Tag Archives: Pathogens

A coat against our troubles: new compound can transform air filters into pathogen-killing machines

A joint research venture between the University of Birmingham and private firms NitroPep Ltd and Pullman AC has produced air filters that are highly effective at killing bacteria, fungi, and viruses, including the SARS-CoV 2 virus, the infamous coronavirus.

Image via Pixabay.

The secret of these filters’ effectiveness is a chemical called chlorhexidine digluconate (CHDG). This is a potent biocide that can kill pathogens within seconds of coming into contact with them. Air filters coated in this substance can prove to be a powerful tool against airborne pathogens around the world, according to the researchers that designed them.

Removing the gunk

“The COVID-19 pandemic has brought to the forefront of public consciousness the real need for new ways to control the spread of airborne respiratory pathogens. In crowded spaces, from offices to large indoor venues, shopping malls, and on public transport, there is an incredibly high potential for transmission of COVID-19 and other viruses such as flu,” says Dr. Felicity de Cogan, Royal Academy of Engineering Industry Fellow at the University of Birmingham, and corresponding author of the paper.

“Most ventilation systems recycle air through the system, and the filters currently being used in these systems are not normally designed to prevent the spread of pathogens, only to block air particles. This means filters can actually act as a potential reservoir for harmful pathogens. We are excited that we have been able to develop a filter treatment which can kill bacteria, fungi and viruses—including SARS-CoV-2—in seconds. This addresses a global un-met need and could help clean the air in enclosed spaces, helping to prevent the spread of respiratory disease.”

The filters were tested in both laboratory and real-life conditions to determine how effective they were at removing air-borne pathogens, and the results are stellar.

In the lab, the filters were covered with viral particles of the Wuhan strain of SARS-CoV-2, alongside control filters. They were then checked periodically over a period of more than one hour to see how these pathogens fared. While much of the initial quantity of viral particles remained on the surface of the control filters for the experiment’s length, all SARS-CoV-2 cells were destroyed within 60 seconds on the treated filters.

Experiments involving bacteria and fungi that commonly cause illness in humans — such as E. coli, S. aureus, and C. albicans— yielded similar results. This showcases the wide applicability of the filters.

To determine how well these fitlers would perform in real-life situations, treated filters were installed in the heating, ventilation, and air conditioning systems on train carriages in the UK alongside control filters in matched pairs on the same train line. These were left to operate for three months before being removed and sent to the lab for analysis — which involved the researchers counting any bacteria colonies that survived on the filters.

No pathogens were found on the treated filters, the team explains. Furthermore, this step showed that the treatment was durable enough to withstand three months of real-world use while maintaining their structure, filtration functions, and anti-pathogen abilities.

“The technology we have developed can be applied to existing filters and can be used in existing heating, ventilation and air conditioning systems with no need for the cost or hassle of any modifications,” Dr. de Cogan explains. “This level of compatibility with existing systems removes many of the barriers encountered when new technologies are brought onto the market.”

NitroPep Ltd is now building on these findings in order to deliver a final marketable version of the coating.

The paper “Efficacy of antimicrobial and anti-viral coated air filters to prevent the spread of airborne pathogens” has been published in the journal Nature Scientific Reports.

15,000-year-old viruses found in Tibetan glacier ice — and we know nothing about them

The viruses, recovered from two ice core samples taken from the Tibetan Plateau, are new species to science, and they’re unlike anything we’ve ever seen. Researchers say these could help us shed new light on viral evolution, but concerns also loom.

Yao Tandong, left, and Lonnie Thompson, right, process an ice core drilled from the Guliya Ice Cap in the Tibetan Plateau in 2015. The ice held viruses nearly 15,000 years old, a new study has found. Credit: Lonnie Thompson, The Ohio State University.

There are diseases in the ice

In a sense, glaciers are time capsules, preserving information from thousands of years ago. This information can relate to past climate, atmospheric chemistry, or even past inhabitants.

“These glaciers were formed gradually, and along with dust and gasses, many, many viruses were also deposited in that ice,” said Zhi-Ping Zhong, lead author of the study and a researcher at The Ohio State University Byrd Polar and Climate Research Center who also focuses on microbiology. “The glaciers in western China are not well-studied, and our goal is to use this information to reflect past environments. And viruses are a part of those environments.”

