New AI diagnostic can predict COVID-19 without testing

New AI diagnostic can predict COVID-19 without testing

Researchers at King's College London, Massachusetts General Hospital and health science company ZOE have developed an artificial intelligence diagnostic that can predict whether someone is likely to have COVID-19 based on their symptoms. Their findings are published today in Nature Medicine.

The AI model uses data from the COVID Symptom Study app to predict COVID-19 infection, by comparing people's symptoms and the results of traditional COVID tests. Researchers say this may provide help for populations where access to testing is limited. Two clinical trials in the UK and the US are due to start shortly.

More than 3.3 million people globally have downloaded the app and are using it to report daily on their health status, whether they feel well or have any new symptoms such as persistent cough, fever, fatigue and loss of taste or smell (anosmia).

In this study, the researchers analysed data gathered from just under 2.5 million people in the UK and US who had been regularly logging their health status in the app, around a third of whom had logged symptoms associated with COVID-19. Of these, 18,374 reported having had a test for coronavirus, with 7,178 people testing positive.

The research team investigated which symptoms known to be associated with COVID-19 were most likely to be associated with a positive test. They found a wide range of symptoms compared to cold and flu, and warn against focusing only on fever and cough. Indeed, they found loss of taste and smell (anosmia) was particularly striking, with two thirds of users testing positive for coronavirus infection reporting this symptom compared with just over a fifth of the participants who tested negative. The findings suggest that anosmia is a stronger predictor of COVID-19 than fever, supporting anecdotal reports of loss of smell and taste as a common symptom of the disease.

The researchers then created a mathematical model that predicted with nearly 80% accuracy whether an individual is likely to have COVID-19 based on their age, sex and a combination of four key symptoms: loss of smell or taste, severe or persistent cough, fatigue and skipping meals. Applying this model to the entire group of over 800,000 app users experiencing symptoms predicted that just under a fifth of those who were unwell (17.42%) were likely to have COVID-19 at that time.

Researchers suggest that combining this AI prediction with widespread adoption of the app could help to identify those who are likely to be infectious as soon as the earliest symptoms start to appear, focusing tracking and testing efforts where they are most needed.

Professor Tim Spector from King's College London said: "Our results suggest that loss of taste or smell is a key early warning sign of COVID-19 infection and should be included in routine screening for the disease. We strongly urge governments and health authorities everywhere to make this information more widely known, and advise anyone experiencing sudden loss of smell or taste to assume that they are infected and follow local self-isolation guidelines."

Story Source:

Materials provided by King's College London. Note: Content may be edited for style and length.

---

Journal Reference:

1. Cristina Menni, Ana M. Valdes, Maxim B. Freidin, Carole H. Sudre, Long H. Nguyen, David A. Drew, Sajaysurya Ganesh, Thomas Varsavsky, M. Jorge Cardoso, Julia S. El-Sayed Moustafa, Alessia Visconti, Pirro Hysi, Ruth C. E. Bowyer, Massimo Mangino, Mario Falchi, Jonathan Wolf, Sebastien Ourselin, Andrew T. Chan, Claire J. Steves, Tim D. Spector. Real-time tracking of self-reported symptoms to predict potential COVID-19. Nature Medicine, 2020; DOI: 10.1038/s41591-020-0916-2

Vitamin D at High Dose Can Worsen MS, Early Study Says

High-dose vitamin D supplements appear to aggravate inflammation and myelin loss in the brain and spinal cord, and worsen the disability associated with multiple sclerosis (MS), a study in a mouse disease model reported.

Excessive use of vitamin D causes calcium levels to spike, which directly increase the inflammatory state of immune cells and their capacity to infiltrate the central nervous system (CNS; the brain and spinal cord), the researchers observed.

Supplements given in moderation, however, may help to ease disease symptoms.

The findings were presented at the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) Forum 2020, held Feb. 27–29 in Florida, in the poster “High Dose Vitamin D Worsens Experimental CNS Autoimmune Disease By Raising T Cell-excitatory Calcium.” The presenter was Sebastian Torke, PhD, with the Institute of Neuropathology, University Medical Center in Göttingen, Germany.

A large body of data suggests that low vitamin D levels raise a person’s risk of developing MS. But whether or not vitamin supplements should be given to people who already have the disease is under debate.

In general, MS patients have relatively low levels of vitamin D. Based on studies showing an association between low levels of this vitamin and a higher risk of relapses and earlier disability, doctors often recommend oral vitamin D3 (cholecalciferol) supplements to their patients.

