A serious pediatric illness has been linked to a similar condition in adults. Coronavirus inhabiting the gut could be the cause—and it may explain long-lasting symptoms, too.
COUNT THE U.S. children who have caught COVID-19 since February, and you’d soon outnumber the population of Boston.
Fortunately, most of these 697,000 confirmed or probable cases have had comparatively mild illness—and somewhere between 16 and 45 percent of children may not manifest any symptoms at all. Yet some in this group—clinically defined as those under the age of 21—go on to develop a serious condition called multisystem inflammatory syndrome in children, or MIS-C.
Thanks to months of urgent research, what began as a mysterious spectrum of symptoms has coalesced into a definable illness, with early signs that include fever, rashes, abdominal pain, diarrhea, and vomiting. Though MIS-C is rare—with 1,027 confirmed cases in the U.S. so far—it can develop into severe inflammation in a matter of hours, often requires intensive care, and is sometimes fatal. A recent report from the U.S. Centers for Disease Control and Prevention analyzed coronavirus fatalities in people under 21 and found that the majority were from MIS-C.
“It happens so rapidly, and the kids are so ill, that 70 percent will require admission into an ICU,” says Alvaro Moreira, a physician scientist at the University of Texas Health Science Center at San Antonio who recently published an analysis of results from multiple scientific papers in EClinicalMedicine based on 662 cases of MIS-C.
An affordable anti-microbial drug used to treat stomach ulcers and bacterial infections has shown promise in combatting the coronavirus in animals, scientists in Hong Kong announced Monday.
Researchers set out to explore whether metallodrugs—compounds containing metal that are more commonly used against bacteria—might also have anti-viral properties that could fight the SARS-CoV-2 coronavirus.
Using Syrian hamsters as tests subjects, they found that one of the drugs, ranitidine bismuth citrate (RBC), was “a potent anti-SARS-CoV-2 agent”.
“RBC is able to lower the viral load in the lung of the infected hamster by tenfold,” Hong Kong University researcher Runming Wang told reporters on Monday as the team presented their study.
“Our findings demonstrate that RBC is a potential anti-viral agent for COVID-19.”
The coronavirus has killed more than a million people since it first emerged in China last December and then spread across the globe.
As scientists scramble to find a vaccine, they have also been scouring readily available drugs that might alleviate symptoms caused by the COVID-19 disease or help the body fight infection.
Remdesivir, a broad-spectrum antiviral drug, and dexamethasone, a type of corticosteroid, have both been identified as having some success against the virus. Both were used by doctors to treat US President Donald Trump after he contracted COVID-19.
The study of Johnson & Johnson’s Covid-19 vaccine has been paused due to an unexplained illness in a study participant.
A document sent to outside researchers running the 60,000-patient clinical trial states that a “pausing rule” has been met, that the online system used to enroll patients in the study has been closed, and that the data and safety monitoring board — an independent committee that watches over the safety of patients in the clinical trial — would be convened. The document was obtained by STAT.
Contacted by STAT, J&J confirmed the study pause, saying it was due to “an unexplained illness in a study participant.” The company declined to provide further details.
“We must respect this participant’s privacy. We’re also learning more about this participant’s illness, and it’s important to have all the facts before we share additional information,” the company said in a statement.
J&J emphasized that so-called adverse events — illnesses, accidents, and other bad medical outcomes — are an expected part of a clinical study, and also emphasized the difference between a study pause and a clinical hold, which is a formal regulatory action that can last much longer. The vaccine study is not currently under a clinical hold. J&J said that while it normally communicates clinical holds to the public, it does not usually inform the public of study pauses.
A new study that researchers conducted in animal models suggests that SARS-CoV-2, the virus that causes COVID-19, may deactivate a pain signaling pathway. This could explain why so many cases of the infection do not cause any symptoms, promoting viral transmission.
Estimates vary widely, but according to the Centers for Disease Control and Prevention’s (CDC) current best estimates, 40% of people with COVID-19 may experience no symptoms.
These people may carry on with their daily activities as usual, without necessarily realizing that they have contracted the virus. This may cause them to spread it unintentionally. For this reason, some scientists refer to people without symptoms as “silent spreaders.”
