Connect with us

NewsMakers

Scientists find evidence that novel coronavirus infects the mouth’s cells

“When infected saliva is swallowed or tiny particles of it are inhaled, we think it can potentially transmit SARS-CoV-2 further into our throats, our lungs, or even our guts.”

Published

on

Photo by Kelsey Curtis from Unsplash.com

An international team of scientists has found evidence that SARS-CoV-2, the virus that causes COVID-19, infects cells in the mouth. While it’s well known that the upper airways and lungs are primary sites of SARS-CoV-2 infection, there are clues the virus can infect cells in other parts of the body, such as the digestive system, blood vessels, kidneys and, as this new study shows, the mouth.

The potential of the virus to infect multiple areas of the body might help explain the wide-ranging symptoms experienced by COVID-19 patients, including oral symptoms such as taste loss, dry mouth and blistering. Moreover, the findings point to the possibility that the mouth plays a role in transmitting SARS-CoV-2 to the lungs or digestive system via saliva laden with virus from infected oral cells. A better understanding of the mouth’s involvement could inform strategies to reduce viral transmission within and outside the body. The team was led by researchers at the National Institutes of Health and the University of North Carolina at Chapel Hill.

“Due to NIH’s all-hands-on-deck response to the pandemic, researchers at the National Institute of Dental and Craniofacial Research were able to quickly pivot and apply their expertise in oral biology and medicine to answering key questions about COVID-19,” said NIDCR Director Rena D’Souza, D.D.S., M.S., Ph.D. “The power of this approach is exemplified by the efforts of this scientific team, who identified a likely role for the mouth in SARS-CoV-2 infection and transmission, a finding that adds to knowledge critical for combatting this disease.”

The study, published online March, 25, 2021 in Nature Medicine, was led by Blake M. Warner, D.D.S., Ph.D., M.P.H., assistant clinical investigator and chief of NIDCR’s Salivary Disorders Unit, and Kevin M. Byrd, D.D.S., Ph.D., at the time an assistant professor in the Adams School of Dentistry at the University of North Carolina at Chapel Hill. Byrd is now an Anthony R. Volpe Research Scholar at the American Dental Association Science and Research Institute. Ni Huang, Ph.D., of the Wellcome Sanger Institute in Cambridge, U.K., and Paola Perez, Ph.D., of NIDCR, were co-first authors.

Researchers already know that the saliva of people with COVID-19 can contain high levels of SARS-CoV-2, and studies suggest that saliva testing is nearly as reliable as deep nasal swabbing for diagnosing COVID-19. What scientists don’t entirely know, however, is where SARS-CoV-2 in the saliva comes from. In people with COVID-19 who have respiratory symptoms, virus in saliva possibly comes in part from nasal drainage or sputum coughed up from the lungs. But according to Warner, that may not explain how the virus gets into the saliva of people who lack those respiratory symptoms.

“Based on data from our laboratories, we suspected at least some of the virus in saliva could be coming from infected tissues in the mouth itself,” Warner said.

To explore this possibility, the researchers surveyed oral tissues from healthy people to identify mouth regions susceptible to SARS-CoV-2 infection. Vulnerable cells contain RNA instructions for making “entry proteins” that the virus needs to get into cells. RNA for two key entry proteins–known as the ACE2 receptor and the TMPRSS2 enzyme–was found in certain cells of the salivary glands and tissues lining the oral cavity. In a small portion of salivary gland and gingival (gum) cells, RNA for both ACE2 and TMPRSS2 was expressed in the same cells. This indicated increased vulnerability because the virus is thought to need both entry proteins to gain access to cells.

“The expression levels of the entry factors are similar to those in regions known to be susceptible to SARS-CoV-2 infection, such as the tissue lining the nasal passages of the upper airway,” Warner said.

Once the researchers had confirmed that parts of the mouth are susceptible to SARS-CoV-2, they looked for evidence of infection in oral tissue samples from people with COVID-19. In samples collected at NIH from COVID-19 patients who had died, SARS-CoV-2 RNA was present in just over half of the salivary glands examined. In salivary gland tissue from one of the people who had died, as well as from a living person with acute COVID-19, the scientists detected specific sequences of viral RNA that indicated cells were actively making new copies of the virus–further bolstering the evidence for infection.