Yet, it is unclear whether such supplements offer therapeutic benefits to MS patients, and if they do, what doses should be advised. While relatively low doses of vitamin D appear to be safe, high doses are likely toxic and potentially harmful.

Researchers set out to model the consequences of this common practice by investigating the effects of long-term vitamin D supplements given to mice.

They fed mice a diet containing either a low concentration (less than 5 IU of vitamin D3/kg of food), a standard amount (1,500 IU/kg), or a high dose (75,000 IU/kg) of vitamin D3 for 15 weeks (about three and a half months).

These three doses were chosen to generate serum levels of 25-hydroxyvitamin D [25(OH)D] — the molecule measured in a vitamin D blood test — reflective of what is typically seen in patients with vitamin D deficiency (less than 30 nmol/l), in those taking modest supplements and achieving normal vitamin D levels (100 nmol/l), and in those with disproportionally high supplements (250 nmol/l).

All three diets contained identical calcium (1%) and phosphate (0.7%) concentrations.

Researchers then induced MS-like disease in the mice and followed their clinical symptoms, CNS inflammation and damage, and immune cell behavior.

Results showed that, compared to MS mice not given supplements, a moderate dose of vitamin D eased disease severity, which was linked to an expansion of regulatory T-cells — immune cells that help to keep immune responses in check.

The opposite, however, happened in mice fed a high-dose vitamin D diet.

“High-dose, long-term vitamin D supplementation lead to much worse disease in these mice,” Torke said.

The animals had excessively high levels of the vitamin in the blood (above 200 nmol/l), and developed “fulminant” disease with severe and persistent disability. This was associated with massive CNS inflammation and the infiltration of activated  T helper 1 (Th1) and Th17 cells — immune cells that can cause inflammation and autoimmune disease — as well as demyelination (loss of myelin), a hallmark of MS.

Researchers decided that calcium is likely at fault for what they considered an “unexpected outcome.”

High-dose vitamin D caused calcium levels to rise to excessive amounts (hypercalcemia) throughout the body, triggering the activation, proliferation, and inflammatory behavior of  T-cells.

Supporting these findings, the researchers also found that exposing mice or human T-cells in vitro (in the lab) to various concentrations of calcium (equivalent to those found in vitamin D-fed mice) increased the entry of calcium into cells, and triggered the activation of pro-inflammatory pathways.

“It is not vitamin D that is bad, but too much vitamin D leads to increased calcium [levels] that promote T-cell proliferation and activation,” Torke said.

Calcium also enhances the ability of T-cells to cross the blood-brain barrier — a highly selective membrane that regulates which substances or cells carried in blood can enter the brain or spinal cord — reflecting a greater ability to infiltrate the CNS.

Inducing hypercalcemia in mice was enough to activate T-cells, confirming that this effect can also occur in a living organism (in vivo).

“These findings highlight excessive vitamin D supplementation and resulting hypercalcemia as novel risk factors promoting worsening of CNS demyelinating disease,” Torke said.

“Our data caution that in light of the currently limited information on a direct beneficial effect of vitamin D in MS, MS patients may be at danger of experiencing untoward immunological and/or clinical effects when vitamin D is supplemented excessively,” Torke concluded.

Dozens of non-oncology drugs can kill cancer cells

Cancer treatment concept (stock image).

Drugs for diabetes, inflammation, alcoholism -- and even for treating arthritis in dogs -- can also kill cancer cells in the lab, according to a study by scientists at the Broad Institute of MIT and Harvard and Dana-Farber Cancer Institute. The researchers systematically analyzed thousands of already developed drug compounds and found nearly 50 that have previously unrecognized anti-cancer activity. The surprising findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.

"We thought we'd be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many," said Todd Golub, chief scientific officer and director of the Cancer Program at the Broad, Charles A. Dana Investigator in Human Cancer Genetics at Dana-Farber, and professor of pediatrics at Harvard Medical School.

The new work appears in the journal Nature Cancer. It is the largest study yet to employ the Broad's Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs). The study also marks the first time researchers screened the entire collection of mostly non-cancer drugs for their anti-cancer capabilities.

Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin's cardiovascular benefits. "We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way," said study first author Steven Corsello, an oncologist at Dana-Farber, a member of the Golub lab, and founder of the Drug Repurposing Hub.