The CDC also estimate that up to 50% of all SARS-CoV-2 transmission occurs before the onset of symptoms.
One recent study provides a possible explanation for asymptomatic cases and the lack of symptoms early in the course of more serious infections.
SARS-CoV-2 gains entry to its host cells via a receptor in their outer membrane called ACE2. The spike proteins that give the coronavirus its characteristic crown-like appearance latch onto these receptors.
However, the virus can also invade cells when its spikes bind to another membrane receptor called neuropilin.
This receptor’s usual binding partner is called vascular endothelial growth factor A (VEGF-A), which, among other things, promotes the growth of blood vessels.
Crucially, when VEGF-A binds to neuropilin, it also stimulates a pain signaling pathway in the nervous system.
Researchers at the University of Arizona in Tucson have now discovered that the spike protein of SARS-CoV-2 blocks these pain pathways when it locks onto neuropilin.
This suggests that the virus numbs the pain of infection, possibly to the extent that people feel few, if any, symptoms early in the disease.
The findings of this study appear in the journal Pain.
The study’s findings were significant — “spectacular” even, in the words of at least one expert commenter.
A team of doctors at Reina Sofía University Hospital in Córdoba, Spain, split 76 newly admitted Covid-19 patients into two groups. One group got the standard treatment at the time, which included a cocktail of antibiotics and immunosuppressant drugs. The second group got the same standard treatment — plus a drug designed to raise vitamin D levels in the blood.
Among the 26 hospitalized people who received standard care alone, fully half went on to the intensive care unit (ICU) because their disease had worsened. Two of them died. But among the 50 people who received the vitamin D treatment on top of standard care, only one person ended up in the ICU. None died.
In their study write-up, published in October in the Journal of Steroid Biochemistry and Molecular Biology, the Spanish researchers explained that their experiment was a “pilot” study that requires follow-up work. But they also pointed out that theirs is not the first piece of evidence linking vitamin D to a reduced risk for severe respiratory infection. Far from it.
“Vitamin D supports a range of innate antiviral immune responses while simultaneously dampening down potentially harmful inflammatory responses,” says Adrian Martineau, PhD, a clinical professor of respiratory infection and immunity at Queen Mary University of London.
Coronavirus antibodies can last at least three months after a person becomes infected with the virus that causes COVID-19, according to a study published in Science Immunology.
Researchers from the University of Toronto and the Lunenfeld-Tanenbaum Research Institute at Sinai Health used both saliva and blood samples from COVID-19 patients to measure and compare antibody levels for over three months post-symptom onset.
They found that antibodies of the IgG class that bind to the SARS-CoV-2 spike protein are detectable for at least 115 days, representing the longest time interval measured. The study is also the first to show these antibodies can also be detected in the saliva.
“Our study shows that IgG antibodies against the spike protein of the virus are relatively durable in both blood and saliva,” said Jennifer Gommerman, professor of immunology in U of T’s Temerty Faculty of Medicine and leader of the saliva testing effort.
“Our study suggests saliva may serve as an alternative for antibody testing. While saliva is not as sensitive as serum, it is easy to collect.” The saliva assay was developed at U of T while a team at Lunenfeld-Tanenbaum, led by senior investigator Anne-Claude Gingras, who is also a professor of molecular genetics at U of T, executed the serum assay.
“The LTRI platform for detection of antibodies in serum, or blood, is incredibly robust and well suited for assessing the prevalence of infection within the community,” said Gingras. “This is another tool that can help us better understand and even overcome this virus.”
In severe cases of COVID-19, Emory researchers have been observing an exuberant activation of immune cells, resembling acute flares of systemic lupus erythematosus (SLE), an autoimmune disease.
Their findings point towards tests that could separate some COVID-19 patients who need immune-calming therapies from others who may not. They also may begin to explain why some people infected with SARS-CoV-2 produce abundant antibodies against the virus, yet experience poor outcomes.
The results were published online on Oct. 7 in Nature Immunology.
