Does your homemade mask work?

If a surgeon arrived at the operating theatre wearing a mask they had made that morning from a tea towel, they would probably be sacked. This is because the equipment used for important tasks, such as surgery, must be tested and certified to ensure compliance with specific standards.

But anyone can design and make a face covering to meet new public health requirements for using public transport or going to the shops.

Indeed, arguments about the quality and standard of face coverings underlie recent controversies and explain why many people think they are not effective for protecting against COVID-19. Even the language distinguishes between face masks (which are normally considered as being built to a certain standard) and face coverings that can be almost anything else.

Perhaps the main problem is that, while we know that well-designed face masks have been used effectively for many years as personal protective equipment (PPE), during the COVID-19 outbreak shortages of PPE have made it impractical for the entire population to wear regulated masks and be trained to use them effectively.

As a result, the argument has moved away from wearing face masks for personal protection and towards wearing “face coverings” for public protection. The idea is that despite unregulated face coverings being highly variable, they do, on average, reduce the spread of virus perhaps in a similar way as covering your mouth when you cough.

But given the wide variety of unregulated face coverings that people are now wearing, how do we know which is most effective?

The first thing is to understand what we mean by effective. Given that coronavirus particles are about 0.08 micrometres and the weaves within a typical cloth face covering have gaps about 1,000 times bigger (between 1 and 0.1 millimetres), “effectiveness” does not mean reliably trapping the virus. Instead, much like covering our mouths when we cough, the aim of wearing cloth coverings is to reduce the distance that your breath spreads away from your body.

The idea is that if you do have COVID-19, depositing any virus you may breathe out on either yourself or nearby (within one metre) is much better than blowing it all over other people or surfaces.

So an effective face covering is not meant to stop the wearer from catching the virus. Although from a personal perspective we might want to protect ourselves, to do so we should be wearing specially designed PPE such as FFP2 (also known as N95) masks. But, as mentioned, by doing so we risk creating mask shortages and potentially putting healthcare workers at risk.

Instead, if you want to avoid catching the virus yourself, the most effective things to do are avoid crowded places by ideally staying at home, don’t touch your face, and wash your hands often.

Two simple tests

If effectiveness for face coverings means preventing our breath travelling too far away from our bodies, how would we go about comparing different designs or materials?

Perhaps the easiest way, as demonstrated by several increasingly shared pictures or videos on social media, is to find someone who “vapes” and film them breathing out the vapour while wearing a face covering. One glance at such a picture dispels any suggestion that these face coverings stop your breath escaping.

Instead, these pictures show that your breath is directed over the top of your head, down onto your chest, and behind you. The breath is also turbulent, meaning that although it does spread out, it doesn’t go far.

In comparison, if you look at a picture of someone not wearing a face covering, you will see that the exhalation goes mostly forward and down, but a significantly further distance than with the face covering.

Such a test is probably ideal for examining different designs and fits. Do coverings that loop around the ears work better than scarves? How far under your chin does a covering need to go? What is the best nose fitting? How do face shields compare to face masks? These are all questions that could be answered using this method.

But, in conducting this experiment, we should appreciate that “vaping” particles are about 0.1 to 3 micrometres – significantly bigger than the virus. While it is probably fair to assume that the smaller virus particles will travel in roughly the same directions as the vaping particles, there is also the chance that they may still go straight forward through the face covering.

To get an idea of how much this might happen, a simple test involving trying to blow out a candle directly in front of the wearer could be tried. Initially, the distance coupled with the strength of exhalation could be investigated, but then face coverings made from different materials and critically with different numbers of layers could be tried. The design of face covering that made it hardest to divert the candle flame will probably provide the best barrier for projecting the virus forward and through the face covering.

Without any more sophisticated equipment, it would be difficult to conduct any further simple experiments at home. However, combining the above two tests would provide wearers with a good idea about which of their face coverings would work the best if the aim was to avoid breathing potential infection over other people.

