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Getting vaccinated for COVID-19 measurably improved the psychological well-being of participants in the Understanding Coronavirus in America study, a large longitudinal look at the impact of the pandemic on individuals in the United States. Vaccination was associated with declines in distress and perceived risks of infection, hospitalization, and death. The study, appearing in the American Journal of Preventive Medicine, published by Elsevier, validates the intuitive but previously unanswered questions of whether becoming vaccinated reduces perceived risks associated with COVID-19, and whether the reduction of these fears leads to improvements in mental health and quality of life.
“Our study documents important psychological benefits of vaccination beyond reducing the risk of severe illness and death associated with COVID-19,” said lead investigator Jonathan Koltai, PhD, Department of Sociology, University of New Hampshire, Durham, NH, USA.
Psychologic distress and anxiety increased sharply across the population following the onset of the COVID-19 pandemic. Several factors contributed, such as widespread job and income loss, food insecurity, social isolation, caregiving burdens, substance abuse, and racialized discrimination. Depressive symptoms persisted and increased into 2021 for those experiencing an accumulation of stress exposures. Not surprisingly, many individuals are also experiencing anticipatory fears that contribute to rising mental health problems.
Data from a nationally representative study of 8,090 adults who were interviewed regularly between March 2020 and June 2021 revealed declines in COVID-related risk perceptions and psychological distress following vaccination. Specifically, adults who received at least one dose of the COVID-19 vaccine between December 2020 and June 2021 reported a 7% relative reduction in mental distress, as measured using the Patient Health Questionnaire 4 (PHQ-4) distress scores, from average levels in the survey period immediately prior to vaccination.
Reductions in distress were partially explained by declining risk perceptions following vaccination. Becoming vaccinated was associated with a 7.77 percentage point decline in perceived risk of infection, a 6.91 percentage point decline in perceived risk of hospitalization, and a 4.68 percentage point decline in perceived risk of death. Adjusting for risk perceptions decreased the vaccination?distress association by 25%.
These effects persisted and became stronger up to at least eight weeks following vaccination. It is noteworthy that while responses from vaccinated and never-vaccinated participants followed similar trends pre-vaccination, they significantly diverged post-vaccination. Becoming vaccinated made people feel safer in addition to being safer.
The impact of vaccination on mental health varied by race/ethnicity. The largest reductions in distress were observed among American Indians (AI) and Alaska Native (AN) individuals, who have suffered disproportionately from COVID-19. The breakout among racial/ethnic groups was proportional to the overall US population during the study period, with the highest rates of vaccination observed among Asian and Pacific Islanders, and the lowest rates of vaccination observed among Black participants.
With the rapid rise of the Omicron variant in late 2021 and early 2022, urgent measures are needed to increase vaccination rates and achieve vaccine equity, both locally and globally. These efforts need to be coupled with effective communication about the benefits, both physical and mental, associated with vaccination.
Dr. Koltai stressed, “To ensure these benefits are widely shared, efforts to increase vaccination and booster rates in early 2022 need to prioritize equitable distribution and access to vaccines.”
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SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesPeople who are vaccinated are less likely to develop long Covid even if they catch the virus, a rapid review by the UK Health Security Agency reveals. It looked at the available evidence to date from 15 studies around the world. The findings suggest that while some who are jabbed catch Covid, vaccines reduce infection risk and illness, including symptoms like fatigue. And unvaccinated people who catch Covid and get symptoms of long Covid, do better if they then get vaccinated. Some of the studies in the review looked at the effect of vaccinations given before infection and found:People with Covid who received two doses of the Pfizer, AstraZeneca or Moderna vaccines or one dose of the Janssen vaccine, were about half as likely as people who received one dose or were unvaccinated to develop long-Covid symptoms lasting more than 28 daysVaccine effectiveness against most long-Covid symptoms was highest in people aged 60 years and overOthers that looked at the effects of vaccines in people who already had long-Covid symptoms found:Vaccines may improve rather than worsen Covid symptoms, either immediately or over several weeksAccording to the UK Health Security Agency (UKHSA), around 2% of the UK population have reported symptoms of long Covid, such as fatigue, shortness of breath and muscle or joint pain. Symptoms like these can last for more than four weeks after the infection. People who received two doses of a vaccine against Covid are less likely to experience this or will have the symptoms for a shorter time. Dr Mary Ramsay, Head of Immunisation at the UKHSA, said: “These studies add to the potential benefits of receiving a full course of the Covid-19 vaccination. Vaccination is the best way to protect yourself from serious symptoms when you get infected and may also help to reduce the longer-term impact. “For most people, symptoms of long Covid are short-lived and resolve over time. But for some, symptoms can be more severe and disrupting to their daily lives. If you’re experiencing unusual symptoms, particularly for longer than four weeks after infection, you should consider contacting your GP.”UKHSAThe BBC is not responsible for the content of external sites.