The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad's Cancer Cell Line Encyclopedia (CCLE). Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment. The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.

They found nearly 50 non-cancer drugs -- including those initially developed to lower cholesterol or reduce inflammation -- that killed some cancer cells while leaving others alone.

Some of the compounds killed cancer cells in unexpected ways. "Most existing cancer drugs work by blocking proteins, but we're finding that compounds can act through other mechanisms," said Corsello. Some of the four-dozen drugs he and his colleagues identified appear to act not by inhibiting a protein but by activating a protein or stabilizing a protein-protein interaction. For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilizing the interaction between PDE3A and another protein called SLFN12 -- a previously unknown mechanism for some of these drugs.

These unexpected drug mechanisms were easier to find using the study's cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.

Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs.

The researchers were also able to predict whether certain drugs could kill each cell line by looking at the cell line's genomic features, such as mutations and methylation levels, which were included in the CCLE database. This suggests that these features could one day be used as biomarkers to identify patients who will most likely benefit from certain drugs. For example, the alcohol dependence drug disulfiram (Antabuse) killed cell lines carrying mutations that cause depletion of metallothionein proteins. Compounds containing vanadium, originally developed to treat diabetes, killed cancer cells that expressed the sulfate transporter SLC26A2.

"The genomic features gave us some initial hypotheses about how the drugs could be acting, which we can then take back to study in the lab," said Corsello. "Our understanding of how these drugs kill cancer cells gives us a starting point for developing new therapies."

The researchers hope to study the repurposing library compounds in more cancer cell lines and to grow the hub to include even more compounds that have been tested in humans. The team will also continue to analyze the trove of data from this study, which have been shared openly (https://depmap.org) with the scientific community, to better understand what's driving the compounds' selective activity.

"This is a great initial dataset, but certainly there will be a great benefit to expanding this approach in the future," said Corsello.

This collaboration involved the Broad's Center for the Development of Therapeutics, the PRISM team, the Cancer Data Sciences team, and the labs of Todd Golub and Matthew Meyerson. The work was funded in part by SIGMA (Carlos Slim Foundation, Slim Initiative in Genomic Medicine for the Americas), the National Institutes of Health, and an anonymous donor.

---

Story Source:

Materials provided by Broad Institute of MIT and Harvard. Original written by Leah Eisenstadt. Note: Content may be edited for style and length.

Pig-Pen effect: Mixing skin oil and ozone can produce a personal pollution cloud

Ozone can produce a personal pollution cloud

When ozone and skin oils meet, the resulting reaction may help remove ozone from an indoor environment, but it can also produce a personal cloud of pollutants that affects indoor air quality, according to a team of researchers.

In a computer model of indoor environments, the researchers show that a range of volatile and semi-volatile gases and substances are produced when ozone, a form of oxygen that can be toxic, reacts with skin oils carried by soiled clothes, a reaction that some researchers have likened to the less-than-tidy Peanuts comic strip character.

"When the ozone is depleted through human skin, we become the generator of the primary products, which can cause sensory irritations," said Donghyun Rim, assistant professor of architectural engineering and an Institute for CyberScience associate, Penn State. "Some people call this higher concentration of pollutants around the human body the personal cloud, or we call it the 'Pig-Pen Effect.'"

The substances that are produced by the reaction include organic compounds, such as carbonyls, that can irritate the skin and lungs, said Rim. People with asthma may be particularly vulnerable to ozone and ozone reaction products, he said.

According to the researchers, who reported their findings in a recent issue of Nature's Communications Chemistry, skin oils contain substances, such as squalene, fatty acids and wax esters. If a person wears the same clothes too long -- for example, more than a day -- without washing, there is a chance that the clothes become more saturated with the oils, leading to a higher chance of reaction with ozone, which is an unstable gas.

"Squalene can react very effectively with ozone," said Rim. "Squalene has a higher reaction rate with ozone because it has a double carbon bond and, because of its chemical makeup, the ozone wants to jump in and break this bond."

Indoors, ozone concentration can range from 5 to 25 parts per billion -- ppb -- depending on how the air is circulating from outside to inside and what types of chemicals and surfaces are used in the building. In a polluted city, for example, the amount of ozone in indoor environments may be much higher.

"A lot of people think of the ozone layer when we talk about ozone," said Rim. "But, we're not talking about that ozone, that's good ozone. But ozone at the ground level has adverse health impacts."