Viruses and other microbes can survive thousands of years, frozen in ice. In a new study conducted by researchers from Ohio State University, researchers analyzed ice cores from the Guliya ice cap in the Tibetan Plateau. The cores, which date as far back as 14,4000 years ago, revealed 33 viruses, 28 of which were completely unknown to science.

Identifying and classifying viruses is harder than with other species, and the process of cataloging them typically takes a while. Still, the viruses would have thrived in cold environments, the researchers believe, based on the genetic analysis.

“These are viruses that would have thrived in extreme environments,” said Matthew Sullivan, co-author of the study, professor of microbiology at Ohio State and director of Ohio State’s Center of Microbiome Science. “These viruses have signatures of genes that help them infect cells in cold environments—just surreal genetic signatures for how a virus is able to survive in extreme conditions. These are not easy signatures to pull out, and the method that Zhi-Ping developed to decontaminate the cores and to study microbes and viruses in ice could help us search for these genetic sequences in other extreme icy environments—Mars, for example, the moon, or closer to home in Earth’s Atacama Desert.”

The researchers were careful to avoid contamination. When studying microbes, it’s always important to ensure that you’re not bringing your own microbes into the mix. So researchers first decontaminated the surface of the ice core, and then looked at the untainted parts. This method could also come in handy when looking for microbes on other planets (or satellites).

Growing importance

While this could help us better understand how viruses evolved and adapted to extreme environments, it’s also becoming increasingly important to study viruses and other pathogens frozen in ice.

So far, this is only the third study to identify viruses in glaciers, and it may pay to carry out more studies of this type. As temperatures continue to rise as a result of man-made greenhouse gas emissions, more and more ice will continue to melt — not just from glaciers, but also from ice caps and permafrost. Ice that has remained frozen for thousands of years is about to melt, bringing dormant viruses and bacteria back to life.

“We know very little about viruses and microbes in these extreme environments, and what is actually there,” Thompson said. “The documentation and understanding of that is extremely important: How do bacteria and viruses respond to climate change? What happens when we go from an ice age to a warm period like we’re in now?”

The study has been published in the journal Microbiome.

Want to avoid new pandemics? Preserving biodiversity is step one, research argues

A growing body of evidence is already showing that preventing new pandemics like COVID-19 will require addressing biodiversity loss from human activities such as deforestation and agriculture. Now, a new study has synthesized the current understanding of how biodiversity affects human health and why it’s so important to preserve and protect it. 

Image credit: Flickr / Ali Rajabali.

Felicia Keesing, a Bard College professor and lead author of the paper, says it’s a myth that wild areas with high levels of biodiversity represent hotspots for diseases. The more animal diversity, the more pathogens — the myth goes. But this is plain wrong, Keesing says. Biodiversity itself isn’t a threat, quite the contrary: it protects us from the species that carry pathogens. 

Zoonotic diseases such as Ebola, SARS, and COVID-19 are caused by pathogens that jump to humans from other species. A pathogen might travel from one host to another in droplets or aerosols from coughs or sneezes; through bodily fluids; through fecal material; or by being transferred during the bite of a vector. It’s never easy to figure out how the next virus may jump.

Cross-species transmission results from a complex interplay between the characteristics of the pathogen, the original host’s infection, behavior, and ecology, how the pathogen is shed into and survives in the environment, how humans are exposed to the pathogen, and how susceptible those humans are to infection. So it’s not that more species directly means more risk — it’s more about how we interact with those species, and how they interact with each other.

Natural biodiversity (and its loss) can affect this pathway at multiple points, potentially affecting the probability that a new pathogen will become established in humans. But do diverse communities of host species serve as sources for new pathogens? Recent research seems to suggest that’s not the case.

“Research is mounting that species that thrive in developed and degraded landscapes are often much more efficient at harboring pathogens and transmitting them to people. In less-disturbed landscapes with more animal diversity, these risky reservoirs are less abundant and biodiversity has a protective effect,” Rick Ostfeld, co-author of the paper, said in a statement.

The researchers argued that innate biodiversity can reduce the risk of infectious diseases through a dilution effect, in which species in diverse communities dilute the impact of host species that thrive when diversity declines. This happens when the transmission of a pathogen increases as diversity declines, as has been demonstrated for a number of disease systems.

