Months after recovering from mild cases of COVID-19, people still have immune cells in their body pumping out antibodies against the virus that causes COVID-19, according to a study from researchers at Washington University School of Medicine in St. Louis. Such cells could persist for a lifetime, churning out antibodies all the while.
The findings, published May 24 in the journal Nature, suggest that mild cases of COVID-19 leave those infected with lasting antibody protection and that repeated bouts of illness are likely to be uncommon.
“Last fall, there were reports that antibodies wane quickly after infection with the virus that causes COVID-19, and mainstream media interpreted that to mean that immunity was not long-lived,” said senior author Ali Ellebedy, PhD, an associate professor of pathology & immunology, of medicine and of molecular microbiology. “But that’s a misinterpretation of the data. It’s normal for antibody levels to go down after acute infection, but they don’t go down to zero; they plateau. Here, we found antibody-producing cells in people 11 months after first symptoms. These cells will live and produce antibodies for the rest of people’s lives. That’s strong evidence for long-lasting immunity.”
COVID-19 is thought to spread mainly through close contact from person to person, including between people who are physically near each other (within about 6 feet). People who are infected but do not show symptoms can also spread the virus to others. We are still learning about how the virus spreads and the severity of illness it causes.
COVID-19 spreads very easily from person to person
How easily a virus spreads from person to person can vary. The virus that causes COVID-19 appears to spread more efficiently than influenza but not as efficiently as measles, which is among the most contagious viruses known to affect people.
The opposite of a gift that keeps on giving is an affliction that keeps on taking away. Latest research seems to indicate that is exactly that case with obesity in relation to COVID-19. Fat chance.
The probability that an obese person will develop severe COVID-19 is high regardless of age, sex, ethnicity, and the presence of co-morbidities such as diabetes, high blood pressure, and heart or lung disease, according to a study by Brazilian researchers published in Obesity Research & Clinical Practice.
The systematic review and meta-analysis of relevant data in the scientific literature focus on nine clinical studies, which in aggregate reported the evolution of 6,577 COVID-19 patients in five countries. The authors conclude that obesity is itself a factor that favors rapid progression to critical illness requiring intensive care and significantly increases the risk of death. The associated research project was supported by São Paulo Research Foundation – FAPESP .
Can you get the seasonal flu along with the raging coronavirus at the same time? That may be the question on everyone’s mind this pandemic pre-flu season. The following is what Johns Hopkins Medicine has to say on the subject.
Unfortunately, yes — and if you have the coronavirus and the flu at the same time, the resulting impact could be even more severe than having either infection alone. By this fall, some areas may have a test available that can look for both the coronavirus and flu viruses so you only need one test.
I have been writing this blog since March 2010. There are approximately 4000 posts in here. Without a doubt, one of the most incendiary topics in that entire time is … flu shots. I get one every year. My doctor tells me to. I listen to her and I got one on Friday. I think you should, too. In view of the pandemic it is even more important.
As the flu season approaches in the United States, health experts are warning that the addition of another respiratory illness on top of the ongoing COVID-19 pandemic could overburden the health care system, strain testing capacity, and increase the risk of catching both diseases at once, according to the University of California San Francisco.
In a bad flu season, which peaks from December to February, 40 million to 50 million Americans may catch the flu, with some 800,000 requiring hospitalization, according to Charles Chiu, MD, PhD, an infectious disease expert at UC San Francisco.
“So the worry is that with the onset of the flu season, you’re going to get peaks of flu and COVID-19 cases at the same time,” he said. “Even with a mild flu season, the convergence with a COVID surge could very rapidly overwhelm our hospital system.”
Unlike COVID-19, however, the flu is a familiar foe, and a safe and effective vaccine is available every year.
Studies indicate that homemade masks help combat the spread of viruses like COVID-19 when combined with frequent hand-washing and physical distancing. Many of these studies focus on the transfer of tiny aerosol particles; however, researchers say that speaking, coughing and sneezing generates larger droplets that carry virus particles. Because of this, mechanical engineer Taher Saif said the established knowledge may not be enough to determine the effectiveness of some fabrics used in homemade masks.
Saif, a mechanical science and engineering professor at the University of Illinois, Urbana-Champaign, led a study that examined the effectiveness of common household fabrics in blocking droplets. The findings are published in the journal Extreme Mechanics Letters.
Few people who have undergone nasopharyngeal swabs for coronavirus testing would describe it as a pleasant experience. The procedure involves sticking a long swab up the nose to collect a sample from the back of the nose and throat, which is then analyzed for SARS-CoV-2 RNA by the reverse-transcription polymerase chain reaction (RT-PCR). Now, researchers reporting in ACS Nano have developed a prototype device that non-invasively detected COVID-19 in the exhaled breath of infected patients.