Temperature fluctuations such as heatwaves can have very different effects on infection rates and disease outcomes depending on the average background temperature, says a report published today in eLife.
The study suggests it will be increasingly difficult to predict the consequences of climate change on host-pathogen interactions as global temperatures rise and extreme weather events become more common.
Infectious diseases have profound ecological effects on human, agricultural and wildlife populations. It is well known that interactions between pathogens and their hosts are sensitive to changes in temperature. But what is less well understood is how sudden and extreme temperature variation affects this relationship and how this influences overall infection rates and disease outcomes.
“Climate change is predicted to increase not only average temperatures but also temperature fluctuations and the frequency and intensity of extreme weather events,” explains co-first author Pepijn Luijckx, William C. Campbell Lecturer in Parasite Biology, Trinity College Dublin, Ireland. “Yet although studies have quantified the effects of rising average temperatures on host and pathogen traits, the influence of variable temperature regimes such as heatwaves remains largely unknown.”
Luijckx and the team examined the effects of different temperatures on various traits in a host organism — a small crustacean called Daphnia magna — and its known gut parasite, Odospora colligata. Transmission of the parasite is representative of classic environmental transmission, similar to that seen with diseases such as SARS-CoV-2 and cholera.
The team looked at how the organisms responded to three distinct temperature regimes: a constant temperature, and two variable regimes, with daily fluctuations of +/- 3°C and three-day heatwaves of 6°C above ambient temperature. They then measured the crustacean’s lifespan, fertility, infection status and the number of parasite spores within their gut. Next, they processed the data into a statistical model to compare the impact of the three different temperature regimes.
The team found that daily fluctuations of temperature reduced the infectivity and spore burden of the parasite compared to those kept at the constant average temperature. However, by contrast, the infectivity of parasites after a heatwave was almost the same as the infectivity of those maintained at the constant temperature.
Moreover, the number of spores in the crustacean host increased following the three-day ‘heatwave’ when the background constant temperature was 16°C, but this burden was reduced at higher temperatures. This suggests that the effects of temperature variation differ depending on the average background temperature and whether this is close to the optimum temperature for the parasite.
Host fitness and reproductive success were generally reduced in the crustacean exposed to either the parasite spores or when experiencing variable temperatures. The difference between the host and pathogen responses suggest that under some circumstances the parasites were able to withstand the sudden change in heat better than their hosts.
“Our findings show that temperature variation alters the outcome of host-pathogen interactions in complex ways. Not only does temperature variation affect different host and pathogen traits in a distinct way, but the type of variation and the average temperature to which it is applied also matter,” concludes Luijckx. “This means that changing patterns of climate variation, superimposed on shifts in mean temperatures due to global warming, may have profound and unanticipated effects on disease dynamics.”
Alongside Pepijn Luijckx, the research team includes co-first author Charlotte Kunze (Carl von Ossietzky University of Oldenburg, Germany, and Trinity College Dublin), Andrew Jackson and Ian Donohue (both Trinity College Dublin).
Their study was funded by Science Foundation Ireland and the Irish Research Council.
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A one-time infusion of stem cells from bone marrow improves the survival of mice with sepsis, shows a study published today in eLife.
The findings could lead to potential new treatments for sepsis, a life-threatening inflammatory condition triggered by bacterial or viral infections.
Sepsis causes an overwhelming immune response that can lead to organ failure and death. Around 20% of deaths worldwide and one-third of hospital deaths are caused by the condition.
“New treatments are urgently needed to help reduce the number of sepsis-related deaths,” explains first author and HHMI Gilliam Scholar Daniel Morales-Mantilla, Predoctoral Fellow at the Katherine King Lab, Baylor College of Medicine, Houston, Texas, US. “We set out to study the effects of sepsis in mice for clues of potential new targets for treatments.”
First, the team examined the effects of sepsis on mice following infection with Streptococcus pyogenes, the pathogen that causes strep throat. They found that a detrimental effect of the condition is a severe drop in the number of hematopoietic stem and progenitor cells (HSPCs) in the animals’ bone marrow. These cells are responsible for the day-to-day production of all blood and immune cells.
The team suspected that the number of HSPCs drops because the cells work overtime to produce the immune and blood cells needed to fight both the infection and the severe inflammation caused by sepsis.