Once the team had found evidence of oral tissue infection, they wondered whether those tissues could be a source of the virus in saliva. This appeared to be the case. In people with mild or asymptomatic COVID-19, cells shed from the mouth into saliva were found to contain SARS-CoV-2 RNA, as well as RNA for the entry proteins.

To determine if virus in saliva is infectious, the researchers exposed saliva from eight people with asymptomatic COVID-19 to healthy cells grown in a dish. Saliva from two of the volunteers led to infection of the healthy cells, raising the possibility that even people without symptoms might transmit infectious SARS-CoV-2 to others through saliva.

Finally, to explore the relationship between oral symptoms and virus in saliva, the team collected saliva from a separate group of 35 NIH volunteers with mild or asymptomatic COVID-19. Of the 27 people who experienced symptoms, those with virus in their saliva were more likely to report loss of taste and smell, suggesting that oral infection might underlie oral symptoms of COVID-19.

Taken together, the researchers said, the study’s findings suggest that the mouth, via infected oral cells, plays a bigger role in SARS-CoV-2 infection than previously thought.

“When infected saliva is swallowed or tiny particles of it are inhaled, we think it can potentially transmit SARS-CoV-2 further into our throats, our lungs, or even our guts,” said Byrd.

More research will be needed to confirm the findings in a larger group of people and to determine the exact nature of the mouth’s involvement in SARS-CoV-2 infection and transmission within and outside the body.

“By revealing a potentially underappreciated role for the oral cavity in SARS-CoV-2 infection, our study could open up new investigative avenues leading to a better understanding of the course of infection and disease. Such information could also inform interventions to combat the virus and alleviate oral symptoms of COVID-19,” Warner said.

Zest Magazine accepts contributions promoting everything about living the good life (and how to make this so). C'mon, give us a yell.

NewsMakers

Patients who are overweight or obese at risk of more severe COVID-19

COVID-19 patients with obesity were more likely to require oxygen and had a 73 per cent greater chance of needing invasive mechanical ventilation. Similar but more modest results were seen in overweight patients. No link was found between being overweight or obese and dying in hospital from COVID-19.

Published

on

Patients who are overweight or obese have more severe COVID-19 and are highly likely to require invasive respiratory support, according to a new international study.

The research, led by the Murdoch Children’s Research Institute (MCRI) and The University of Queensland and published in Diabetes Care, found obese or overweight patients are at high risk for having worse COVID-19 outcomes. They are also more likely to require oxygen and invasive mechanical ventilation compared to those with a healthy weight.

MCRI researcher Dr Danielle Longmore said the findings, which highlighted the relationship between obesity and increased COVID-19 disease burden, showed the need to urgently introduce strategies to address the complex socio-economic drivers of obesity, and public policy measures such as restrictions on junk food advertising.

“Although taking steps to address obesity in the short-term is unlikely to have an immediate impact in the COVID-19 pandemic, it will likely reduce the disease burden in future viral pandemics and reduce risks of complications like heart disease and stroke,” she said.

The study looked at hospitalised SARS-CoV-2 patients from 18 hospitals in 11 countries including China, America, Italy, South Africa and The Netherlands.

Among the 7244 patients aged 18 years and over, 34.8 per cent were overweight and 30.8 per cent were obese.

COVID-19 patients with obesity were more likely to require oxygen and had a 73 per cent greater chance of needing invasive mechanical ventilation. Similar but more modest results were seen in overweight patients. No link was found between being overweight or obese and dying in hospital from COVID-19.

Cardiovascular and pre-existing respiratory diseases were associated with increased odds of in-hospital deaths but not a greater risk for needing oxygen and mechanical ventilation. For patients with pre-existing diabetes, there was increased odds of needing invasive respiratory support, but no additionally increase in risk in those with obesity and diabetes.

Men were at an increased risk of severe COVID-19 outcomes and needing invasive mechanical ventilation. In those aged over 65 years, there was an increased chance of requiring oxygen and higher rates of in-hospital deaths.

The University of Queensland’s Dr Kirsty Short, who co-led the research, said almost 40 per cent of the global population was overweight or obese.