Wearing clean clothes might be a good idea for a lot of reasons, but it might not necessarily lead to reducing exposure to ozone, said Rim. For example, a single soiled t-shirt helps keep ozone out of the breathing zone by removing about 30 to 70 percent of the ozone circulating near a person.

"If you have clean clothes, that means you might be breathing in more of this ozone, which isn't good for you either," said Rim.

Rim said that the research is one part of a larger project to better understand the indoor environment where people spend most of their time.

"The bottom line is that we, humans, spend more than 90 percent of our time in buildings, or indoor environments, but, as far as actual research goes, there are still a lot of unknowns about what's going on and what types of gases and particles we're exposed to in indoor environments," said Rim. "The things that we inhale, that we touch, that we interact with, many of those things are contributing to the chemical accumulations in our body and our health."

Rather than advising people whether to wear clean or dirty clothes, the researchers suggest that people should focus on keeping ground ozone levels down. Better building design and filtration, along with cutting pollution, are ways that could cut the impact of the Pig-Pen Effect, they added.

To build and validate the models, the researchers used experimental data from prior experiments investigating reactions between ozone and squalene, and between ozone and clothing. The researchers then analyzed further how the squalene-ozone reaction creates pollutants in various indoor conditions.

The team relied on computer modeling to simulate indoor spaces that vary with ventilation conditions and how inhabitants of those spaces manage air quality, Rim said.

In the future, the team may look at how other common indoor sources, such as candle and cigarette smoke, could affect the indoor air quality and its impact on human health.

---

Story Source:

Materials provided by Penn State. Original written by Matt Swayne. Note: Content may be edited for style and length.

Social media stress can lead to social media addiction

Social media stress can lead to social media addiction

Social network users risk becoming more and more addicted to social media platforms even as they experience stress from their use.

Social networking sites (SNS) such as Facebook and Instagram are known to cause stress in users, known as technostress from social media. However, when faced with such stress, instead of switching off or using them less, people are moving from one aspect of the social media platforms to another -- escaping the causes of their stress without leaving the medium on which it originated.

Research into the habits of 444 Facebook users revealed they would switch between activities such as chatting to friends, scanning news feeds and posting updates as each began to cause stress. This leads to an increased likelihood of technology addiction, as they use the various elements of the platform over a greater timespan.

Researchers from Lancaster University, the University of Bamberg and Friedrich-Alexander Univeristät Erlangen-Nürnberg, writing in Information Systems Journal, found that users were seeking distraction and diversion within the Facebook platform as a coping mechanism for stress caused by the same platform, rather than switching off and undertaking a different activity.

Professor Monideepa Tarafdar, Professor of Information Systems and Co-Director of the Centre for Technological Futures at Lancaster University Management School, who co-authored the study, said: "While it might seem counter-intuitive, social media users are continuing to use the same platforms that are causing them stress rather than switching off from them, creating a blurring between the stress caused and the compulsive use."

Assistant Professor Christian Maier, of the University of Bamberg, who collected the data from the Facebook users along with Professor Sven Laumer, Schöller Endowed Professor and Chair of Information Systems and the Deputy Director of the Dr. Theo und Friedl Schöller Research Center. said: "Because social network sites offer such a wide range of features, users can find they act both as stressors and as a distraction from that stress."

"Even when users are stressed from SNS use, they are using the same platforms to cope with that stress, diverting themselves through other activities on the SNS, and ultimately building compulsive and excessive behaviour. As a result, they embed themselves in the social network environment rather than getting away from it, and an addiction is formed."

The research team looked at various different forms of technostress caused by using social media, such users feeling that SNS were invading their personal life, adapting their SNS use to conform to that of their friends, experiencing excessive social demands and too much social information, and facing constant changes and updates to the SNS platform.

They further examined two separate ways of coping with the stress. The first included users creating a diversion by partaking in other activities away from social media, which is the more obvious path. They would switch off, talk to friends or family about issues they were experiencing and spend less time on the platform.

However, the other method consisted of diversion through engaging in different activities within the same SNS app itself, and potentially moving on a pathway towards SNS addiction. This method was more prevalent among those social media users who used the sites more regularly.

Professor Sven Laumer said: "We found that those users who had a greater social media habit- needed less effort to find another aspect of the platforms, and were thus more likely to stay within the SNS rather than switch off when they needed to divert themselves. The stronger the user's SNS habit, the higher the likelihood they would keep using it as a means of diversion as a coping behaviour in response to stressors, and possibly develop addiction to the SNS."

