, the virus that causes COVID-19?

A new study tested how temperatures and humidity affect the structure of individual SARS-Cov-2 virus-like particles on surfaces. They found that just moderate temperature increases broke down the virus’ structure, while humidity had very little impact. In order to remain infectious, the SARS-Cov-2 membrane needs a specific web of proteins arranged in a particular order. When that structure falls apart, it becomes less infectious. The findings suggest that as temperatures begin to drop, particles on surfaces will remain infectious longer.

This is the first study to analyze the mechanics of the virus on an individual particle level, but the findings agree with large-scale observations of other coronaviruses that appear to infect more people during the winter months.

“You would expect that temperature makes a huge difference, and that’s what we saw. To the point where the packaging of the virus was completely destroyed by even moderate temperature increases,” said Michael Vershinin, assistant professor in the Department of Physics & Astronomy at the University of Utah and co-senior author of the paper. “What’s surprising is how little heat was needed to break them down—surfaces that are warm to the touch, but not hot. The packaging of this virus is very sensitive to temperature.

The paper published online on Nov. 28, 2020, in the journal Biochemical Biophysical Research Communications. The team also published a separate paper on Dec. 14, 2020, in Scientific Reportsdescribing their method for making the individual particle packaging. The virus-like particles are empty shells made from the same lipids and three types of proteins as are on active SARS-Cov-2 viruses, but without the RNA that causes infections. This new method allows scientists to experiment with the virus without risking an outbreak.

The SARS-CoV-2 is commonly spread by exhaling sharply, (e.g. sneezing or coughing), which ejects droplets of tiny aerosols from the lungs. These mucus-y droplets have a high surface to volume ratio and dry out quickly, so both wet and dry virus particles come into contact with a surface or travel directly into a new host. The researchers mimicked these conditions in their experiments.

They tested the virus-like particles on glass surfaces under both dry and humid conditions. Using atomic force microscopy they observed how, if at all, the structures changed. The scientists exposed samples to various temperatures under two conditions: with the particles inside a liquid buffer solution, and with the particles dried out in the open. In both liquid and bare conditions, elevating the temperature to about 93 degrees F for 30 minutes degraded the outer structure. The effect was stronger on the dry particles than on the liquid-protected ones. In contrast, surfaces at about 71 degrees F caused little to no damage, suggesting that particles in room temperature conditions or outside in cooler weather will remain infectious longer.

They saw very little difference under levels of humidity on surfaces, however, the scientists stress that humidity likely does matter when the particles are in the air by affecting how fast the aerosols dry out. The research team is continuing to study the molecular details of virus-like particle degradation.

“When it comes to fighting the spread of this virus, you kind of have to fight every particle individually. And so you need to understand what makes each individual particle degrade,” Vershinin said. “People are also working on vaccines and are trying to understand how the virus is recognized? All of these questions are single-particle questions. And if you understand that, then that enables you to fight a hoard of them.”

Abhimanyu Sharma, Benjamin Preece, Heather Swann, and Saveez Saffarian of the University of Utah and Xiangyu Fan, Richard .J. McKenney and Kassandra M. Ori-McKenney of University of California, Davis were also authors of the Biochem Biophys Res Comms study. Heather Swann,  Abhimanyu Sharma, Benjamin Preece, Abby Peterson, Crystal Eldridge, David M. Belnap and Saveez Saffarian of the University of Utah also co-authored the Scientific Reports study.

Find the original post here.

Portable, reusable test for COVID-19

“Testing, testing, testing.” It’s a mantra that health officials have been constantly promoting because screening people for COVID-19 is the best way to contain its spread. In the U.S., however, that crucial necessity has been hampered due to a lack of supplies.

But University of Utah electrical and computer engineering professor Massood Tabib-Azar has received a $200,000 National Science Foundation Rapid Response Research (RAPID) grant to develop a portable, reusable coronavirus sensor that people can always carry with them. The sensor, about the size of a quarter, works with a cellphone and can detect COVID-19 in just 60 seconds.

“It can be made to be a standalone device, but it can also be connected to a cellphone,” says Tabib-Azar. “Once you have it connected either wirelessly or directly, you can use the cellphone software and processor to give a warning if you have the virus.”

Health officials say the U.S. needs to conduct at least five million COVID-19 tests per day to effectively understand and contain the spread of the virus. But at most, 319,000 per day have been given, according to The COVID Tracking Project, mostly due to a lack of testing supplies such as swabs and reagents. Typically, a 6-inch swab is inserted through the nose to the back of the cavity for 15 seconds to obtain a sample that is sent to a lab for analysis. Most tests take between four to seven days for the results.