“Obesity is associated with numerous poor health outcomes, including increased risk of cardiometabolic and respiratory disease and more severe viral disease including influenza, dengue and SARS-CoV-1,” she said.

Dr Short said while previous reports indicated that obesity was an important risk factor in the severity of COVID-19, almost all this data had been collected from single sites and many regions were not represented. Moreover, there was a limited amount of evidence available about the effects of being overweight or obese on COVID-19 severity.

“Given the large scale of this study we have conclusively shown that being overweight or obese are independent risk factors for worse outcomes in adults hospitalised with COVID-19,” she said.

MCRI Professor David Burgner, who co-led the research, said the data would help inform immunisation prioritisation for higher-risk groups.

“At the moment, the World Health Organization has not had enough high-quality data to include being overweight or obese as a risk factor for severe COVID-19 disease. Our study should help inform decisions about which higher-risk groups should be vaccinated as a priority,” he said.

Continue Reading

NewsMakers

Omega-3 supplements do double duty in protecting against stress

A high daily dose of an omega-3 supplement may help slow the effects of aging by suppressing damage and boosting protection at the cellular level during and after a stressful event, new research suggests.

Published

on

Photo by Michele Blackwell from Unsplash.com

A high daily dose of an omega-3 supplement may help slow the effects of aging by suppressing damage and boosting protection at the cellular level during and after a stressful event, new research suggests.

Researchers at The Ohio State University found that daily supplements that contained 2.5 grams of omega-3 polyunsaturated fatty acids, the highest dose tested, were the best at helping the body resist the damaging effects of stress.

Compared to the placebo group, participants taking omega-3 supplements produced less of the stress hormone cortisol and lower levels of a pro-inflammatory protein during a stressful event in the lab. And while levels of protective compounds sharply declined in the placebo group after the stressor, there were no such decreases detected in people taking omega-3s.

The supplements contributed to what the researchers call stress resilience: reduction of harm during stress and, after acute stress, sustained anti-inflammatory activity and protection of cell components that shrink as a consequence of aging.

The potential anti-aging effects were considered particularly striking because they occurred in people who were healthy but also sedentary, overweight and middle-aged – all characteristics that could lead to a higher risk for accelerated aging.

“The findings suggest that omega-3 supplementation is one relatively simple change people could make that could have a positive effect at breaking the chain between stress and negative health effects,” said Annelise Madison, lead author of the paper and a graduate student in clinical psychology at Ohio State.

The research is published today (Monday, April 19, 2021) in the journal Molecular Psychiatry.

Madison works in the lab of Janice Kiecolt-Glaser, professor of psychiatry and psychology and director of the Institute for Behavioral Medicine Research at Ohio State. This paper is a secondary analysis of one of Kiecolt-Glaser’s earlier studies showing that omega-3 supplements altered a ratio of fatty acid consumption in a way that helped preserve tiny segments of DNA in white blood cells.

Those short fragments of DNA are called telomeres, which function as protective caps at the end of chromosomes. Telomeres’ tendency to shorten in many types of cells is associated with age-related diseases, especially heart disease, and early mortality.

In the initial study, researchers were monitoring changes to telomere length in white blood cells known as lymphocytes. For this new study, the researchers looked at how sudden stress affected a group of biological markers that included telomerase, an enzyme that rebuilds telomeres, because levels of the enzyme would react more quickly to stress than the length of telomeres themselves.

Specifically, they compared how moderate and high doses of omega-3s and a placebo influenced those markers during and after an experimental stressor. Study participants took either 2.5 grams or 1.25 grams of omega-3s each day, or a placebo containing a mix of oils representing a typical American’s daily intake.

After four months on the supplements, the 138 research participants, age 40-85, took a 20-minute test combining a speech and a math subtraction task that is known to reliably produce an inflammatory stress response.

Only the highest dose of omega-3s helped suppress damage during the stressful event when compared to the placebo group, lowering cortisol and a pro-inflammatory protein by an average of 19% and 33%, respectively.

Results from blood samples showed that both doses of omega-3s prevented any changes in telomerase levels or a protein that reduces inflammation in the two hours after participants experienced the acute stress, meaning any needed stress-related cell repair – including telomere restoration – could be performed as usual. In the placebo group, those repair mechanisms lost ground: Telomerase dropped by an average of 24% and the anti-inflammatory protein decreased by an average of at least 20%.