"Users go to different areas of the platform which they see as being separate and that they use in different ways. With Facebook, there are features that take you into different worlds within the same platform. You can be in many different places all from the same application, for example following friends' activities, posting pictures about daily activities, switching to a chat feature or playing games."

Professor Monideepa Tarafdar added: "The idea of using the same environment that is causing the stress as means of coping with that stress is novel. It is an interesting phenomenon that seems distinctive to technostress from social media."

---

Story Source:

Materials provided by Lancaster University. Note: Content may be edited for style and length.

Milk from teeth: Dental stem cells can generate milk-producing cells

Milk from teeth

The ability of adult stem cells to generate various tissue-specific cell populations is of great interest in the medical and dental research fields. These cells can replace damaged cells and therefore represent a good alternative to classical medical treatments for tissue regeneration. This may even allow the de novo formation of entire tissues and organs in the future.

Dental stem cells capable of regenerating mammary gland

Dental epithelial stem cells are able to generate all epithelial cell types of the teeth; however, it was not yet clear whether these cells could also produce non-dental cell populations. In a recent paper published in the open access journal Cells, a team of researchers led by Thimios Mitsiadis, professor at the Institute of Oral Biology of the University of Zurich (UZH), has shown for the first time that epithelial stem cells isolated from the continuously growing incisors of young mice are indeed able to form mammary glands in female mice.

In a first set of experiments, after removing all cells of mammary origin, dental epithelial stem cells and mammary epithelial cells were directly injected into the areas where the mammary glands normally develop. The researchers used advanced genetic, molecular and imaging tools that allow the precise follow-up of the transplanted dental stem cells in the mammary gland fat pad of the animals. "The results show that the dental stem cells contribute to mammary gland regeneration, and are able to generate all mammary cell populations and, even more strikingly, milk-producing cells," says Mitsiadis.

This work demonstrates the exceptional plasticity of dental epithelial stem cells to generate not only dental tissues but also other tissues of the body. "These findings represent a major contribution to the understanding of the cellular and molecular mechanisms involved in the regenerative capacity of dental stem cells, and, furthermore, indicate the clinical potential of these specific stem cell populations," Mitsiadis adds.

Stem cell-based therapies could be used for breast tissue regeneration

In a second set of experiments, dental epithelial stem cells were injected alone, without mammary epithelial cells. In this case, the dental stem cells were also able to form small ductal systems consisting of branching rudiments. However, in some cases this resulted in the formation of cysts. "This plasticity might be unique for dental epithelial stem cells, since all other non-mammary epithelial cells examined so far have never shown the ability to generate mammary ducts without the support of mammary epithelial cells," states co-author Pierfrancesco Pagella from the Institute of Oral Biology.

One of the most severe pathological conditions is breast cancer, which is often treated with surgery. "Our discovery that dental epithelial stem cells are able to replace cells from the mammary gland opens up new paths for developing stem cell-based therapies that could be used for breast regeneration in the future," says Thimios Mitsiadis.

---

Story Source:

Materials provided by University of Zurich. Note: Content may be edited for style and length.

Stressed to the max? Deep sleep can rewire the anxious brain

Deep sleep concept

When it comes to managing anxiety disorders, William Shakespeare's Macbeth had it right when he referred to sleep as the "balm of hurt minds." While a full night of slumber stabilizes emotions, a sleepless night can trigger up to a 30% rise in anxiety levels, according to new research from the University of California, Berkeley.

UC Berkeley researchers have found that the type of sleep most apt to calm and reset the anxious brain is deep sleep, also known as non-rapid eye movement (NREM) slow-wave sleep, a state in which neural oscillations become highly synchronized, and heart rates and blood pressure drop.

"We have identified a new function of deep sleep, one that decreases anxiety overnight by reorganizing connections in the brain," said study senior author Matthew Walker, a UC Berkeley professor of neuroscience and psychology. "Deep sleep seems to be a natural anxiolytic (anxiety inhibitor), so long as we get it each and every night."

The findings, published today, Nov. 4, in the journal Nature Human Behaviour, provide one of the strongest neural links between sleep and anxiety to date. They also point to sleep as a natural, non-pharmaceutical remedy for anxiety disorders, which have been diagnosed in some 40 million American adults and are rising among children and teens.