Despite abundant evidence for the dilution effect, the more general idea that biodiversity can reduce human disease risk has been controversial, in large part because biodiversity was thought to be a source of new zoonotic pathogens via spillover. This is why we need to reconcile the effects of biodiversity on the emergence and ongoing transmission, Ostfeld and Keesing said.

Human impacts like land-use change have been linked to emerging infectious diseases of humans in many studies. When this happens, long-lived and larger-bodied species tend to disappear first, while smaller-bodied species with fast life histories tend to proliferate. Bats, primates and rodents have been highlighted as the ones more likely to transmit pathogens to humans. 

“When we erode biodiversity, we favor species that are more likely to be zoonotic hosts, increasing our risk of spillover events,” Ostfeld said. “Managing this risk will require a better understanding of how things like habitat conversion, climate change, and overharvesting affect zoonotic hosts, and how restoring biodiversity to degraded areas might reduce their abundance.”

The researchers argued we debating the importance of one taxonomic group or another and instead focus on the host attributes linked with diseases transmissions. Getting a better understanding of the features of effective zoonotic hosts such as their habitat preferences and resilience to disturbance will be essential to protect public health, they argued. 

The study was published in the journal PNAS. 

Robots might soon be sanitizing hospital rooms, killing far more bacteria than humans

With drug-resistant bacteria being more dangerous than ever, we need all the help we can get.

Image credits: Infection Prevention Technologies / Youtube.

Technology could help temper this ever-growing problem — hospital infections are running rampant, but they may be pushed back by ultraviolet (UV) Robots.

Current cleaning techniques, almost always manual, are nearly helpless in tackling resilient bacteria. This is where the disinfection robots enter the stage.

At certain wavelengths, UV light is mutagenic to bacteria, viruses, and other microorganisms. Particularly at wavelengths around 260 to 270 nanometers (the visible range is around 380 to 750 nanometers), UV light breaks molecular bonds within microorganismal DNA, severely disabling or killing the organisms.

The use of UV as a disinfectant isn’t new. It’s been used in medical sanitation and sterile work facilities since the mid-20th century, and more recently, it’s also been used to sterilize drinking and wastewater facilities.

Now, researchers have fitted UV lamps on disinfection robots which ensure full-room sterilization. Nursing homes, field hospitals, and biohazard zones could all be sterilized in a matter of minutes. The robots are faster and more efficient than human workers, and their ability to move around enables them to cover the entirety of the room, including shadowy areas and corners, as well as door handles and bed frames.

Infection Prevention Technologies (iPT), the company which built the robot, has reportedly tested the technology and found that after 10 minutes, the rooms were completely sterilized. This could go a long way towards reducing hospital infections.

“A 6-month, hospital-wide study showed a 34% drop in the incidence of healthcare associated infections with the use of the IPT 3200 UV robot and specially trained disinfection teams.” iPT claims.

Results have been presented in a new paper.

“One of the problems facing our healthcare system is hospital-associated infections,” says Nicholas Fitzkee, an independent scientist of the paper. Infections cost “thousands of lives and billions of dollars annually”, he adds.

Another advantage of the technology is that it requires minimal human intervention: just one person to guide and monitor the robot.

At the currently used levels, the radiation is harmless to humans. However, it’s still recommended that humans exit the room during the sterilization process.

According to the World Health Organization, drug-resistant pathogens are one of the biggest threats to mankind, and things are only expected to get worse. The CDC also warns that unusual germs with unusual drug-resistance are now widespread in the US. Technologies such as UV sanitizing could go a long way towards fighting that problem where it matters most (hospitals) and kill off some of the most resilient pathogens.

Disease surprise.

Why the WHO put a mysterious ‘Disease X’ on its most-feared list

The World Health Organisation (WHO) has added a mysterious affliction — dubbed ‘Disease X’ — to the list of diseases they fear could start a global pandemic in the future.

Disease surprise.

Image credits: Bruno Glätsch.

Each year, the Geneva-based WHO — tasked with monitoring and safeguarding world health — convenes a high-level meeting of senior scientists, listing diseases that risk prompting a major international public health emergency. Contenders are weighed primarily on their potential to rapidly epidemics of huge proportions, even global pandemics, as well as the real-life damage they have proven capable of.

In previous years, the listing was made up of viruses that had seen outbreaks in recent years, such as Ebola, Zika, Lassa fever, or Sars (severe acute respiratory syndrome). But for the first time the WHO introduces a mysterious condition on the list, dubbed “Disease X“.

