Publisher Health

Kickstarting the brain’s natural ability to adjust to new circumstances, or neuroplasticity, improves how effectively a cochlear implant can restore hearing loss, a new study in deaf rats shows. The investigation, researchers say, may help explain the extreme variation in hearing improvements experienced by implant recipients.
Unlike hearing aids, which amplify, balance, and sharpen incoming sound, cochlear implants send electrical signals that represent sounds directly to the brain. Unfortunately, experts say, it can take time to understand the meaning of the signals. Past studies had shown that, while some cochlear implant users understand some speech hours after receiving their device, others required months or years to do so. However, the mechanisms that determine how quickly the brain can adjust to an implant have been unclear.
Led by researchers at NYU Langone Health, the new investigation in rats evaluated whether stimulating the locus coeruleus, a major site of neuroplasticity deep in the brainstem of mammals, improved how quickly they learned to use their devices. It showed that within just three days of receiving their implants, rodents given the extra boost could effectively complete tasks that required accurate hearing. By contrast, those without the stimulation needed up to 16 days to do so.
“Our findings suggest that differences in neuroplasticity, particularly in parts of the brain such as the locus coeruleus, may help explain why some cochlear implant users improve faster than others,” says study lead author and neuroscientist Erin Glennon, PhD, a medical student at NYU Grossman School of Medicine.
In an earlier investigation, the research team found that electrically stimulating the locus coeruleus in rodents increases neuroplasticity and changes how the brain’s hearing system represents sound. However, the new study, publishing online Dec. 21 in the journal Nature, is the first to demonstrate that stimulating this brain region hastens hearing among cochlear implant recipients, according to Glennon.
For the investigation, the study authors trained normal hearing rats to press a button after they heard a particular sound and to ignore the button if they heard a different tone. Once deafened, the rats were unable to complete the task. Then they were given cochlear implants and retrained to perform the same challenge by relying on the device.
Among the findings, the study showed that locus coeruleus activity changed dramatically as the rats learned to use their implants. At first, the brain region was most active when the animals received food after hearing the tone and pressing the correct button. As they learned to associate pressing the button with receiving the reward, activity instead peaked when they just heard the tones. Notably, the faster this change occurred, the faster the rats consistently succeeded at the task.
“Our results suggest that improving neuroplasticity in the locus coeruleus may speed up and bolster the effectiveness of cochlear implants,” says study co-senior author and neuroscientist Robert Froemke, PhD, the Skirball Foundation Professor of Genetics in the Department of Neuroscience and Physiology at NYU Langone.
Froemke says the team next plans to explore ways of stimulating the brain region in humans that do not require invasive surgery. Froemke also serves as a professor in Department of Otolaryngology — Head and Neck Surgery at NYU Langone.
“Since our goal is to activate the locus coeruleus, we need to determine what noninvasive mechanisms may be used to trigger the brain region,” says study co-senior author Mario Svirsky, PhD. Svirsky is the Noel L. Cohen Professor of Hearing Science in the Department of Otolaryngology — Head and Neck Surgery at NYU Langone.
Svirsky, also a professor in NYU Langone’s Department of Neuroscience and Physiology, cautions that the rats’ hearing was examined using simple sounds in a straightforward task, while humans need to respond to nuanced speech patterns in noisy environments. Further research, he says, is needed into other brain regions that may be involved.
Funding for the study was provided by National Institutes of Health grants F30DC017351, T32GM007308, R01DC003937, R01DC012557, P30CA016087, and P41EB017183. Additional funding support was provided by Cochlear Ltd, a NYU vendor, which also sells equipment and technical support to NYU Langone. The terms and conditions of these agreements are being managed in accordance with the policies of the health system.