"Our study strongly suggests that insufficient sleep amplifies levels of anxiety and, conversely, that deep sleep helps reduce such stress," said study lead author Eti Ben Simon, a postdoctoral fellow in the Center for Human Sleep Science at UC Berkeley.

In a series of experiments using functional MRI and polysomnography, among other measures, Simon and fellow researchers scanned the brains of 18 young adults as they viewed emotionally stirring video clips after a full night of sleep, and again after a sleepless night. Anxiety levels were measured following each session via a questionnaire known as the state-trait anxiety inventory.

After a night of no sleep, brain scans showed a shutdown of the medial prefrontal cortex, which normally helps keep our anxiety in check, while the brain's deeper emotional centers were overactive.

"Without sleep, it's almost as if the brain is too heavy on the emotional accelerator pedal, without enough brake," Walker said.

After a full night of sleep, during which participants' brain waves were measured via electrodes placed on their heads, the results showed their anxiety levels declined significantly, especially for those who experienced more slow-wave NREM sleep.

"Deep sleep had restored the brain's prefrontal mechanism that regulates our emotions, lowering emotional and physiological reactivity and preventing the escalation of anxiety," Simon said.

Beyond gauging the sleep-anxiety connection in the 18 original study participants, the researchers replicated the results in a study of another 30 participants. Across all the participants, the results again showed that those who got more nighttime deep sleep experienced the lowest levels of anxiety the next day.

Moreover, in addition to the lab experiments, the researchers conducted an online study in which they tracked 280 people of all ages about how both their sleep and anxiety levels changed over four consecutive days.

The results showed that the amount and quality of sleep the participants got from one night to the next predicted how anxious they would feel the next day. Even subtle nightly changes in sleep affected their anxiety levels.

"People with anxiety disorders routinely report having disturbed sleep, but rarely is sleep improvement considered as a clinical recommendation for lowering anxiety," Simon said. "Our study not only establishes a causal connection between sleep and anxiety, but it identifies the kind of deep NREM sleep we need to calm the overanxious brain."

On a societal level, "the findings suggest that the decimation of sleep throughout most industrialized nations and the marked escalation in anxiety disorders in these same countries is perhaps not coincidental, but causally related," Walker said. "The best bridge between despair and hope is a good night of sleep."

Co-authors of the study are Aubrey Rossi and Allison Harvey, both at UC Berkeley.

---

Story Source:

Materials provided by University of California - Berkeley. Original written by Yasmin Anwar. Note: Content may be edited for style and length.

Insulin can increase mosquitoes' immunity to West Nile virus

Mosquito

A discovery by a Washington State University-led research team has the potential to inhibit the spread of West Nile virus as well as Zika and dengue viruses.

In a study published today in the journal Cell Reports, researchers demonstrated that mammalian insulin activated an antiviral immunity pathway in mosquitoes, increasing the insects' ability to suppress the viruses.

Mosquito bites are the most common way humans are infected with flaviviruses, a virus family that includes West Nile, dengue and Zika. In humans, both West Nile and dengue can result in severe illness, even death. Zika has been linked to birth defects when pregnant women are infected.

"It's really important that we have some sort of protection against these diseases because currently, we don't have any treatments. If we're able to stop the infection at the level of the mosquito, then humans wouldn't get the virus," said Laura Ahlers, the study's lead author and a recent Ph.D. graduate from WSU. Ahlers is now a post-doctoral fellow with the National Institutes of Health in Bethesda, Maryland.

Working first with fruit flies, which have similar immune responses to mosquitoes, Ahlers and her colleagues identified an insulin-like receptor in the insects that, when activated, inhibits the replication of the West Nile virus in the flies. The researchers then elicited this same response in mosquitoes by feeding them blood containing elevated insulin. Subsequent tests showed activating this receptor was also effective in suppressing dengue and Zika in insect cells.

While it was already known that insulin boosts immune responses in mosquitoes, this is the first time insulin's connection to a particular immune response pathway, called JAK/STAT, has been identified. It is a significant step toward the long-term goal of creating an intervention, said Alan Goodman, WSU assistant professor and the corresponding author on the paper.

"If we can activate this arm of immunity through the insulin receptor in the mosquito, we can reduce the overall viral load in the mosquito population," Goodman said. "If the mosquitoes are carrying less virus when they bite you, they will transmit less of the virus, and there's a better chance you won't acquire the disease."

---

Story Source:

Materials provided by Washington State University. Original written by Sara Zaske. Note: Content may be edited for style and length.