Eyes on the horizon

Despite its name, disease X is not spread around by one group of highly-gifted mutant children in both comic and film. In fact, it’s not actually ‘real’ in the strict sense of the word — Disease X is a hypothetical virus. It’s something that could emerge and then go on to cause widespread infection across the globe.

Luckily, for now, it all hinges on that ‘could’. Disease X is a placeholder: a reminder not to get complacent in our fight against would-be pathogens.

“Disease X represents the knowledge that a serious international epidemic could be caused by a pathogen currently unknown to cause human disease”, the WHO said in a statement.

The statement went on to explain that adding it to the list should help promote and guide “research and development preparedness that is relevant for an unknown Disease X as far as possible.” The mysterious nature of the disease is meant to ensure flexible planning of diagnostics tests and vaccine strategies, so that that they may be applied to a wide range of possible scenarios.

“History tells us that it is likely the next big outbreak will be something we have not seen before”, John-Arne Rottingen, chief executive of the Research Council of Norway and a scientific adviser to the WHO committee, said for The Telegraph.

“We want to see ‘plug and play’ platforms developed which will work for any, or a wide number of diseases; systems that will allow us to create countermeasures at speed.”

Disease X could spring up from a lot of different sources and infect us via innumerable vectors, Mr. Rottingen says, although zoonotic transmission (an animal virus evolving to infect humans) is the most likely. Ebola, salmonella, and HIV are believed to be zoonoses.

In modern times, humans have spread across the face of the planet, inhabiting and shaping virtually all ecosystems. This has also brought us in closer contact and closer contact with more species of animals than ever before, exponentially increasing the likelihood of zoonoses.

“It’s a natural process and it is vital that we are aware and prepare. It is probably the greatest risk,” Mr. Rotingen adds.

Given the rapid development of gene-editing technologies, Disease X could also spring up from human error or malevolence — in which case, having a flexible, widely-applicable plan of action is of paramount importance. Last week’s events showed just how far the reticence of governmental or private actors on using chemical and bio-weapons has decayed, further fanning concerns that Disease X might come from a human laboratory.

Whatever the case may be, the WHO hopes its list will spur governments across the globe to invest more into strengthening local health systems. Primary care systems (local doctors and nurses) are key to safeguarding public health, as they’re our best bet for detecting outbreaks of a new disease early on, and containing it before it spreads.

The WHO says it omitted several groups of diseases, such as hemorrhagic fevers and emergent non-polio enteroviruses from its priority list. However, it also warned that these pathogens still pose a serious risk to public health, and should be “watched carefully”. These classes will be considered for inclusion on next year’s list.

How Ancestry Shapes Our Immune Cells

People of African descent are thought to be partially protected against malaria thanks to a genetic variant. There now seems to be another far bigger advantage to the genetic variation, that is the development of immune cells better armed to fight infections.

A T helper cell – a type of T cell that play an important role in the immune system. Image via Pixabay.

After having a routine blood test, Mr. B found out that he had an unusually low count of immune cells called neutrophils. Neutrophils are white blood cells, which are particularly good at rapidly eliminating microbial pathogens. Yet, Mr. B is perfectly healthy and a new report published in Nature Immunology now indicates that his neutrophils may be even better armed for fighting specific infections. Mr. B was born in Ghana and like virtually all individuals of African ancestry, carries a specific genetic variation, a polymorphism, of a molecule called the Duffy antigen. This polymorphism has been linked with having innocuous low neutrophil counts.

The drastic effects of the Duffy antigen on neutrophils had long been puzzling scientists jointly working at the Ludwig Maximilian University Munich and the University of York.

“Individuals of African ancestry, who carry the polymorphism, lack Duffy antigen on their red blood cells, they are Duffy-negative” explains Rot, Chair of Biomedical Sciences at the University of York, and lead scientist of the study.

This protects them against a malaria parasite, which otherwise highjacks the Duffy antigen in order to invade red blood cells. The group of scientists now reveals that there is much more to the Duffy polymorphism than malaria protection. They studied bone marrow cells of mice, which were deficient in Duffy antigen.