Simon Kolstoe, Senior Lecturer in Evidence Based Healthcare and University Ethics Advisor, University of Portsmouth

This article is republished from The Conversation under a Creative Commons license. Read the original article.

How we found coronavirus in a cat

Since the outset of the coronavirus pandemic, the potential role of animals in catching and spreading the disease has been closely examined by scientists. This is because the virus that causes COVID-19 belongs to the family of coronaviruses that cause disease in a variety of mammals.

The evidence suggests that this virus arose in bats and my colleagues at the University of Glasgow have recently determined that the sub-type of coronavirus to which the virus belongs has been circulating in the bat population since the 1940s.

So it makes sense for researchers to ponder whether the virus can be transmitted to companion animals, whether these animals can show symptoms of infection, and whether they may play any role in the epidemiology of the disease.

Cats are the UK’s most popular pet – a 2019 survey revealed there are almost 11 million felines in households across the country. Public concern about felines was initially raised when tigers and lions at the Bronx Zoo in New York were found to be infected with SARS-CoV-2, the virus which causes COVID-19.

There have also been sporadic reports of cats from COVID-19 households in Hong Kong, Belgium, France, Spain and the US which have tested positive for the virus.

So, could our domestic cat population be somehow involved in this pandemic here in the UK? We decided to find out.

Searching for coronavirus in UK cats

In early May, my colleagues and I were given ethical approval to retrospectively test cats for SARS-CoV-2 and work soon began screening routine respiratory samples taken from cats throughout the UK. We also launched an appeal to veterinary surgeons asking for samples from suspect cases.

After screening hundreds of samples, this collaborative effort eventually resulted in the detection of a cat with SARS-CoV-2 in the south of England, which had been sampled in mid-May. Further samples submitted to our veterinary colleagues at the Animal and Plant Health Agency revealed that this cat had developed an antibody response to the virus, demonstrating that it had indeed experienced a genuine infection and confirming it was not a simple case of sample contamination.

Circumstances indicate that the cat contracted the virus from its owners, who had previously tested positive for COVID-19.

At this point, the World Organisation for Animal Health was notified by the UK Chief Veterinary Officer and the press was alerted. We are currently preparing a paper on our findings for publication.

Should I be worried about my cat?

So, what does this case tell us? Our research coincided with the UK COVID-19 outbreak, focusing on cats experiencing respiratory symptoms. Our finding of a single infected individual among the hundreds screened tells us that infection in cats is relatively uncommon. This is reinforced by the fact that the other cat in the household never became infected, either by the owners or the infected cat.

Although the cat had been experiencing mild symptoms, including runny eyes and a snotty nose, these signs were consistent with feline herpesvirus infection, for which this cat also tested positive. There is no evidence that SARS-CoV-2 was making this cat ill and thankfully, the cat and its owners have all made a full recovery.

It is important to appreciate that while, to date, about 18 million people have tested positive for COVID-19, only a handful of infected cats have been detected around the world.

All available evidence suggests, therefore, that cats are not involved in spreading COVID-19. However, the importance of this type of animal surveillance work is clear, considering that a million mink have recently been culled in the Netherlands and Spain as they have been implicated in disease spread.

Our suspicion in the case of cats is that feline infections simply represent a “spill over” from the human epidemic, and we are currently analysing the genome sequence of the virus from the case we found to investigate this hypothesis.

Our results and those from other studies, such as work in the US showing experimentally infected cats were only transiently infected, can provide reassurance to the pet-owning public.

It’s very unlikely your cat has coronavirus, and if it does, it probably won’t be involved in spreading it any further.

Willie Weir, Professor of Veterinary Infectious Disease, University of Glasgow

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Air pollution exposure linked to higher COVID-19 cases and deaths – new study

The global death toll from COVID-19 has now passed half a million. To slow the spread of the disease, we need to better understand why some places have higher numbers of cases and deaths than others.

