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Coronavirus: What makes it so deadly. Why COVID-19 kills.

This virus particle – just 50 millionths of a millimetre across – is responsible for bringing the world to its knees.The SARS-CoV-2 virus is just a microscopic bundle of proteins, fat and genetic material called RNA.But hundreds of thousands have been killed by the illness it causes, COVID-19.Here’s what we know about the virus, how it attacks the body, who it kills and how.

When it is outside the body, the virus lives in droplets of moisture. People pick up the virus by touching surfaces it lands on.It can live for many hours or even days on those surfaces. The most common way it gets into the body is when people inhale it through their mouth or nose.

The virus can live outside the body but not forever.

It is sensitive to heat, but at room temperature lasts on surfaces like stainless steel for up to seven days. As it survives in microscopic droplets of moisture, it waits until it can transfer into a host – that’s us.

The most common way it gets into our cells is when we inhale droplets that have been sneezed or coughed from an infected person.

But, because it lives on surfaces, people who touch those surfaces can become infected if they touch their nose, mouth or eyes, which gives the virus a route into the body.

Once in the body, it makes its way to the cells that allow it to replicate, most often in the airways and lungs.

Once it is inside our body, it targets our cells. After injecting its RNA, it replicates, producing many copies of itself. This it does through something called viral shedding, the process by which a virus leaves cells and moves on to inhabit another one.

A swab from the back of the throat of an infected person found hundreds of millions of viral particles.
The back of the throat called the pharynx, is where it is most active in its early stage, causing a dry cough.
If a person coughs or touches their mouth, they will spread virus particles into the environment.

Ongoing studies have identified another commonly occurring symptom – loss of taste and smell.

The medical community has not yet come to a consensus about whether loss of taste should be considered a marker for COVID-19.

Other studies have found the virus causes a range of symptoms which vary widely from person to person, including: a sore throat, shortness of breath, aches and diarrhoea.

Experts think it may be the virus attacking cells in the back of the throat or the nose that leads to the loss of taste and smell.

There has been much debate about how many people are asymptomatic – that is they are infected but show no symptoms.

Some studies have put the potential figure as high as 87%, depending on the community being studied, but a consensus is growing it could be around 40% to half of those infected in general.

There are also suggestions that the virus can be spread by people who are asymptomatic or presymptomatic – meaning they can transmit the virus before they show any signs of being ill.

A Chinese study of 94 patients showed that the highest level of viral shedding took place at the exact point when symptoms were starting to show – meaning patients would have been emitting viral particles before they showed any symptoms.

The scientists worked out that as many as 44% of those who were infected by the 94 were given the virus before the person knew they were sick.

Other studies have put the number of cases caused by asymptomatic and presymptomatic carriers at between 40% and 80%.

While the main route to infection may be coughed droplets, there is also growing evidence that one of the ways that people are infected is through carriers’ breath.

Lidia Morawska and Junji Cao, in a review of the evidence for Science, said that because the SARS virus was found to travel in the air, it was highly likely SARS-CoV-2 does too.

It led the British Medical Journal to state in an editorial in April: “We know that patients with influenza shed substantial titres of infectious virions during normal breathing… these data support the idea that seemingly well individuals shedding high titres of SARS-CoV-2 may represent a substantial risk for onward transmission.”

The virus goes on to attack in more severe cases special cells in the lungs.These goblet and ciliated cells have the job of keeping lungs moist.Ejecting anything unwanted from the airways. All these cells are killed, they fall into the lungs creating blockages. But, because these cells normally have the job of clearing blockages, there are fewer to fix the problem. This can lead to pneumonia, a condition in which the air sacs that allow us to take in oxygen become inflamed.

If a patient has failed to improve within about a week, the illness frequently becomes more serious.

The virus appears to be particularly attracted to lung cells. It binds on to an enzyme called ACE2, which sits on the surface of some of the cells in the air sacs – a compartment in the lungs. SARS-CoV-2 then uses the ACE2 to gain entry and attack the cells.

This causes them to become inflamed, and leads to pneumonia.

Studies have shown that the damage to the lungs from COVID-19 can be so severe that patients who survive can be left with lifelong breathing difficulties.

The damage can be caused by the pneumonia or by acute respiratory distress syndrome (ARDS), which can be a consequence of the infection, and means the lungs are not providing the body with the oxygen it needs. This leads to something called hypoxia – a lack of oxygen in the bloodstream.