Whether radiation exposure of fathers can have consequences on their children is one of the most long-standing questions in radiation biology. Using the nematode Caenorhabditis elegans as a model, Professor Dr Björn Schumacher and his team discovered that radiation damage to mature sperm cannot be repaired but is instead passed on to the offspring. In contrast, female eggs either accurately repair the damage or, if the damage is too severe, are eliminated and no damage is passed on. However, when the egg is fertilized with a sperm that has been damaged by radiation, the maternal repair proteins that are provided by the egg try to repair the paternal DNA.
For this purpose, a highly error-prone repair mechanism is used and fuses the broken DNA pieces randomly. These random fusions of the breaks then lead to structural changes in the paternal chromosomes. The offspring that result from this now carry the chromosome damage and in turn their offspring show severe developmental defects. The work done on C. elegans lays the foundation for a better understanding of the mechanisms for the heritable effects of paternal radiation exposure.
This work has now been published under the title ‘Inheritance of paternal DNA damage by histone-mediated repair restriction’ in Nature.
The offspring that results from male animals that have been exposed to radiation and healthy female worms carry on the so-called structural variations — random connections of chromosome parts. In the offspring, these aberrations lead to recurrent breaks but this damage can no longer be repaired. Instead, the damaged chromosomes are shielded from accurate repair by proteins, so-called histones, that densely pack the long strands of DNA. In the densely packed DNA, the breaks can no longer be reached by the repair proteins. The packed DNA structures are held tightly together by the specific histone proteins, HIS-24 and HPL-1. When those histone proteins are removed, the paternally inherited damage is completely eliminated and viable offspring can be produced. The finding that histone proteins govern the accessibility of DNA for repairs could provide effective therapeutic targets for treating radiation damage.
Is this also relevant for radiation damage in humans? In addition to the work on nematodes, the team detected the same structural variants, or randomly assembled chromosomes, in humans. Also here, the chromosome aberrations were specifically passed on from the fathers but not the mothers. For this, the scientists analysed various data sets from the 1000 Genome Project that contains genetic data from more than a thousand people and the Islandic deCODE project with genetic data from the respective mothers, fathers and children.
“Genome aberrations, especially structural variations in chromosomes, which develop in the paternal germline, are thought to increase the risk of disorders like autism and schizophrenia,” Schumacher said. This means that also in humans, mature sperm needs to be especially protected from radiation damage, and damaged mature sperm should not be used for conception. He added, “Such damage could potentially be inflicted during radiotherapy or chemotherapy and thus pose a risk in the two months that it takes to generate new sperm to replace the damaged one.” This is because in contrast to mature sperm, newly generated sperm have the capacity to accurately repair the damage.
Interestingly, the scientists found those structural variations in the chromosomes also in nematodes in the wild and in the human population. These results suggest that damage to mature sperm and the inaccurate repair of paternal DNA in the zygote could be major drivers for genetic diversity during evolution and might be responsible for genetic diseases in humans.
The study was carried out at the Institute for Genome Stability in Ageing and Disease at the CECAD Cluster of Excellence for Aging Research in the University of Cologne and received funding from the German Research Foundation (DFG).
Story Source:
Materials provided by University of Cologne. Note: Content may be edited for style and length.

Evolutionary pressure across male mammals to guarantee the procreation of their own offspring led to a rapid evolution of the testicle. Bioinformatic studies — conducted by an international team of researchers led by Prof. Dr Henrik Kaessmann from the Center for Molecular Biology of Heidelberg University — show that this pressure particularly accelerated the evolution of later stages of sperm formation. The aim of these contrastive studies was, for the first time, to decode the genetic regulation of sperm formation in various species of mammals and in human beings, thereby tracing the evolution of this spermatogenesis. At the same time, the researchers were also able to detect genes whose activity had remained unchanged in the course of evolution.
Spermatogenesis in the testicle is controlled by a finely coordinated, complex interplay of the activity of different genes — also known as gene expression. Hitherto the understanding of these genetic programmes had been largely confined to the mouse. “Consequently little was known about the genetic foundations that constitute the big differences in spermatogenesis across different mammals, both with regard to the number of sperm cells formed and also to their properties,” explains Noe Mbengue, a doctoral researcher in Prof. Kaessmann’s group “Evolution of the mammalian genome.” The Heidelberg scientists have now succeeded in defining the expression of all genes at the level of individual cells during the whole of spermatogenesis for ten different mammals. The organisms they studied represent all major groups of mammals and include humans as well as their closest relatives, great apes. To do so, the researchers used state-of-the-art single-cell genomics technologies.