One factor that could partially explain this is air pollution. Research has shown that long term exposure to pollutants such as fine particulate matter (often called PM2.5, as these are particles smaller than 2.5 micrometres), nitrogen dioxide (NO₂) and sulphur dioxide (SO₂) can reduce lung function and cause respiratory illness. These pollutants have also been shown to cause a persistent inflammatory response even in the relatively young and to increase the risk of infection by viruses that target the respiratory tract.

The pathogen that causes COVID-19 – SARS-CoV-2 – is one such virus. Several studies have already suggested that poor air quality can leave people at greater risk of contracting the virus, and at greater risk of serious illness and death. A study of the US found that even a small increase in PM2.5 concentrations of 1 microgram per cubic metre is associated with an 8% increase in the COVID-19 death rate. Our new research looked at the relationship between COVID-19 cases and exposure to air pollution in the Netherlands and found that the equivalent figure for that country could be up to 16.6%.

Read more: What you need to know about how coronavirus is changing science

The unusual case of the Netherlands

After analysing data for 355 Dutch municipalities, we found that an increase in fine particulate matter concentrations of 1 microgram per cubic metre was linked with an increase of up to 15 COVID-19 cases, four hospital admissions and three deaths.

The first confirmed COVID-19 case in the Netherlands occurred in late February and by late June over 50,000 cases had been identified. The national spread of COVID-19 cases shows a greater number in the south-eastern regions.

Unusually, these hotspots of disease transmission are in relatively rural regions where there are fewer people living close together. The Dutch media offered one potential explanation. In late February and early March each year, these areas hold carnival celebrations which attract thousands of people to street parties and parades – 2020 was no exception, so does that explain the rapid spread of COVID-19 there?

While it’s likely that the carnival celebrations played a role, the pattern of cases across these regions suggest other factors may be at least as important.

The south-eastern provinces of North Brabant and Limburg house over 63% of the country’s 12 million pigs and 42% of its 101 million chickens. Intensive livestock production produces large amounts of ammonia. These particles often form a significant proportion of fine particulate matter in air pollution. Concentrations of this are at their highest in air samples from the south-east of the Netherlands.

The correlation between these indicators of air pollution and cases of COVID-19 is clear to see, but is it just a coincidence?

Pollutants associated with COVID-19

Our analysis used COVID-19 data up to June 5 2020, capturing almost the entire known course of the Dutch epidemic. The relationship we found between pollution and COVID-19 exists even after controlling for other contributing factors, such as the carnival, age, health, income, population density and others.

To put our results in context, the highest annual average concentration of fine particulate matter in a Dutch municipality is 12.3 micrograms per cubic metre, while the lowest is 6.9. If concentrations in the most polluted municipality fell to the level of the least polluted, our results suggest this would lead to 82 fewer disease cases, 24 fewer hospital admissions and 19 fewer deaths, purely as a result of the change in pollution.

Read more: What we do and don't know about the links between air pollution and coronavirus

The correlation we found between exposure to air pollution and COVID-19 is not simply a result of disease cases being clustered in large cities where pollution may be higher. After all, COVID-19 hotspots in the Netherlands were in relatively rural regions. Still, region-level data can only get us so far. Within regions, pollution levels and COVID-19 cases can vary considerably from place to place, making it hard to estimate the precise relationship between the two.

Being able to study this link among individual people would allow us to more precisely eliminate the influence of age and health conditions. But until this kind of data is available, the evidence of a relationship between pollution and COVID-19 can never be conclusive.

Matt Cole, Professor of Environmental Economics, University of Birmingham; Ceren Ozgen, Assistant Professor in Economics, University of Birmingham, and Eric Strobl, Professor of Economics, Université de Berne

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Bats are hosts to a range of viruses but don't get sick – why?