Of those who develop symptoms, about 20% have the more serious form of COVID-19 and require treatment in hospital.

This often becomes apparent when people develop breathing difficulties.

In many cases, help is required to get oxygen into their bloodstream, whether by breathing pure oxygen, using a ventilator to help their weakened lungs, or using a technique called extracorporeal membrane oxygenation (ECMO), when blood is artificially oxygenated outside the body before being returned.

Sometimes, patients have no problems breathing yet are found to have dangerously low blood oxygen levels.

A curious and as yet unexplained feature of COVID-19 is many patients have a level of hypoxia that would, under normal circumstances, result in death. But some patients are fully conscious and apparently unaware of the severity of their illness.

It has been dubbed ‘happy hypoxia’, because they should be dying yet describe themselves as “comfortable” and are often, for example, able to talk to people and use their phones while in hospital.

Normally, people should have a blood oxygen saturation of around 95%, when it is measured in a finger clip test. But some have been experiencing levels as low as 50 or 60%. This is thought to be linked to the virus causing blood clotting, but much study is under way.

Medical experts are struggling to understand the variety of ways COVID-19 is killing people. Some COVID-19 patients have suffered strokes, seizures and brain inflammation. Some patients go on to develop more severe pneumonia and die from respiratory failure, as their immune systems are damaged and unable to protect them.

Significant numbers of people with severe COVID-19 are suffering liver damage. A common cause of death is multiple organ failure. Patients are also succumbing to a form of inflammatory syndrome called a cytokine storm, which can attack many sites in the body at the same time.

The death rates being reported for COVID-19 in some countries, including the UK, sound horrific.

Several health systems around the world are having to deal with one in 10 or more of those who test positive dying.

There are anecdotal reports from intensive care that patients are being affected in many different ways.

But what is actually killing people remains a topic of debate.

Some experts believe that the severity of the disease depends on the amount of a virus someone was exposed to. This could explain why so many health or care professionals have died or been badly affected, when they have had difficulty accessing personal protective equipment (PPE). But others say more evidence is needed.

What is clear is that the virus in its more serious form attacks many parts of the body.

COVID-19 patients have been dying from:
· Catastrophically low blood oxygen levels
· Organ failure (with the liver and kidneys particularly vulnerable)
· Heart failure
· Respiratory failure
· Severe blood clotting and embolisms

Although there is much debate about this, these causes of death may stem from the virus’s tendency to target cells in the heart, blood vessels, lungs, gut, liver and kidneys. These organs have large numbers of cells that have ACE2 on their surface.

One of the biggest causes of death, however, appears to be the body’s defences going into overdrive.

This can start when the body sends an exceptionally high number of defensive cells to fend off the virus in the lungs. It is this defensive action that actually prevents oxygen entering the bloodstream.

Then, as the virus spreads further to other organs, the body reacts to its defences being overwhelmed by launching what is known as a cytokine storm – a surge of tiny proteins – in an attempt to fend it off, but which can result in hyperinflammation.

A cytokine storm is a type of septic shock in which white blood cells release cytokines, which instruct other white blood cells to release more, and so on in what is effectively a feedback loop.

Seizures, catastrophic loss of blood pressure or multiple organ failure can occur, frequently leading to death.

Despite headline figures of over 10%, the true death rate is likely to be much lower than that, as many countries that have higher rates have lower levels of testing.

Medical researchers say that many deaths in which COVID-19 was a factor have not occurred directly as a result of the virus, and the people may have died anyway – for example there have been documented cases of pensioners falling badly, coming into hospital where they caught coronavirus, but then dying of their injuries. COVID-19 is still among the causes of death mentioned on the death certificate.

Studies have found that the disease hits some groups harder than others. They include – men, black and ethnic minorities, those with pre-existing conditions and the elderly.

An early study of 44,000 Chinese patients established early on that the virus more frequently attacks men, the elderly and those with some pre-existing medical conditions.

Early theories were that Chinese men led less healthy lifestyles than women so were more vulnerable. But previous studies have found that men are less able to fend off other viruses too, like HIV and Ebola, because women’s immune systems are able to mount a stronger defence.

A consensus of opinion is yet to form, but it is thought, so far, to be down to a combination of immunological sex differences and variances in lifestyle and behaviour.