The Emory team’s results converge with recent findings by other investigators, who found that high inflammation in COVID-19 may disrupt the formation of germinal centers, structures in lymph nodes where antibody-producing cells are trained. The Emory group observed that B cell activation is moving ahead along an “extrafollicular” pathway outside germinal centers – looking similar to they had observed in SLE.
B cells represent a library of blueprints for antibodies, which the immune system can tap to fight infection. In severe COVID-19, the immune system is, in effect, pulling library books off the shelves and throwing them into a disorganized heap.
Before the COVID-19 pandemic, co-senior author Ignacio (Iñaki) Sanz, MD and his lab were focused on studying SLE and how the disease perturbs the development of B cells.
Sanz is head of the division of rheumatology in the Department of Medicine, director of the Lowance Center for Human Immunology, and a Georgia Research Alliance Eminent Scholar. Co-senior author Frances Eun-Hyung Lee, MD is associate professor of medicine and director of Emory’s Asthma/Allergy Immunology program.
A new study suggests that face masks have a negligible negative effect on the levels of carbon dioxide and oxygen that a person breathes.
The findings even hold true for individuals with chronic obstructive pulmonary disease (COPD).
The research, which appears in the journal Annals of the American Thoracic Society, contributes to dispelling some of the myths surrounding the use of face masks in the context of the ongoing COVID-19 pandemic.
As the world gains access to more information about SARS-CoV-2, the virus that causes COVID-19, scientists have become increasingly convinced that masks can help reduce its spread.
The primary way that SARS-CoV-2 transmits involves viral particles entering a person’s respiratory tract. This typically happens after another person coughs, sneezes, or speaks near them, producing droplets or aerosols that transport the virus.
Consequently, face masks play an important role in reducing exposure to the virus and limiting the amount of the virus that a person can project toward others.
There is a growing consensus about the value of face masks in reducing the spread of SARS-CoV-2, though this has not always been the case.
Initially, little was known about the new virus and policy had to be developed based on the best available evidence, following scientific models that drew on data from earlier epidemics involving similar viruses.
As a consequence, guidance about mask wearing has varied from country to country, and some major health bodies, including the World Health Organization (WHO), have changed their advice over time.
A study of 160 people in the United States finds associations between worries around COVID-19 and substance use. The authors warn that the pandemic may increase the risk of substance abuse in some people and advocate for specific interventions to protect mental health.
Beyond the physical effects of the novel coronavirus, the onset and continuation of the COVID-19 pandemic have dramatically affected people’s mental health in the United States and worldwide.
Understandably, the pandemic generates fear in many people, as the world finds itself in an unprecedented situation filled with uncertainty.
People manage uncertainties in different ways, but there is a risk that the stress the pandemic causes may trigger an ongoing mental health problem in some people.
A recent study led by the University of Houston, TX, finds that worry about COVID-19 may be a risk factor for substance use, which could, in turn, lead to misuse in some people.
The findings, which appear in Psychiatry Research, suggest the pandemic could adversely affect mental health for years to come.
At almost 7 months into the COVID-19 pandemic, what reasons for (cautious) optimism does recent research offer us when it comes to controlling the spread and impact of the new corona virus?
Almost 7 months ago, the World Health Organization (WHO) declared that the COVID-19 outbreak had become a pandemic.
Since then, scientists all over the world have been working ceaselessly to find effective ways to prevent and treat infections with SARS-CoV-2 and help people recover from COVID-19.
At Medical News Today, we present regular roundups of the most recent research advances that offer hope and reassurance that scientists continue to look for ways out of the pandemic.
In this installment, we look at the latest research around SARS-CoV-2 infection prevention, emerging evidence that could help inform new COVID-19 therapies, and what specialists are doing to advance knowledge about the mysterious “long COVID” and support people it affects.
Alpaca nanobodies to the rescue?
At the start of September, researchers from Karolinska Institutet in Sweden published a study paper in the journal Nature Communications. In it, they suggest that a nanobody, or an antibody fragment, that alpacas naturally produce could help prevent infection with SARS-CoV-2.
Antibodies are a type of protein that recognize antigens. Antigens are structural sequences that are present on infectious agents.