PROFESSOR HUGH PENNINGTON explains how Covid-19 spreads

The killer virus that just keeps breeding: PROFESSOR HUGH PENNINGTON explains how Covid-19 spreads, what its ‘aggressive strain’ is and whether it will die down in the summer


‘Coronavirus’ is the name given to a family of viruses that we have known about since the mid-1960s. Covid-19, the cause of the current outbreak, is a new strain of coronavirus.

In total, we know of seven coronaviruses that can infect humans. They include certain strains of the common cold and the SARS (severe acute respiratory syndrome) and MERS (Middle East respiratory syndrome).

SARS, MERS and Covid-19 are coronaviruses that evolved from animals to infect humans.

At the virus’s core is a bundle of RNA (ribonucleic acid), one of the two main types of genetic material underpinning all life (the other being DNA or deoxyribonucleic acid).

A woman wears a surgical mask while walking through Terminal 5 at Heathrow Airport in London today 

This is protected by a protein coating that assists the virus in its sole aim in life: to replicate and pass on its genes.

To do this it must invade the cells of other organisms, using long tendrils on its protein coat which reach out like fingers to grasp on to protein molecules on the surfaces of the cell it is trying to infect.

These tendrils have knobs on the end which make the virus look like a crown – corona in Latin, hence its name.


The virus’s preferred home is in the mucous membranes of the lungs. Each package of newly-replicated viral RNA is wrapped in a protective coating of its own and can be passed on in various ways: most commonly being coughed out of the airways in the form of airborne droplets and then inhaled by other people.

Alternatively, it can be transferred manually – for example, if you touch a hard surface onto which the droplets have fallen, hence the importance of current advice to wash your hands thoroughly and regularly.

Today, March 6, saw the biggest one-day jump in the number of people confirmed to have the coronavirus – there were 47 new cases, bringing the UK’s new total from 116 to 163

From the hands, coronavirus can get into the body when you touch your mouth, your nose or your eyes – the latter being connected to the throat via tear-ducts – and then breathed back down into the lungs.

The virus can also be found in human stools. This is a theoretical method of transmission – poor sanitation caused many SARS infections – but there is no evidence yet that Covid-19 has been passed on like this.


By forcing the lung cells of the infected person to replicate its RNA, Covid-19 disrupts normal respiratory functioning. This includes the constant waving motion of cilia: tiny hair-like projections in the lungs which sweep out mucus and dirt or particles that have been breathed in from the air around us.

With this vital defence mechanism impaired, the lungs are more vulnerable to potentially deadly infections like pneumonia.

We know that our immune systems are strongest when we are younger, so it is not surprising that children appear to be the least vulnerable to developing the worst symptoms of coronavirus.

The opposite is true of elderly people, especially if their lung function is already compromised – for example, by life-long smoking or conditions like COPD (chronic obstructive pulmonary disease).

In people of all ages, the symptoms can be worsened when the body’s immune system goes into overdrive in its response to infection. White blood cells dispatched to fight the virus and reduce the inflammation in the lungs can damage healthy cells in the process.

The fever experienced by many victims is another immune response, with the body raising its internal temperature to a level at which the virus can no longer operate.

The majority of people infected with Covid-19 will experience symptoms so mild that they will not even know that they have had the disease.


Viruses mutate all the time and what the Chinese scientists have identified is a minor variation (known as L-type) to the existing Covid-19 (S-type) rather than a new and insidious new virus.

The word ‘aggressive’ is being used to describe it but the facts are less alarming. The S-type which kicked off the epidemic in China appears to be milder and less infectious; L-type seems to be more infectious – it currently accounts for 70 per cent of cases – but does not appear to be causing symptoms that are any worse.

Bear in mind that new strains of influenza are evolving constantly. That is why our annual flu jabs contain two or three different vaccines which change year on year.

Any future vaccine against Covid-19 will similarly take account of the different strains out there.


Respiratory infections are certainly more common in winter. There is no simple explanation for this, but one theory is that viruses can survive longer in colder weather when there is less UV radiation (which can kill microbes) from sunlight bearing down on the hard surfaces on which they linger.

Or it may be that people get together in confined spaces more often in winter.

Whatever the explanation, there is no way of knowing what warmer weather will bring for the coronavirus. During the 2009 swine flu pandemic, UK cases peaked in July.


Short of wearing a spacesuit, or stopping the people around you from breathing, the answer is no.

But public health control measures proved highly effective in eradicating SARS in 2002/2003.

Even if we are not completely rid of Covid-19, it may eventually evolve into different strains of the common cold – a recurring winter infection which many of us build immunity to, having caught it once.

That said, there is no room for complacency. And if we can draw anything positive from the spread of Covid-19, it’s as a reminder that we cannot skimp on funding if science is to keep pace with the ever-evolving threats to our health both now and in the future.


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