A headshot of an engineer standing in front of technological equipment, in a brown jacket, red tie, blue shirt, wearing glasses.

University of Utah electrical and computer engineering professor Massood Tabib-Azar.

Tabib-Azar’s technology, which was profiled in two papers published last month in IEEE Sensors Journal, involves just a drop of saliva and can produce results in a minute. It is based on a sensor Tabib-Azar first began developing for the NSF about a year ago to detect the Zika virus. He is now converting the same technology to work with COVID-19.

The sensor would use single-strand DNA called aptamers in the sensor that would attach to the proteins in the COVID-19 virus molecule if it is present. A person would plug the small sensor into the cellphone’s power jack and launch an app made for the device. To test for the presence of the virus, the user would place a drop of saliva on the sensor, and the results would appear on the phone. It is designed to also test for the virus on the surface of something, like a table or desk, by brushing a swab on the surface and then on the sensor. And it might be able to detect the presence of COVID-19 in floating microscopic particles in the air in enclosed spaces such as an elevator (while the virus is currently considered not airborne, studies are being conducted to determine if minute particles of the virus can hang in floating droplets in the air.).

If the virus is present, the DNA strands in the sensor would bind to the virus’ proteins and electrical resistance is measured in the device, signaling a positive result.

Tabib-Azar says the sensor would include an array of tiny devices inside it, each with a DNA strand that looks for a different protein. A specific combination of proteins would be unique to just COVID-19.

“By increasing the number of devices and single-strand DNA, we can increase the sensor’s accuracy and reduce the false positives and false negatives,” he says.

The sensor is designed to be reusable because it can destroy the previous sample on it by producing a small electrical current that could heat up and remove or disintegrate the virus. Tabib-Azar says the entire process would use little battery power from the cellphone.

Another possible method would involve putting the saliva sample on disposable sheets that are placed on top of the sensor like a sticky note. This would decrease cross-contamination on the sensor and eliminate the need to heat up and destroy the sample afterward.

The device also can be designed to upload the results to a central server that maps out positive results in an area, giving researchers a clearer and more accurate picture of where hotspots are with big outbreaks of the virus.

Because Tabib-Azar has already developed the technology—and a prototype—to detect the Zika virus, he said he could have a prototype of the new COVID-19 sensor for clinical trials in two to three months.

Mucus and the coronavirus

As the lethal COVID-19 coronavirus propagates around the globe, we know a sneeze, a cough or simply touching a surface with the virus can spread the infection.

What researchers don’t know is exactly the role different compositions of mucus, the slimy substance on human tissue, play in the transmission and infection of coronaviruses. Nor do they know why some people known as “super-spreaders” will spread the disease more than others. But University of Utah biomedical engineering assistant professor Jessica R. Kramer is now researching how mucus plays a part in transferring coronaviruses from person to person.

“Not everyone spreads the disease equally. The quality of their mucus may be part of the explanation,” Kramer says. “One person may sneeze and transmit it to another person, and another may not, and that is not well understood.”

She has received a one-year, $200,000 Rapid Response Research (RAPID) grant from the National Science Foundation for the research.

PHOTO CREDIT: Dan Hixson/University of Utah College of Engineering

University of Utah biomedical engineering assistant professor Jessica R. Kramer has received a new grant to research how mucins, the slimy substance in human tissue, plays a role in spreading coronaviruses such as COVID-19.

Understanding how different compositions of the proteins that make up mucus spread coronaviruses could help identify those who are “super-spreaders” as well as those who could be more vulnerable to becoming infected, says Kramer. That could lead to faster, more accurate data on who will spread the virus or more effective quarantine measures for high-risk populations. The nation’s epidemiologists have said since the arrival of COVID-19 that accurate testing to know where the infection is growing is a key factor to containing its spread.

Kramer and her team will create different forms of synthetic mucins, the proteins that make up mucus, and test them with non-hazardous versions of coronaviruses. COVID-19, which is the cause of the worldwide pandemic, is a novel coronavirus that by the end of March has so far killed more than 37,000 people since it was first discovered late last year. But it is only one of many forms of coronaviruses.

Kramer will use special aerosols in a closed environment to simulate coughing to help determine how different mucins carry the virus through the air. She will also test the viability of the virus when it lands on a surface based on the mucins that carry it. Her lab will also examine how mucin composition on the next victim’s mouth, eyes or lungs affects whether the virus makes it through the mucus into their cells to replicate.