In addition to being uncomfortable, the current gold standard for COVID-19 testing requires RT-PCR, a time-consuming laboratory procedure. Because of backlogs, obtaining a result can take several days. To reduce transmission and mortality rates, healthcare systems need quick, inexpensive and easy-to-use tests. Hossam Haick, Hu Liu, Yueyin Pan and colleagues wanted to develop a nanomaterial-based sensor that could detect COVID-19 in exhaled breath, similar to a breathalyzer test for alcohol intoxication. Previous studies have shown that viruses and the cells they infect emit volatile organic compounds (VOCs) that can be exhaled in the breath.
The researchers made an array of gold nanoparticles linked to molecules that are sensitive to various VOCs. When VOCs interact with the molecules on a nanoparticle, the electrical resistance changes. The researchers trained the sensor to detect COVID-19 by using machine learning to compare the pattern of electrical resistance signals obtained from the breath of 49 confirmed COVID-19 patients with those from 58 healthy controls and 33 non-COVID lung infection patients in Wuhan, China. Each study participant blew into the device for 2-3 seconds from a distance of 1–2 cm. Once machine learning identified a potential COVID-19 signature, the team tested the accuracy of the device on a subset of participants. In the test set, the device showed 76% accuracy in distinguishing COVID-19 cases from controls and 95% accuracy in discriminating COVID-19 cases from lung infections. The sensor could also distinguish, with 88% accuracy, between sick and recovered COVID-19 patients. Although the test needs to be validated in more patients, it could be useful for screening large populations to determine which individuals need further testing, the researchers say.
Influenza viruses can spread through the air on dust, fibers and other microscopic particles, according to new research from the University of California, Davis, and the Icahn School of Medicine at Mount Sinai. The findings, with obvious implications for coronavirus transmission as well as influenza, are published Aug. 18 in Nature Communications.
“It’s really shocking to most virologists and epidemiologists that airborne dust, rather than expiratory droplets, can carry influenza virus capable of infecting animals,” said Professor William Ristenpart of the UC Davis Department of Chemical Engineering, who helped lead the research. “The implicit assumption is always that airborne transmission occurs because of respiratory droplets emitted by coughing, sneezing or talking. Transmission via dust opens up whole new areas of investigation and has profound implications for how we interpret laboratory experiments as well as epidemiological investigations of outbreaks.”
Respiratory droplets from a cough or sneeze travel farther and last longer in humid, cold climates than in hot, dry ones, according to a study on droplet physics by an international team of engineers. The researchers incorporated this understanding of the impact of environmental factors on droplet spread into a new mathematical model that can be used to predict the early spread of respiratory viruses including COVID-19, and the role of respiratory droplets in that spread.
The team developed this new model to better understand the role that droplet clouds play in the spread of respiratory viruses. Their model is the first to be based on a fundamental approach taken to study chemical reactions called collision rate theory, which looks at the interaction and collision rates of a droplet cloud exhaled by an infected person with healthy people. Their work connects population-scale human interaction with their micro-scale droplet physics results on how far and fast droplets spread, and how long they last.r
Their results were published June 30 in the journal Physics of Fluids.
“The basic fundamental form of a chemical reaction is two molecules are colliding. How frequently they’re colliding will give you how fast the reaction progresses,” said Abhishek Saha, a professor of mechanical engineering at the University of California San Diego, and one of the authors of the paper. “It’s exactly the same here; how frequently healthy people are coming in contact with an infected droplet cloud can be a measure of how fast the disease can spread.”
They found that, depending on weather conditions, some respiratory droplets travel between 8 feet and 13 feet away from their source before evaporating, without even accounting for wind. This means that without masks, six feet of social distance may not be enough to keep one person’s exhalated particles from reaching someone else.
“Droplet physics are significantly dependent on weather,” said Saha. “If you’re in a colder, humid climate, droplets from a sneeze or cough are going to last longer and spread farther than if you’re in a hot dry climate, where they’ll get evaporated faster. We incorporated these parameters into our model of infection spread; they aren’t included in existing models as far as we can tell.”
The researchers hope that their more detailed model for rate of infection spread and droplet spread will help inform public health policies at a more local level, and can be used in the future to better understand the role of environmental factors in virus spread.