Following this discovery, the researchers investigated whether an infusion of new healthy HSPCs could improve sepsis outcomes. To answer this question, they gave mice with sepsis an infusion of approximately 10,000 healthy new HSPCs around 24 hours following infection. The treatment increased the animals’ survival by 50-60% compared with mice that did not receive an HSPC infusion. This treatment also decreased the number of inflammatory molecules called cytokines in the animals.
“Surprisingly, we found that HSPC infusion did not reduce the amount of bacteria in the mice,” Morales-Mantilla says. “Instead, it increased the numbers of immune cells that reduce inflammation.”
Currently, clinicians sometimes transfuse a different type of immune cell, called granulocytes, to treat sepsis patients with depleted immune cells. But these transfusions offer a limited benefit to patients. Additionally, granulocyte transfusions require large numbers of donor cells and must be given repeatedly.
“Our work demonstrates a potential alternative to granulocyte transfusions that uses a fraction of the number of cells in a single infusion,” concludes senior author Katherine King, Associate Professor of Pediatric Infectious Diseases at Baylor College of Medicine and Texas Children’s Hospital, Houston. “If our findings are verified by further studies, this could pave the way to a much-needed treatment alternative for sepsis patients.”
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By investigating changes in the metabolic profile of neural stem cells, a research team led by Professor Dr. Matteo Bergami from the CECAD Cluster of Excellence for Aging Research at the University of Cologne discovered that the protein YME1L is essential in coordinating the shift between cellular proliferation (cell division) and quiescence (a resting state). The protein YME1L is responsible for balancing the conversion of the brain’s neural stem cells, which are limited in number and cannot be produced again, into neurons. Defects in the functioning of this protein can lead to a premature conversion of neural stem cells into specialized cells, and hence impair neural regeneration in the long term. The article ‘Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L’ has been published in Cell Reports.
Neural stem cells are maintained in only a few regions of the adult mammalian brain, where they sustain the production of new neurons throughout life. Understanding how neural stem cell activity is regulated and maintained in these regions has critical implications for regenerative approaches following brain trauma and disease. Mutations in YME1L have also been linked to brain disorders and intellectual disability in human patients.
YME1L is a protease (an enzyme which cleaves other proteins) localized in mitochondria, the powerhouses of the cells. As for other mitochondrial proteases, YME1L plays an important role in the quality control of proteins within mitochondria. By analysing the level of those proteins known to be targeted by YME1L, the scientists now found that the enzymatic activity of YME1L precisely reflects different metabolic states in neural stem cells. Higher YME1L activity marks a quiescent (dormant) state while lower YME1L activity matches with a proliferative state.
This balance in YME1L activity is required to maintain the stemness properties of neural stem cells, as impairments in YME1L function force cells to exit their status of stem cells and prematurely specialize into different types of nerve cells, leading to the overall loss of stem cells from brain tissue. Ultimately, this stem cell loss has a major impact on the long-term neurogenic capacity of the brain, as no further neurons can be produced.
‘Our results show that the activity of a single mitochondrial protease can significantly affect the fate of neural stem cells and the production rate of new nerve cells. These findings not only reveal a new layer of regulation in the biology of neural stem cells but may also have important implications for patients bearing mutated YME1L,’ Bergami said.
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It was a medical mystery: When University of Pittsburgh School of Medicine scientists induced a particular genetic mutation in mouse eggs, the resulting embryos would all die in the womb within a week.
And yet, people with the same troublesome gene are thriving.
“This gene is clearly very deleterious — the mice did not even develop a heartbeat, let alone survive to birth,” said Cecilia Lo, Ph.D., distinguished professor and F. Sargent Cheever Chair of Pitt’s Department of Developmental Biology. “That led us to wonder: How are people who we know have this gene walking around?”
The team found that a protective gene was countering the bad one, explaining why some people with this very deleterious gene not only survived but did so with only an atrial septal defect — a hole in the heart. The findings — reported today in Cell Reports Medicine — provide valuable clinical and personal information to guide families with a history of the disease and could lead to future genetic treatments.
Congenital heart disease is one of the most common birth defects, affecting about 1% of live births. Atrial septal defects — which involve a hole in the wall between the upper chambers of the heart, allowing blood to flow in ways that can damage the heart and lungs — are among the most common forms of congenital heart disease, affecting as many as 10,000 babies born in the U.S. each year.