The composition of mucus changes from person to person based on their genetics, environmental factors, or their lifestyle such as whether the person smokes or what their diet is. “It’s important that people understand that it’s not only the amount of mucus that is a factor but how the molecular composition is different,” she says.

Kramer’s lab at the University of Utah has been creating synthetic mucins and more recently studying how mucins and bacteria interact with each other. She says researching how mucins interact with viruses is a natural extension of this work.

Kramer’s award is the second NSF RAPID grant to be given to U researchers related to the spread of the COVID-19 coronavirus. Michael Vershinin and Saveez Saffarian of the U’s Department of Physics & Astronomy will study how the structure of the coronavirus withstands changes in humidity and temperature and under what conditions the virus falls apart.

Find original post here.

COVID-19 antibody tests can guide public health, policy decisions

It’s too soon to use COVID-19 antibody testing to issue “immunity passports,” antibody tests that are available today. But they are good enough to inform public health decisions about relaxing social distancing interventions, says an international group of infectious disease and public health experts in Science Immunology today.

“We don’t need to wait for the perfect test to monitor populations,” says University of Utah Health infectious disease physician-researcher Daniel Leung. “We can use what we have if we go in with our eyes open.” Leung is the corresponding author on the editorial together with specialists from seven different countries and leading public health institutions in the U.S., including Johns Hopkins Bloomberg School of Public Health, Harvard School of Public Health, University of California, San Francisco and Pennsylvania State University.

Today’s tests are ready for populations, not people

Some have suggested that detecting antibodies to SARS-CoV-2—the coronavirus that causes COVID-19—become the basis of “immunity passports” that enable people to return to work, school, or travel. Yet facts indicate that it is premature to take that step. Scientists have yet to determine whether the antibodies or perhaps a threshold level of antibodies, protect a person from being re-infected. In addition, there are multiple antibody tests, none with the levels of specificity needed to declare someone immune.

In short, we are far from being at a place where a positive antibody test guarantees that a person cannot get COVID-19 nor spread it to someone else, say Leung and colleagues. And the stakes are too high to risk getting it wrong.

Regardless, these same tests are good enough to monitor the spread of COVID-19 in populations. “There is no need to throw out the baby with the bathwater,” Leung says. “We can use serological testing at the population level to get valuable information about transmission and the impact of interventions—and we don’t need a perfect serology test to do it.”

Understanding trends such as where outbreaks are occurring and which regions are quiet, along with the characteristics of who is getting ill and who is protected, can provide information to guide policy. Is a specific state or county ready to ease restrictions? Are students safe to go back to school? Do certain populations need extra protection?

Fine-tuning existing tests to meet different needs

One reason many of today’s tests can work for public-level decisions is that they do not just provide black and white answers. Instead, their parameters can be adjusted to fit different needs. One of these characteristics is specificity—how well a test detects antibodies to SARS-CoV-2 and not to antibodies against other coronaviruses. The other is sensitivity—the minimum level of antibodies someone must have in their blood in order to test positive.

In general, there is a tradeoff between the two. Adjusting a test to prioritize sensitivity makes it not as specific, and making a test more specific makes it less sensitive. But, according to the editorial, it’s OK to sacrifice one for the other in order to answer certain questions.

Take the situation in a rural countryside where relatively few people per capita have had COVID-19. In that setting, a test with high sensitivity and low specificity would not be optimal. These characteristics could easily result in the same number of people testing positive who never had COVID-19 as the number of people who really are positive. In this situation, the results would be practically meaningless.

However, the same test can be used if it is tuned for that situation. This can be done by designating a higher cutoff and saying that a test does not count as positive unless it has a stronger signal. Doing so lowers the false positive rate by increasing specificity. In this scenario, positive tests are more likely to be truly positive—and that data can be safely used to monitor that population.

On the other hand, an urban setting where higher proportions of the population have been infected would do better with a test prioritized for higher sensitivity. That would provide a better snapshot of the spread of COVID-19 by capturing a greater segment of the population.

“While we should certainly collect these data, we need to make sure the right studies are put in place so we can meaningfully interpret these data for individuals and for populations,” says Andrew Azman, assistant scientist at Johns Hopkins Bloomberg School of Public Health.

Additional studies will only make the results of antibody testing more informative. The editorial stipulates that we still need to understand whether antibodies remain in the body for months or years, what levels of antibodies provide immunity, and how responses might differ in people who had various severities of infection or who have other medical conditions.