“We found that the lack of this molecule had a profound influence on the stem cells and the very early development of immune cells, particularly the progenitor cells of neutrophils,” says Duchêne, group leader at the Ludwig Maximilian Univeristy Munich and first author of the study. “As a result of their changed development, mature neutrophils of Duffy-negative individuals carry more molecular “weapons” against infectious pathogens” says Duchêne.

The scientists also show that these distinctive neutrophils readily leave the blood stream, which explains the apparent lower numbers of neutrophils in the blood of Mr. B.

“Although an alternative “super-armed” immune system may be an advantage to fight infections, a stronger immune response may be detrimental in the context of chronic inflammation and autoimmune diseases” argues Rot.

Indeed, individuals of African ancestry are more susceptible to heart disease, stroke and several autoimmune and inflammatory diseases. This study comes as a serious warning to today’s genomic medicine, which aims to map disease traits with genetic variants based on 96% of participants from European descent. “Black lives Matter,” Rot likes to say. He hopes the findings will lead to “therapies specifically tailored to tackle diseases in individuals of African ancestry”. Mr. B too.

This is a guest post by Anne Rigby (photo below). Anne is a former Biologist, particularly fascinated by Immunology. She gets excited by new scientific ideas and hypotheses which challenge our current thinking.

 

Journal Reference: Duchene J et al. Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis. 2017. Nat. Immunol. doi:10.1038/ni.3763

Ladybugs.

If you like having sex, you should thank pathogens for making it possible

The arms race between pathogens and the organisms they infect may be the fundamental reason why animals have taken to having sex and then stuck with it, a new paper reports.

So why do we have sex? Well, it’s obvious isn’t it — we do it to make more humans. But there is a small chink in that explanation, something which has been bothering evolutionary geneticists for about as long there have been any around: sexual reproduction is hard work, whereas asexual reproduction is easy and much more efficient — so why bother with it?

Ladybugs.

Image via Pixabay.

That’s something we’ve all asked ourselves at one point or another but Dr. Jack da Silva and James Galbraith from the University of Adelaide have actually set out to get an answer. After using a computer model to simulate how the genomes of Caenorhabditis elegans (non-parasitic roundworms) shift throughout several generations, the duo suggests that sexual reproduction imposed itself because organisms needed to constantly adapt their genomes to fight off co-evolving pathogens.

“Asexual reproduction, such as laying unfertilised eggs or budding off a piece of yourself, is a much simpler way of reproducing,” says Dr da Silva, Senior Lecturer in the University of Adelaide’s School of Biological Sciences.

“It doesn’t require finding a mate, and the time and energy involved in that, nor the intricate and complicated genetics that come into play with sexual reproduction. It’s hard to understand why sex evolved at all.”

One decades-old theory has been attracting more attention recently, da Silva said. Known as the Hill-Robertson Interference, it holds that sexual reproduction evolved because it allows DNA recombination between mates, allowing offspring to ‘hoard’ more beneficial mutations. In the case of asexual reproduction, where there is no pooling of genes, beneficial mutations compete with each other and natural selection grinds down.

But de Silva says this theory doesn’t explain why sexual reproduction would be maintained in a stable, well-adapted population — where maintaining the status quo makes more evolutionary sense.

 

“It is hard to imagine why this sort of natural selection should be ongoing, which would be required for sex to be favoured,” he says.

“Most mutations in an adapted population will be bad. For a mutation to be good for you, the environment needs to be changing fairly rapidly. There would need to be some strong ongoing selective force for sex to be favoured over asexual reproduction.”

The team’s suggestion is to bring another, less influential evolutionary theory into the mix. Known as the Red Queen theory, it holds that because bacteria, viruses, or parasites are continuously trying to adapt and overcome our natural or artificial defenses, our genomes are also trying to keep one step ahead by continuously mutating, becoming more resistant to them.

‘Good enough’ is better than ‘the best’

While we may be really well adapted to our environments, there’s a constant sort of biological arms race going on. Staying unpredictable — by having the ability to develop new mutations and pool them in offspring — thus becomes more advantageous than reaching a hypothetical ‘best-adapted’ genome and keeping with it.

So in the end, organisms may have chosen sexual reproduction over cloning because, although it’s harder and (on those lonely Saturday nights) more frustrating to pull off, it keeps us all similar but different enough so the germs can’t get us all in one shot. Which I feel is win for us.