Based on this data they were subsequently able to trace the evolution of spermatogenesis with the aid of bioinformatic comparisons between the different mammals. According to Prof. Kaessmann, these comparative studies uncovered a time-related pattern. “While the genetic programmes in the early stages of spermatogenesis are very similar among mammals, in later stages they differ greatly; that means that the rapid evolution of the testicle is a result of major differences in cells during late spermatogenesis,” underlines Dr Florent Murat, a former postdoc in Henrik Kaessmann’s research group and now a group leader at the National Research Institute for Agriculture, Food and Environment (INRAE) in Rennes (France). Further analyses by the scientists revealed genes whose activity had remained unchanged in the course of evolution. They regulate fundamental processes of sperm cell formation that are the same for all mammals. “Hence our data also supplies valuable elements for researching fertility disorders in men,” Prof. Kaessmann explains.
Finally, the scientists’ data enabled them for the first time to distinguish sperm cells that carry either an X or a Y chromosome and thus determine the sex of the offspring. With the aid of this division, the researchers succeeded in systematically studying the gene expression on these sex chromosomes. As these investigations showed, gene expression on the sex chromosomes of all male mammals is downregulated during the maturation division known as meiosis. This mechanism is presumably fundamental for preventing a disadvantageous genetic exchange between the X and Y chromosome during meiosis.
The results of the study on the evolution of spermatogenesis across mammals were published in the journal Nature. The European Research Council, the German Research Foundation, the Australian Research Council and the Novo Nordisk Foundation supported the investigations.
Story Source:
Materials provided by Heidelberg University. Note: Content may be edited for style and length.

The most comprehensive lung cell atlas to date, from the Wellcome Sanger Institute and collaborators, has revealed 11 new lung cell types and offers detailed insight into an immune process involved in fighting lung infections.
Published today (21 December 2022) in Nature Genetics, this freely available resource highlights multiple immune cells, barrier cells, and their environments in the lung that are implicated in respiratory diseases and infections.
This new lung cell atlas, which is part of the wider international Human Cell Atlas Initiative*, combined single cell sequencing with spatial transcriptomics to provide a fuller picture of how cells interact and communicate with each other.
While single cell studies have advanced the understanding of lung function, the lungs are made up of complex structures and environments that cannot be investigated by single cell sequencing alone. For example, there are many unanswered questions about how the cells are organised and how specific cell types, especially rare cell types, contribute to lung disease.
Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) and interstitial lung disease, are leading causes of death worldwide1. Understanding communication between cells within their local environment in healthy lungs can help determine what is disrupted in disease, and give clues on how to prevent or treat this.
In this study, researchers from the Wellcome Sanger Institute and collaborators, genetically profiled nearly 200,000 cells from lung tissue of 13 donors, discovering 11 new cell types, and showing the exact location of 80 cell types in total.

New research from the University of Virginia School of Medicine and collaborators reveals how microorganisms found in our guts can worsen dangerous C. difficile infections. The discovery could help doctors identify patients at risk for severe illness and open the door to new treatments.
C. difficile is a bacterium that can cause potentially deadly infections, particularly among the elderly and people on long-term antibiotics. These infections are characterized by diarrhea, nausea and fever. C. diff, as it is commonly known, strikes more than 350,000 Americans a year. Once infected, patients are prone to suffer re-infections; among those who survive, one in six will develop another case within eight weeks, according to the federal Centers for Disease Control and Prevention. As such, C. diff can be a major problem for hospitals and nursing facilities.