Equally as important as leveraging the technologies at hand, the authors say, is building an infrastructure that allows states and countries to share protocols, standardize methods, share results, and coordinate activities. This would not only improve the response to the current pandemic but could build a foundation for monitoring other infectious diseases, including influenza, cholera, malaria, and future pandemics.

The knowledge gained now may help re-frame the future, they say. “The current crisis presents an opportunity to rethink how health systems generate and use surveillance data and how to harness the power of serological tests and seroepidemiology.”

Find original post here.


In addition to Leung, co-authors are Juliet Bryant, Andrew Azman, Matthew Ferrari, Benjamin Arnold, Maciej Boni, Yap Boum, Kyla Hayford, Francisco Luquero, Michael Mina, Isabel Rodriguez-Barraquer, Joseph Wu, Djibril Wade and Guy Vernet. In addition to the institutions mentioned, collaborators come from Fondation Mérieux, Médecins Sans Frontières, Epicentre in Yaounde and Paris, University of Hong Kong, IRESSEF, Dakar and Institut Pasteur de Bangui.

The editorial was published as “Serology for SARS-CoV-2: apprehensions, opportunities, and the path forward.”

People who live together may not get COVID-19 together

If anyone I live with were to get COVID-19, I would be resigned to the idea that I would get it too. After all, my family breathes the same air without wearing masks and touches the same doorknobs, day in and day out. And yet, it’s not necessarily a foregone conclusion that members of a shared household will share the virus.

Once one person becomes infected, there is a 12% likelihood that someone they are living with will become infected too, according to the University of Utah’s Utah HERO phase one study. Reports from China (also here) indicate that what we’re seeing in Utah is similar to what’s happening elsewhere in the world.

Scientists arrived at the number by performing antibody tests on more than 8,000 Utahns in randomly chosen households across four counties in the state. A positive test indicates that a person has had COVID-19 sometime in the past. Among households where at least one person tested positive, the scientists calculated the proportion of remaining members who also had antibodies.

It’s thought that, typically, when two or more people in a household test positive, one passed the virus to the other. But in some cases, they each may have been infected by someone outside the household. Either way, the frequency that two or more people in a household test positive is lower than one might expect considering how quickly COVID-19 is spreading all around us.

“You might think, ‘Wow if I’m in a household with an infected person, I’m a goner,’” says U of U Health epidemiologist Matthew Samore. “But that’s just not true. The interesting thing is, what are the implications?”

Superspreader or super unlucky?

Close examination of COVID-19 cases worldwide has already taught us that new coronavirus infection spreads more readily when people are close to one another indoors for long periods of time. That characterizes the living condition of many homes—and yet spread from one person in a household to another fails to happen about 88% of the time. What, then, could make the difference between who is likely to spread the virus and who is not?

Perhaps you’ve heard of the term “superspreaders”? One explanation, says Samore and his colleague Damon Toth, is that there is a large variability in infectiousness, and certain conditions are conducive to spreading the virus to large numbers of people. There is support for the idea that a relatively small proportion of people could be responsible for much of the spread of the disease. Research suggests that 10% to 20% of infected people were responsible for 80% of the cases examined.

“If we can understand the factors that make people superspreaders, or that make people minimally infectious, then we can create better policies that better control spread,” Samore says. What could those factors be? Scientists are trying to answer the question, but several possibilities exist.

Biological differences that lead infected people to shed more virus—and for longer periods of time—could boost their infectivity. Characteristics like these could come from being in a certain age group, from changes in the immune system and from other reasons scientists have yet to uncover.

The surrounding environment presents another set of conditions that could make a big difference. Imagine that households with a large number of people in tight quarters, multigenerational families or poor ventilation could be particularly conducive to spreading the disease.

Whether superspreading conditions are the main culprit or transmission mainly comes from many mild spreading events, chances are spreading happens more frequently outside the home. An infected person is more likely to encounter a greater number of people in the community, and a superspreader can potentially infect dozens of others. That suggests that community spread—rather than household transmission—may be a main driver of the pandemic.

Regardless, Toth points out that it is still important to take precautions at home if you know that someone you live with either has COVID-19 or has come in close contact with someone who does. Utah HERO has found that about 1% of Utahns tested positive for antibodies, meaning that about 99% were still susceptible to the disease.

“Twelve percent is still a pretty high risk if you have someone coming home with the virus,” Toth says. “It is a lot higher than before you had someone in your household who is positive.”

Find original post here.