“These two theories have been pushed around and analysed independently but we’ve brought them together,” says Dr da Silva. “Either on their own can’t explain sex, but looking at them together we’ve shown that the Red Queen dynamics of co-evolving pathogens produces that changing environment that makes sex advantageous through the simple genetic mechanism of the Hill-Robertson theory.”

“This is not a definitive test but it shows our model is consistent with the best experimental evidence that exists.”

The paper “Hill-Robertson Interference Maintained by Red Queen Dynamics Favours the Evolution of Sex” has been published in the Journal of Evolutionary Biology.

Europeans picked up a customized immune system by having sex with Neanderthals

Researchers have discovered that people of European and African descent have very different immune responses to infections. They believe these traits could be the result of modern humans breeding with Neanderthals after leaving Africa.

Image credits Paul Hudson / Flickr.

Sometime between one hundred to a few tens of thousands of years ago, as modern humans migrated out of Africa, they met strange peoples which weren’t completely like them, but not too different either — the Neanderthals. So, naturally, they had sex with them.

The genes we acquired in that exchange may be responsible for a whole range of diseases, but it’s possible they gave our ancestors the means to better adapt to their new environment. Scientists studying the immune system of humans today have found that people of European descent have significantly different immune responses from their African counterparts — a direct consequence of the exchange, they believe.

The finding could explain why Africans generally have more robust immune systems than Europeans, but also why they’re more predisposed to certain autoimmune conditions.

“I was expecting to see ancestry-associated differences in immune response but not such a clear trend towards an overall stronger response to infection among individuals of African descent,” says University of Montreal geneticist and paper co-author Luis Barreiro.

Barreiro’s team examined samples taken from 175 American patients, roughly half and half of African and European ancestry. They extracted macrophages from their blood — white cells that kill pathogens by “eating” them — and infected the cells with Listeria and Salmonella. They let them go about their business for 24 hours, then analyzed them.

The cells retrieved from the African group had reduced the bacterial growth three times faster than the European group thanks to a stronger inflammatory response. That’s a definite plus when combating infections, but the team points out it’s a double edged sword.

“The immune system of African Americans responds differently, but we cannot conclude that it is better,” Barreiro said, “since a stronger immune response also has negative effects, including greater susceptibility to autoimmune inflammatory diseases such as Crohn’s disease.”

The team also examined the genetic makeup of the cells’ active genes, and found a link between the European sample and Neanderthal DNA — but didn’t find any similar link in the African sample.

The team says that when early humans migrated into Europe around 100,000 years ago, they encountered a continent already colonized by the Neanderthal. Finding traces of their DNA in modern European subjects suggests that the two species actively bred with each other. It makes sense, too. The new genes would have offered our ancestors an evolutionary edge in Europe, where environmental conditions were very different from those in Africa. A lower inflammatory response would also make more sense in the colder climate compared to Africa’s sweltering heat, which promotes infections.

“Our results suggest that the immune systems of African- and European-descended individuals have evolved to better respond to the specific needs imposed by their specific environments,” Barreiro told Live Science.

“What is advantageous in one context is likely to be detrimental in another.”

Too much of a good thing

A separate study also found a lower inflammatory tendency in monocytes against bacterial and viral threats in people of European descent compared to those from Africa. The study included 200 participants from France. The team, led by Lluis Quintana-Murci from the Institut Pasteur, also tied the differences to Neanderthal-like genes in the European participants. In broad lines, the results are the same. The French team also suggests that a powerful inflammatory response could actually be dangerous in Europe, so this effect could have provided an inherent evolutionary benefit — weeding out the more inflammatory-prone genes over time.

“Reducing immune inflammatory responses is a way to avoid autoimmunity, inflammatory, and allergic reactions,” Quintana-Murci told ResearchGate.

“Finding that reduced immune responses has conferred an advantage highlights the tradeoff between recognising pathogens while avoiding exacerbated, aberrant reactions that can be also harmful for the host.”

Both studies say more work needs to be done before we understand where these differences stem from. But it could help us develop things like personalized treatments or medications tailored for certain ethnicities’ needs.

“There is still much to do,” says Barreiro. “[Genetics] explains only about 30 percent of the observed differences in immune responses. Our future studies should focus on other factors, emphasising the influence of the environment and our behaviour.”

Barreiro’s and Quintana-Murci’s studies are published in the journal Cell.