UVA’s new findings help explain why certain patients are at particular risk. The researchers determined that a group of antibiotic-resistant “opportunistic pathogens” found in the gut called enterococci can make C. diff more potent and dangerous.
“The interactions between C. diff, other microbes and the human gut are highly complex. This study leveraged expertise from a large, multidisciplinary team across several institutions to disentangle these complex interactions and discover key mechanisms that help C. diff cause disease,” said researcher Jason Papin, PhD, of UVA’s Department of Biomedical Engineering, a joint program of the School of Medicine and School of Engineering. “With this greater understanding, we have an opportunity to develop new therapeutic strategies to treat this dangerous infection.”
A More Dangerous C. difficile
Enterococci are bacteria that can, on their own, cause dangerous infections that are difficult to treat. For example, they can cause meningitis, urinary tract infections (which can be very serious in the elderly) and the painful gastrointestinal disease diverticulitis, as well as other illnesses. But the researchers found that the threat they pose does not end there.
The research team collected stool samples from patients with C. difficile infections at Vanderbilt University Medical Center, Children’s Hospital of Philadelphia and the Hospital of the University of Pennsylvania. They then used a combination of lab tests and advanced computer modeling to better understand how C. diffinteracts with other microorganisms in the gut.
They found that enterococci make for a dangerous ally for C. diff. Enterococci produce amino acids, including leucine and ornithine, which make C. difficile a more potent threat for patients whose gut compositions have been disrupted by antibiotics.
Papin and his team developed powerful computer models that helped the researchers understand and predict the complex changes in the gut. Their work, combined with lab research performed in other labs, showed that enterococci can dramatically reshape the “metabolome” — the collection of metabolites such as amino acids — in the gut. These changes, the researchers report, ultimately reprogram C. difficile and enhance its disease-causing behaviors.
“The computational modeling that Matthew Jenior [UVA postdoctoral fellow in the Papin lab] performed was instrumental in discovering the role of amino acids in the interaction between C. diff and enterococci,” Papin said. “The computational models that Matthew constructed will continue to help us better understand the molecular processes in C. diff that cause disease.”
By better understanding how C. diff interacts with enterococci and other microorganisms in the gut, doctors will be better positioned to battle this common and serious infection, the researchers say.
“Biology is a data-rich science and the power of computational models to use these data is only in its infancy,” Papin said. ” We’re excited about the innumerable opportunities to use data science and computer modeling to drive biological discovery.”

Making an intentional effort to recognize positive life events and achievements while gathering for food and drink will leave you feeling more socially supported, new research shows.
The research, published online in the Journal of Public Policy & Marketing, finds that celebrations with three conditions — social gathering, eating or drinking, and intentionally marking a positive life event — will increase perceived social support. Perceived social support, according to previous research, is the belief you have a social network that will be there for you in case of future, negative life events. That belief is associated with health and well-being outcomes, including increased life-span and decreased anxiety and depression.
“Many celebrations this time of year include two of the three conditions — eating and drinking while gathering together,” said Kelley Gullo Wight, assistant professor at the Indiana University Kelley School of Business and co-author of the study. “Adding the third condition, making an intentional effort to recognize other’s positive achievements, is key. For example, take the time to congratulate someone for getting accepted to their first-choice university, or a work project that went well, or a new job offer. This will maximize the benefits to your well-being and the well-being of all the attendees at that holiday party.”
Wight and her co-authors, including professors Danielle Brick of the University of Connecticut, and James Bettman, Tanya Chartrand, and Gavan Fitzsimons of Duke University, used behavioral experiments to survey thousands of participants over several years.
The research revealed that even if gatherings are virtual, if everyone has food and drink (no matter if it’s healthy or indulgent) and they’re celebrating positive events, this also increases a person’s perceived social support, and they can receive the same well-being benefits from it.
It also has implications for marketing managers or anyone looking to raise funds for a good cause.