A recent Office for National Statistics study found that men working as taxi, bus and coach drivers, security guards, chefs and plant processing and construction workers were among those who face the greatest likelihood of dying in the UK.

Some of those categories could be put down to the risk of exposure – such as bus and taxi drivers – but the study also found healthcare workers – among the most exposed – were no more likely to die from the disease than others, and security guards were the most likely. The study further hinted that income inequality and lifestyle may be a factor.

The risk to the elderly has been backed up by death rate figures from many other countries since the pandemic spread outside of China.

In England, more than half of those aged 80 or over who test positive for COVID-19 die and four in 10 of those aged 60-79.

It was initially thought that Italy had been so hard hit because it had an elderly population, compared to other countries, but it has since emerged that death rates are likely to end up similar to many other European countries, and may in fact be lower.

Some have suggested that the reason elderly people are being hit so hard is because they have weaker immune systems than younger people. Except that, the very young and other groups with naturally weaker defences like pregnant women have also been viewed as vulnerable to pandemic infections and with COVID-19 this doesn’t appear to be the case.

Work is ongoing to establish which part of a weaker immune system makes the elderly – and those with pre-existing conditions – so much more likely to die.

The list of pre-existing conditions which people can have that are said to make them more vulnerable to COVID-19 is well known and long.

What is less well understood is why these people are more vulnerable.

Some of the conditions do not occur in isolation – for example, many people with obesity also suffer from conditions like diabetes, or heart problems.

Many of the pre-existing conditions merely make people more vulnerable because they have weaker immune systems, that means they are less able to fight off any infection, including COVID-19.

But work is ongoing to establish if there is a link between the disease’s targeting of ACE2 in the blood stream and organs, particularly the heart, and added vulnerability due to diseases like coronary heart disease, or high blood pressure.

Others who are apparently more at risk are those from black, Asian and minority ethnic backgrounds (BAME).

The UK government has launched a study to work out why more black people or people of Asian origin are being affected than should be the case.

In a study released in early April of UK patients on ventilators in intensive care, nearly 30% were black, Asian or mixed race – double the proportion in the general public, 15% BAME, according to the latest ONS estimates.

Sky News analysis in the week ending Sunday 3 May found that 62% of those who had died up to that point in NHS hospitals were BAME, and the Office for National Statistics (ONS) found that black people were four times more likely to die with COVID-19 than their white counterparts.

There are many theories about why that may be, including that people from some ethnic minorities have higher levels of ACE2, BAME people are more likely to come from disadvantaged backgrounds, or that there is a greater level of diabetes among the BAME population.

But it is too early at this stage to say whether one is more likely than the others, or whether the reason is a combination of the above. Others have said it may be that, generally, people from disadvantaged backgrounds are more at risk.

What is known is that children are not generally badly affected.

Studies in several countries have found that less than 2% of those who test positive are under 18 and of those only a tiny fraction are seriously affected. Younger children seem to be even less affected, with some screening studies finding no positive under-10s. Part of the reason for this may be because children seem to be less likely to acquire the virus.

There are suggestions, but this is yet to be confirmed, that children do not transmit the disease as easily as adults or even, possibly, at all.

More perplexing, however, are other studies that have found that children can have large amounts of the virus in their system.

Although a handful of children are dying – including some as young as newborn – the conundrum is why, in general, elderly people are dying in large numbers and infants and pre-schoolers – who often have less developed immune systems – are getting off lightly.

Dr Jeremy Rossman, honorary senior lecturer in virology at the University of Kent, has hypothesized it may be because the body remembers how to attack viruses and older people, who have a greater reservoir of defensive memory against coronaviruses, could be priming their system to overreact. This could, in some cases, be killing them. Youngsters, meanwhile, have systems with little memory of attacks, preventing an overreaction.

Others have claimed the opposite is possible – that children’s regular exposure to colds and viruses – as they interact with other infected youngsters – makes them better at fighting off SARS-CoV-2.

Even more of a puzzle is why the vast majority of children show few or no symptoms, but a tiny minority are critically affected.

The Paediatric Intensive Care Society has issued an alert, seeking more information, about a phenomenon affecting youngsters called multisystem inflammatory state or toxic shock syndrome, which is presenting itself as a very rare illness called Kawasaki disease. A link between Kawasaki and COVID-19 remains under investigation, but cases are “very rare”.

– SkyNews/photo/EvaluatePharma

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