Working with Brian Feingold, M.D., M.S., medical director of the pediatric heart failure and heart transplant programs at UPMC Children’s Hospital of Pittsburgh, Lo’s team obtained genetic samples from eight members of a family who all had large atrial septal defect. Whole genome sequencing revealed that they all carried an extremely rare mutation in a gene called TPM1 that didn’t appear in more than 900 unrelated samples from people with congenital heart disease; worldwide, it has been seen only twice.

Researchers have successfully used CRISPR-Cas9 to edit the genomes of the black-legged tick. To accomplish this feat, they developed an embryo injection protocol that overcame a major barrier in the field.The work appears February 15 in the journal iScience.
“Despite their capacity to acquire and pass on an array of debilitating pathogens, research on ticks has lagged behind other arthropod vectors, such as mosquitoes, largely because of challenges in applying available genetic and molecular tools,” says Monika Gulia-Nuss (@gulianusslab) a co-senior author of the study and a molecular biologist at the University of Nevada, Reno.
“Having genome-editing tools available will allow us to unlock some of the secrets of the tick genome and allow us to determine how these unique animals survive in the environment, how they interact with pathogens, and how we might prevent ticks from spreading diseases to humans and livestock,” she says.
Despite the public health relevance of ticks — which are vectors of a wide variety of pathogens to humans, wildlife, and domestic animals — knowledge of the biology of ticks on a molecular level is still limited. This is in contrast to insects such as mosquitoes, for which numerous tools for transgenic development and genome editing are now available. “Progress in this area is critical for the advancement of research to solve the growing problem of tick-borne diseases,” says Andrew Nuss, the other co-senior author of the study and an entomologist at the University of Nevada, Reno.
CRISPR-Cas9 has revolutionized functional genetics research in many organisms. This gene-editing technique has been applied to mosquitoes and other arthropod disease vectors, but successful gene editing has not yet been reported in ticks. Technical challenges for injecting tick embryos to attempt gene editing have further slowed research progress. Tick embryos are extremely difficult to inject because of high pressure inside the eggs, a hard chorion (the outer shell of the egg), and a wax layer outside the embryo that must be removed before injection. Female ticks use a specialized organ called Gene’s organ to coat their eggs with a tough wax layer.
In the iScience study, the researchers developed a successful tick-embryo injection protocol and targeted gene disruption with CRISPR-Cas9 using two methods: embryo injection and Receptor-Mediated Ovary Transduction of Cargo (ReMOT Control) — a less-labor-intensive method of gene editing in arthropods. The researchers ablated Gené’s organ to prevent wax deposition and then treated the eggs with chemicals called benzalkonium chloride and sodium chloride to remove the chorion and to decrease the pressure inside the eggs.
“We were able to carefully dissect gravid female ticks to surgically remove the organ responsible for coating the eggs with wax, but still allowing the females to lay viable eggs. These wax-free eggs permitted injection of tick embryos with materials necessary for genome modification,” Gulia-Nuss says. “Another major challenge was understanding the timing of tick embryo development. So little is known about tick embryology that we needed to determine the precise time when to introduce CRISPR-Cas9 to ensure the greatest chance of inducing genetic changes.”
The survival rate of injected embryos was approximately 10%, comparable to well-established insect models. For ReMOT Control, all injected ticks survived. The data show the feasibility of tick embryo injection and genetic manipulation in ticks by both methods, which had comparable editing efficiency for the Proboscipedia (ProbP) gene, which is expressed in appendages.
“Previously, no lab has demonstrated genome modification is possible in ticks. Some considered this too technically difficult to accomplish,” Nuss says. “This is the first study to demonstrate that genetic transformation in ticks is possible by not only one, but two different methods.”
More research is needed to fully understand the molecular mechanisms underlying efficient gene editing in ticks. While these tools will accelerate tick genetic research, improvements are needed in the embryo injection protocol to enhance survival and larval hatching and gene-editing efficiencies.
“We expect that the tools we developed here will open new research avenues that will dramatically accelerate our understanding of the molecular biology of this and related tick species,” Gulia-Nuss says. “Targeted disruption of genes in tick vectors of human pathogens is a powerful method to uncover the underlying biology of tick-pathogen-host interactions that can inform the development and application of new approaches to tick-borne disease control.”
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A modeling study raises questions about how far respiratory droplets, like those that transmit the virus that causes COVID-19, can travel before becoming harmless. Can the airborne particles that carry the virus remain infectious not just for a few feet but rather more than 200 feet, farther than the length of a hockey rink?
Experiments dating to the 1930s proposed two paths for respiratory droplets like those from a sneeze or cough. Either they are big and heavy, plummeting to the ground without much chance of infecting another person. Or they are so small and light that they dry out almost instantly, remaining airborne but becoming harmless very quickly. The dryness renders “enveloped” viruses like coronaviruses unable to infect.