“We found that when people feel supported socially after a celebration, they’re more ‘pro-social,’ and more willing to volunteer their time or donate to a cause,” said Danielle Brick, assistant professor of marketing at the University of Connecticut and co-author on the study. “This would be a good time for non-profits to market donation campaigns, around the time many people are celebrating positive life events, like holidays or graduations.”
The researchers note that hosting celebrations that increase perceived social support can be especially beneficial at places serving populations more at-risk of loneliness and isolation, like nursing homes or community centers.
They also note the importance of understanding the well-being benefits of celebrations for policymakers looking to implement regulations or measures that could impact social gatherings, like COVID lockdowns, to avoid negative consequences to mental health. They recommend that if organizers need to have virtual celebrations, they should involve some type of consumption and the marking of a separate, positive life event, so people leave the celebration feeling socially supported.
Story Source:
Materials provided by Indiana University. Note: Content may be edited for style and length.

Rising to meet the formidable challenge of the timely diagnosis of dementia, research scientists from Regenstrief Institute, IUPUI and the medical schools of Indiana University and University of Miami are conducting the Digital Detection of Dementia study, a real-world evaluation of the use of an artificial intelligence (AI) tool they developed for early identification of Alzheimer’s disease and related dementias in primary care, the setting where most adults receive healthcare. Individuals identified as cognitively impaired will be referred for diagnostic services.
The AI tool, called a passive digital marker, is a machine learning algorithm the researchers developed, trained and tested. The tool uses natural language processing to cull unstructured information in combination with structured data from a patient’s electronic health record. These could include mention of memory issues, a notation of vascular concerns, comorbid conditions or other factors potentially linked to dementia.
“Between 50 to 80 percent of dementia cases are unrecognized by the healthcare system in the U.S. And, if you include patients living with mild cognitive impairment, that number might actually climb to higher than 80 percent of cases that are not recognized,” said Regenstrief Institute and Indiana University School of Medicine faculty member Malaz Boustani, M.D., MPH, senior author of the Digital Detection of Dementia study protocol paper, published in the peer reviewed journal Trials. “In this new study we are evaluating the practical use of our tool when used alone and when used with an accompanying patient-reported outcomes survey.
“Unfortunately, the lay public believe there’s nothing you can do if you find out you or a family member has Alzheimer’s disease, but that is not true. Over the past 20 years we have developed, validated and have been operating a comprehensive collaborative care model for dementia that reduces the disease burden for the patient, reduces caregiver stress and reduces inappropriate hospitalizations, keeping people living at home longer and lowering overall costs to them and to the healthcare system,” he said.
Few primary care practices are designed for the timely detection of Alzheimer’s disease. The limited time that primary care clinicians have to spend with patients, the need to focus on the health problems which brought the patient to the clinic, as well as the stigma of dementia are the major reasons for lack of recognition of the condition, according to Dr. Boustani. In addition, he notes, there is no demand from the public for dementia diagnoses, most likely driven by the stigma of dementia, lack of public knowledge about benefits of early recognition of Alzheimer’s, and issues related to health insurance coverage.
The first aspect of the Digital Detection of Dementia study is a clinical trial, already underway in Indianapolis enrolling patients seen in primary care clinics at federally qualified health centers affiliated with Eskenazi Health. The participants in this trial are expected to be predominantly people who are Black and reside in urban areas. The second clinical trial of the study commences early in 2023 in Miami, Florida, at University of Miami primary care clinics. The participants are expected to be predominantly Hispanic and include a high percentage of rural residents.

Nothing beats a good soak in a hot bath, and when it really hits the spot, you can almost feel your worries and ailments diffusing out into steam.
Perhaps there is nowhere better to treat what ails you than the hot springs at the historical city of Beppu, located on the north-east shores of Kyushu. Not only does the city boast the most onsen — Japanese for hot springs — in the country, it is also a research hotbed for investigating the health benefits of onsen and treatments based on them.
In a paper published in Scientific Reports, researchers from Kyushu University’s Beppu Hospital report that onsen bathing in the evening hours is linked to lower prevalence of hypertension in Japanese adults over 65.