“You could consider an increase in cortisol and inflammation potential factors that would erode telomere length,” Madison said. “The assumption based on past work is that telomerase can help rebuild telomere length, and you want to have enough telomerase present to compensate for any stress-related damage.

“The fact that our results were dose-dependent, and we’re seeing more impact with the higher omega-3 dose, would suggest that this supports a causal relationship.”

The researchers also suggested that by lowering stress-related inflammation, omega-3s may help disrupt the connection between repeated stress and depressive symptoms. Previous research has suggested that people with a higher inflammatory reaction to a stressor in the lab may develop more depressive symptoms over time.

“Not everyone who is depressed has heightened inflammation – about a third do. This helps explain why omega-3 supplementation doesn’t always result in reduced depressive symptoms,” Kiecolt-Glaser said. “If you don’t have heightened inflammation, then omega-3s may not be particularly helpful. But for people with depression who do, our results suggest omega-3s would be more useful.”

The 2.5-gram dose of omega-3s is much higher than what most Americans consume on a daily basis, but study participants showed no signs of having problems with the supplements, Madison said.

Continue Reading

NewsMakers

Heart patients advised to move more to avoid heart attacks and strokes

To prevent heart disease, European guidelines recommend at least 150 minutes a week of moderate intensity or 75 minutes a week of vigorous intensity aerobic physical activity or an equivalent combination.

Published

on

Photo by @chanderr from Unsplash.com

Elevated blood pressure, high cholesterol and diabetes increase the risk of heart disease. But a large study today reveals that in people with these conditions, increasing activity levels is associated with a reduced likelihood of heart events and mortality. The research is presented at ESC Preventive Cardiology 2021, an online scientific congress of the European Society of Cardiology (ESC).

Study author Dr. Esmée Bakker of Radboud University Medical Center, Nijmegen, the Netherlands said: “Previous research showed that improvements in physical activity are beneficial to health. However, those studies were performed in the general population. In our study, we were interested to see if there were similar effects in individuals with cardiovascular risk factors such as high blood pressure, high cholesterol, and diabetes.”

The study included 88,320 individuals from the LifeLines Cohort Study. Participants underwent a physical examination and completed questionnaires about their medical history and lifestyle including exercise. The questionnaires were repeated after approximately four years.

Study participants were divided into five groups according to activity levels at baseline and four years: large reduction, moderate reduction, no change, moderate improvement, and large improvement. Participants were followed-up for a median of seven years after the first assessment for the occurrence of cardiovascular disease or death.

A total of 18,502 (21%) individuals had high blood pressure, high cholesterol, and/or diabetes at the start of the study. The average age of this group was 55 years. After adjusting for age, sex, and baseline physical activity, the researchers found that those with a moderate to large improvement in physical activity were around 30% less likely to develop cardiovascular disease or die during follow-up compared to those who did not change their activity level.

The remaining 69,808 (79%) participants did not have high blood pressure, high cholesterol, or diabetes at the start of the study. The average age of this group was 43 years. After adjusting for age, sex, and baseline physical activity, the researchers found that those with large reductions in physical activity had a 40% higher risk of cardiovascular disease or death compared to those who did not change their activity level.

Dr. Bakker said: “Our study suggests that to prevent heart attacks and strokes and boost longevity, healthy individuals should maintain their physical activity levels, while those with risk factors need to become more active. The associations we found were even more pronounced in people who were relatively sedentary at the start of the study, indicating that inactive people have the most to gain.”

To prevent heart disease, European guidelines recommend at least 150 minutes a week of moderate intensity or 75 minutes a week of vigorous intensity aerobic physical activity or an equivalent combination.

Dr. Bakker said: “If you are currently sedentary, walking is a good activity to start with. If you are already hitting the recommended amount, try doing 10 minutes more each day or increasing the intensity.”

Continue Reading
Advertisement
Advertisement

Like Us On Facebook

Facebook Pagelike Widget

Most Popular

Copyright ©FRINGE PUBLISHING. All rights reserved.