Bats harbour many diverse viruses, including coronaviruses. Indeed, Sars, Mers and COVID-19 – which are all caused by coronaviruses – are thought to have emerged from bats. These diseases can be deadly to humans, yet bats seem to be unaffected by them.

Like all animal species, bats possess their own range of pathogens – viral, bacterial and fungal. Organisms are part of an interconnected system of other living things that evolved to exploit and be exploited in turn. Bats have therefore evolved with a set of viruses that infect them and continuously circulate through the bat population.

SARS-CoV-2, the virus that causes COVID-19 is a member of a family of viruses called the coronaviridae (coronaviruses). Coronaviruses, or “CoVs”, infect a variety of animals, with human infections ranging from HCoV-229E, which causes some cases of the common cold, to MERS-CoV, which is fatal in up to 30% of cases.

Read more: Coronavirus: three misconceptions about how animals transmit diseases debunked

Since the original SARS-CoV outbreak in 2002, coronaviruses closely related to SARS-CoV have been discovered in bats from countries all over the world. Scientists in China studying Chinese horseshoe bats in 2013, identified several SARS-like CoVs that use the same ACE2 receptor to bind to cells as the current SARS-CoV-2. These viruses were similar enough to SARS-CoV that they were termed SARS-like coronaviruses. New viruses have been added to this group since then. So there is a significant diversity of coronaviruses circulating in bats, which may increase the probability that one of these viruses has the potential to become a zoonotic infection – in other words, can jump to humans.

Bats are excellent hosts for viruses in general and coronaviruses as a group have been particularly successful at infecting and diversifying within bats. The highly social nature of many bat species leads to the constant exchange of viral pathogens between bats – and this may act to drive viral diversification within a population.

Unique among mammals

With so many potentially dangerous viruses circulating among them, why do the bats themselves not die off from these constant infections? Clearly, bats can maintain a balance between control of a viral infection and the excessive inflammatory response that can kill other hosts. Perhaps the answer lies in their unique feature among mammals – flight.

Read more: Bat flu can spread to humans: should we be worried?

The physiological requirements of flight have affected the bat immune system. Flight causes bats to have elevated metabolic functions and raises their core body temperature about 38°C. This means that bats are often in a state that, for humans, would be considered a fever. Researchers in the UK have suggested that this may be a mechanism to help bats survive viral infections.

Viral infections can harm the host, in part, by causing an out-of-control inflammation response called a “cytokine storm”, which can be a fatal complication in several respiratory diseases, including COVID-19. If bats adaptation to flight also allows them to tolerate high body temperatures better, it means they can tolerate at least some potential damaging effects of the inflammation response better than other mammals.

In addition to traits that allow bats to tolerate a high body temperature, bats may also have other adaptations that mark their immune system as unusual or unique among mammals.

A sting in the tale

In 2018, scientists in China and Singapore identified a mutation in a gene that helps to control the antiviral response in bats during a viral infection. The mutation is in a gene called the stimulator of interferon genes (STING), which is common to all mammals and has a crucial role in triggering the inflammation response during a viral infection.

The mutation identified in bats has been shown to reduce the production of specific inflammation-causing proteins, called interferons, during a viral infection.

It may seem counter-intuitive that reduced production of an antiviral component could be better for the host, but it appears that damping down the inflammation response may allow the bats to avoid the damage caused an excessive immune response – the previously mentioned cytokine storm.

Adaptation to flight and mutation in STING both serve to control and tolerate inflammation. But these changes are probably only part of how bats have adapted to persistent viral infections in a way that other species have not.

Although we have known for a long time that bats are a potential source of novel viruses, research into bat immunity remains at the cutting edge of science, and new research is emerging all the time. It is likely that further discoveries will be made and that each new piece of data will enhance our understanding of bats, viruses and provide insights into our own immune systems.

Keith Grehan, Postdoctoral Researcher, Molecular Biology, University of Leeds

This article is republished from The Conversation under a Creative Commons license. Read the original article.