They found that at 35C (95F) and 40 percent relative humidity, a droplet can travel about 8 feet. However, at 5C (41F) and 80 percent humidity, a droplet can travel up to 12 feet. The team also found that droplets in the range of 14-48 microns possess higher risk as they take longer to evaporate and travel greater distances. Smaller droplets, on the other hand, evaporate within a fraction of a second, while droplets larger than 100 microns quickly settle to the ground due to weight.
This is further evidence of the importance of wearing masks, which would trap particles in this critical range.
The team of engineers from the UC San Diego Jacobs School of Engineering, University of Toronto and Indian Institute of Science are all experts in the aerodynamics and physics of droplets for applications including propulsion systems, combustion or thermal sprays. They turned their attention and expertise to droplets released when people sneeze, cough or talk when it became clear that COVID-19 is spread through these respiratory droplets. They applied existing models for chemical reactions and physics principles to droplets of a salt water solution–saliva is high in sodium chloride–which they studied in an ultrasonic levitator to determine the size, spread, and lifespan of these particles in various environmental conditions.
Many current pandemic models use fitting parameters to be able to apply the data to an entire population. The new model aims to change that.
“Our model is completely based on “first principles” by connecting physical laws that are well understood, so there is next to no fitting involved,” said Swetaprovo Chaudhuri, professor at University of Toronto and a co-author. “Of course, we make idealized assumptions, and there are variabilities in some parameters, but as we improve each of the submodels with specific experiments and including the present best practices in epidemiology, maybe a first principles pandemic model with high predictive capability could be possible.”
There are limitations to this new model, but the team is already working to increase the model’s versatility.
“Our next step is to relax a few simplifications and to generalize the model by including different modes of transmission,” said Saptarshi Basu, professor at the Indian Institute of Science and a co-author. “A set of experiments are also underway to investigate the respiratory droplets that settle on commonly touched surfaces.”
Despite reports that children and young people may be less likely to get coronavirus disease 2019 (COVID-19) than older adults, there may be substantial indirect adverse effects of the disease on their physical and mental health, according to an analysis in CMAJ (Canadian Medical Association Journal).
“While children and young people seem rarely to be victims of severe COVID-19, we should anticipate that they will experience substantial indirect physical, social and mental health effects related to reduced access to health care and general pandemic control measures,” says Dr. Neil Chanchlani, University of Exeter, United Kingdom.
The authors describe a range of potential adverse effects and contributing factors as well as mitigation strategies for health care providers and health systems.
We all know the expression – a gift that keeps on giving. Well, it appears the coronavirus is the opposite of that – an affliction that keeps on taking.
One in four adults in the UK are experiencing food insecurity, which is likely to have left them susceptible to hunger and potential malnutrition, during the COVID-19 pandemic. That is the main finding of a survey published today by Feeding Britain and Northumbria University’s Healthy Living Lab.
The survey finds that 25% of adults have struggled during the pandemic to access food they can afford, and are likely to have been susceptible to hunger and potential malnutrition as a result. Meanwhile, nearly one in four adults looking after children have eaten less so they can feed the children in their household.
They worked in hospitals hundreds of miles from the epicenter of COVID-19. Their city of 24 million people locked down hard enough, and did enough testing, that it only had a few hundred cases of the disease.
But hundreds of young Chinese doctors in a new study still experienced a sharp drop in mood, a rise in depression and anxiety symptoms, and a doubling of their fear of workplace violence, in just the first month of the coronavirus pandemic.
As if smoking weren’t bad enough for you, it seems the new coronavirus likes it, too.
The lungs of people who smoke may contain more of the receptors that the new coronavirus uses to invade cells. This could explain why people with the virus who also smoke appear to be particularly vulnerable to severe illness.
The majority of people who acquire SARS-CoV-2, the virus that causes COVID-19, experience mild-to-moderate symptoms and will fully recover without hospital treatment.
However, several studies suggest that people who smoke are significantly more likely than people who do not to develop a severe form of the illness.
For example, according to a recent study of COVID-19 cases in hospitals in mainland China, 11.8% of people who smoked had a nonsevere form of the disease, while 16.9% had severe disease.
To break into cells and start replicating itself, the virus latches onto a protein receptor called angiotensin-converting enzyme 2 (ACE2), which is present in the cells’ membranes.
As if smoking per se weren’t bad enough, now, it turns out that smoking significantly worsens COVID-19, according to a new analysis by UC San Francisco of the association between smoking and progression of the infectious disease.
In a meta-analysis of studies that included 11,590 COVID patients, researchers found that among people with the virus, the risk of disease progression in those who currently smoke or previously smoked was nearly double that of non-smokers. They also found that when the disease worsens, current or former smokers had more acute or critical conditions or death. Overall, smoking was associated with almost a doubling of the risk of disease progressing.