But a new study from scientists at the Department of Energy’s Pacific Northwest National Laboratory suggests a third option — that small respiratory particles can remain moist and airborne for a longer time and greater distance than scientists have recognized.
“There are reports of people becoming infected with a coronavirus downwind of an infected person or in a room several minutes after an infected person has exited that room,” said Leonard Pease, the corresponding author of the study. The findings were published in the February issue of the journal International Communications in Heat and Mass Transfer.
“The idea that enveloped virions may remain well hydrated and thus fully infective at substantial distances is consistent with real-world observations. Perhaps infectious respiratory droplets persist longer than we have realized,” Pease added.
The PNNL team took a long look at the mucus that coats the respiratory droplets that people spew from their lungs. Scientists know that mucus allows many viruses to travel further than they otherwise would, enabling them to journey from one person to another.

Vaccine-associated myocarditis shows a similar injury pattern on cardiac MRI compared to other causes of myocarditis, but abnormalities are less severe, according to a new study published in the journal Radiology.
Myocarditis, or inflammation of the heart muscle, often occurs as a result of a viral infection, including COVID-19. It can affect the heart’s rhythm and ability to pump blood and may leave behind lasting damage in the form of scarring of the heart muscle. Myocarditis has also been reported as a rare complication of the messenger RNA (mRNA)-based COVID-19 vaccines.
Cardiac MRI has an important role in the assessment of acute myocarditis with unparalleled ability for noninvasive characterization of myocardial tissue. Understanding the pattern and extent of myocardial injury and its implications will allow for improved care of these patients and may help to address vaccine hesitancy.
Therefore, cardiac radiologist Kate Hanneman, M.D., M.P.H., and colleagues at University Health Network, University of Toronto, set out to determine the pattern and extent of cardiac MRI findings in myocarditis associated with COVID-19 vaccination and to compare these findings to other causes of myocarditis, including COVID-19.
“We know that the risk of myocarditis following COVID-19 vaccination is very low. However, there is very limited data on the extent of injury in the heart in comparison to other causes of myocarditis,” Dr. Hanneman said.
For this retrospective study, the researchers analyzed data from 92 consecutive adult patients with myocarditis and abnormalities on cardiac MRI performed at a tertiary referral hospital between 2019 and 2021. Patients were classified into one of three groups: myocarditis following COVID-19 vaccination, myocarditis following COVID-19 illness, and myocarditis not associated COVID-19 vaccination or illness.

For at least six months after COVID-19 vaccination, antibodies produced by immune cells become steadily more formidable and more precisely targeted against the virus that causes COVID-19, according to a study of the antibody response to the Pfizer-BioNTech vaccine by researchers at Washington University School of Medicine in St. Louis.
The idea that antibodies increase in quality as they decrease in quantity will come as no surprise to immunologists. The process was described in animals by Washington University immunologists Herman Eisen, MD, and Gregory Siskind, MD, in 1964. But this study, published Feb. 15 in Nature, is the first to track the maturation of the antibody response in detail in people.
The findings suggest that declining antibody levels in the months after vaccination primarily represent a shift to a sustainable immune response. Producing vast quantities of antibodies burns a lot of energy. The immune system cannot sustain such a high level of activity indefinitely, so it gradually switches to producing smaller amounts of more powerful antibodies.
Even quite low levels of antibodies would continue to provide some protection against disease, the researchers said — as long as the virus doesn’t change.
“If the virus didn’t change, most people who got two doses of this vaccine would be in very good shape,” said senior author Ali Ellebedy, PhD, an associate professor of pathology & immunology, of medicine and of molecular microbiology. “The antibody response we saw is exactly what we’d expect from a robust immune response. We never thought that six months following that second injection, many people would still be actively improving the quality of their antibodies. To me, that is remarkable. The problem is that this virus keeps evolving and producing new variants. So, the antibodies are getting better at recognizing the original strain, but unfortunately the target keeps changing.”
Immune cells that produce antibodies are from the B cell family. Following the B cell response through all of its stages — from initiation through peak antibody production to the emergence of memory cells that can quickly churn out new antibodies the next time the body encounters the same virus — requires repeatedly taking samples from parts of the body that can be hard to access. At different stages in the process, key members of the B cell family are located in the blood, the lymph nodes and the bone marrow. Getting B cells from the lymph nodes is technically challenging and involves using ultrasound to locate minuscule immune structures called germinal centers within the lymph nodes. Obtaining a sample of bone marrow involves inserting a needle into the pelvic bone.