Humanity’s history with hot springs can be found as far back as ancient Egypt over 5,000 years ago. Onsen themselves are even referenced in Japan’s oldest books and creation myths, and people have touted the health benefits of soaking in hot springs well into the modern age.
In 1931, Kyushu University founded the ‘Onsen Therapy Research Institute’ in the historical city of Beppu to study the therapeutic benefits of onsen. Over the 90 years since, the institute has grown to cover a range of modern medical fields including internal and external medicine, rehabilitation, gynecology, and cardiology. Nonetheless, it still conducts research on the health benefits of onsen and continues to make a name for itself as a national hot spring treatment research center.
“In 2011, the institute partnered with the city and conducted a massive survey of Beppu residents over 65 about their health and onsen habits,” explains Satoshi Yamasaki, a Lecturer of internal medicine at the Beppu Hospital and first author of the study. “This is something we can uniquely do here in Beppu because onsen are a part of everybody’s daily lives, especially for the elderly. There are local onsen facilities everywhere, and you can even connect onsen to your home utilities.”
The survey collected information regarding medical history, onsen habits, and even the type of onsen frequented from over 11,000 people — nearly one-third of Beppu city residents over 65. Since then, researchers like Yamasaki have been going through the trove of data, analyzing the connection between health and onsen use.
“I wanted to find out if long-term onsen bathing had any preventative effects on hypertension. Past research has shown that traditional thermal therapy and hot spring bathing are effective against various diseases including hypertension,” continues Yamasaki. “In Japan especially, it is the leading cause of hospital visits and long-term prescription medication use.”
In their data set, the team was able to pull out 4,001 individuals who currently have, or a history of, hypertension. Their first analysis found that having hypertension also increased the likelihood for the individual to have a history of other pathologies.
“These were the usual suspects of pathologies correlated with hypertension such as gout, arrhythmia, renal disease, and diabetes,” Yamasaki explains. “But it was when we looked at an individual’s onsen habits that we found something interesting. We found that individuals who bathed in onsen after 19:00 were roughly 15% less likely to have hypertension.”
The team hypothesizes two main reasons for these findings: lower stress and faster sleep onset. Previous research has shown that faster onset of sleep can improve sleep quality and improved hypertension control. Moreover, thermal therapies such as sauna bathing have been shown to alter levels of stress markers in the blood and lead to better mitigation of hypertension.
“Of course, we must acknowledge some limitations in our study. Selection bias is expected whenever a questionnaire is used. We also could not account for the respondent’s daily lifestyle that could affect hypertension, or if they are being treated for hypertension medically or with onsen,” concludes Yamasaki. “Nonetheless, we found that habitual nighttime onsen bathing was associated with a lower prevalence of hypertension. To understand these results further, we will need more data from patients.”
Story Source:
Materials provided by Kyushu University. Note: Content may be edited for style and length.

Researchers at the University of Tokyo have used artificial DNA to target and kill cancer cells in a completely new way. The method was effective in lab tests against human cervical cancer- and breast cancer-derived cells, and against malignant melanoma cells from mice. The team created a pair of chemically synthesized, hairpin-shaped, cancer-killing DNA. When the DNA pairs were injected into cancer cells, they connected to microRNA (miRNA) molecules that are overproduced in certain cancers. Once connected to the miRNA, they unraveled and joined together, forming longer chains of DNA which triggered an immune response. This response not only killed the cancer cells but prevented further growth of cancerous tissue. This method is different from conventional anticancer drug treatments and is hoped to bring about a new era of drug development.
Cancer is a sadly familiar global health concern and current methods of treatment have their limitations. However, drugs based on nucleic acids — namely DNA and RNA, the vital information-carrying molecules — can control the biological functions of cells, and are expected to transform the future of medicine and provide a significant boost towards efforts to overcome cancer and other hard-to-treat illnesses, caused by viruses and genetic diseases.
A research group at the University of Tokyo, led by Assistant Professor Kunihiko Morihiro and Professor Akimitsu Okamoto from the Graduate School of Engineering, were inspired to create a new anticancer drug using artificial DNA. “We thought that if we can create new drugs that work by a different mechanism of action from that of conventional drugs, they may be effective against cancers that have been untreatable up to now,” said Okamoto.
Nucleic acid drug use for cancer treatment has been challenging because it is difficult to make the nucleic acids distinguish between cancer cells and other healthy cells. This means there is a risk of adversely affecting the patient’s immune system if healthy cells are inadvertently attacked. However, for the first time, the team was able to develop a hairpin-shaped DNA strand that can activate a natural immune response to target and kill specific cancerous cells.
Cancer cells can overexpress, or make too many copies of, certain DNA or RNA molecules, causing them to not function normally. The team created artificial oncolytic (cancer-killing) hairpin DNA pairs called oHPs. These oHPs were triggered to form longer DNA strands when they encountered a short (micro) RNA called miR-21, which is overexpressed in some cancers. Typically, oHPs don’t form longer strands due to their curved hairpin shape. However, when the artificial oHPs enter a cell and encounter the target microRNA, they open up to combine with it and form a longer strand. This then causes the immune system to recognize the presence of the overexpressed miR-21 as dangerous and activate an innate immune response, which ultimately leads to the death of the cancer cells.
The tests were effective against overexpressed miR-21 found in human cervical cancer-derived cells, human triple-negative breast cancer-derived cells, and mouse malignant melanoma-derived cells. “The formation of long DNA strands due to the interaction between short DNA oHPs and overexpressed miR-21, found by this research group, is the first example of its use as a selective immune amplification response which can target tumor regression, providing a new class of nucleic acid drug candidates with a mechanism that is completely different from known nucleic acid drugs,” said Okamoto.
“The results of this study are good news for doctors, drug discovery researchers and cancer patients, as we believe it will give them new options for drug development and medication policies. Next, we will aim for drug discovery based on the results of this research, and examine in detail the drug efficacy, toxicity and potential administration methods.” This research still has many steps to go before a treatment can be made available, but the team is confident in the benefits of nucleic acids for new drug discovery.
Funding:
This work was supported by JST ACT-X (JPMJAX1911 to K.M.) JSPS KAKENHI (19K15408 and 20H04698 to K.M., and 21K19040 to A.O.) AMED Grant (JP22ym0126805j0001 to A.O.) and the Hitachi Global Foundation (the Kurata Grants to K.M.).
Story Source:
Materials provided by University of Tokyo. Note: Content may be edited for style and length.

Viruses such as SARS-CoV-2, influenza virus and others travel from person to person essentially by hitchhiking on aerosols. These are finely dispersed particles containing liquid suspended in the air that an infected person expels when coughing, sneezing, or simply exhaling, and can be inhaled by someone else.
That’s why it is generally seen as important to ventilate rooms effectively and filter indoor air: lowering aerosol particle concentrations in homes, offices and public transport vehicles can reduce the risk of infection.
How do suspended particles become acidic?
It’s not clear how long viruses in aerosols remain infectious. Some studies suggest that the humidity and temperature of the air may play a role in virus persistence. A factor that has been underestimated so far is the exhaled aerosols’ chemical composition, in particular its acidity and its interactions with the indoor air. Many viruses, such as influenza A virus, are acid-sensitive; exhaled aerosol particles can absorb volatile acids and other airborne substances, among them acetic acid, nitric acid or ammonia, from the indoor air, which in turn affects the acidity (pH) levels of the particles.
No research had yet been conducted on the effect the acidification of aerosols post exhalation has on the viral load they carry. Now a team of researchers from ETH Zurich, EPFL and the University of Zurich has investigated exactly that.
In a new study, they show for the first time how the pH of aerosol particles changes in the seconds and hours after exhalation under different environmental conditions. Further, they show how this impacts the viruses contained in the particles. The study has just been published in the journal Environmental Science & Technology.