Rhys Davies is an Academy Coach Development Officer at London Irish, as well as head coach with HAC mens team in London and Berkshire Ladies. He has taken social media by storm with his great resources around being more effective as a coach when using different games. In this podcast, we develop his themes around challenges, effective coaching and how to manage training to give players a fantastic game experience. MORE
Coronavirus and athletes: the truth, the whole truth and nothing but the truth
Exclusive from Peak Performance
Coronavirus is spreading to every corner of the globe, and is almost certainly going to have a huge impact on the way we live our lives, including the way we participate in sport, exercise and leisure. In the first part of a three-part article, we take an in-depth look at the characteristics of coronavirus and the challenges it poses to all of us
Note to the reader: This is a three-part series. In part one, we look at the characteristics and epidemiology of the novel coronavirus. In parts two and three, we will look at the science of infection prevention and enhancing immunity with antiviral nutrition should infection occur. We make no apologies for quoting the science where necessary; as always, Peak Performance is an evidence-based publication, and the information we present to you is not framed by ‘experts’, governments, famous athletes and their coaches or anyone else. We are, and always will be, driven solely by peer-reviewed data from scientific studies, which we use to inform our conclusions.
In December 2019 in the city of Wuhan in China, a strange phenomenon began to occur. An increasing number of patients began presenting to local hospitals with serious breathing difficulties, which were caused by an unusual viral pneumonia. What also mystified doctors was that many of these patients appeared to be linked in some way or other to the Wuhan seafood wholesale market(1). Subsequent genetic analysis of the virus responsible showed that the virus responsible was a type of coronavirus (see panel 1)(2). However, while it was genetically related to two previous viruses – SARS-Cov and MERS-Cov – it had hitherto never been observed in humans, and was therefore named ‘2019-Cov’ or ‘SARS-Cov2’. However, since the term ‘novel coronavirus’ or just ‘coronavirus’ is now used ubiquitously by most people, this is the term we will use in this article.
The coronavirus family
Coronaviruses are ‘enveloped’ (where the virus machinery is enclosed by a shell) RNA viruses that are the cause of widespread infection in humans, other mammals, and birds, resulting in a variety of respiratory, gastrointestinal, hepatic, and neurological diseases. In particular, there are six coronavirus species that are known to cause human disease(3). Four of these viruses – known as 229E, OC43, NL63, and HKU1 are common in humans, typically causing common cold symptoms in individuals.
The two other strains of coronavirus are ‘Severe Acute Respiratory Syndrome’ coronavirus (SARS-CoV) and ‘Middle East Respiratory Syndrome’ coronavirus (MERS-CoV). These are both far more serious infections of the lower respiratory tract (lungs), and which often resulted in fatal outcomes during virus outbreaks in 2003 and 2012 respectively. Like the new 2019-Cov virus (the 7th coronavirus to evolve and infect humans), both SARS and MERS were ‘zoonotic’ in origin, meaning they emerged as a result of a coronavirus from another species evolving and mutating into a form that can infect humans. This is a particular problem with coronaviruses because of their large genetic diversity, frequent recombination of their gene sequences and because of human-animal interactions, which allows cross-species infections to occur(4).
Figure 1: Coronavirus caught on camera*
Novel coronavirus (in orange) isolated from a patient in the U.S is seen emerging from the surface of cells (in gray). Close examination reveals a spherical envelope coated with tiny spikes protruding. These ‘spike’ proteins are used to lock onto receptors on the surface of human cells, gain entry into cells where infection can take place. Once inside the cell, the virus ‘hijacks’ the cell’s genetic machinery, reprogramming it to make copies of the coronavirus. * Image courtesy of National Institute of Allergy and Infectious Diseases/Rocky Mountain Laboratories, USA.
On January 2nd of this year, the Chinese authorities reported 41 patients in Wuhan had contracted coronavirus and were receiving hospital treatment. By 5th January, the number of patients increased to 59, with seven in a critical condition. The virus spread rapidly, and by the end of January, over 11,700 cases had been confirmed in China, with over 250 fatalities. Not only had it spread widely across China, cases had begun to occur in over a dozen other countries around the world. February witnessed an accelerating trend and at the time of writing (13th March), nearly 140,000 of coronavirus cases have been reported across the globe, with over 5,000 deaths. And while it’s true that China has managed to get the virus under control –thanks to the use of extraordinary quarantine measures – the spread outside of China is accelerating rapidly, with the World Health Organisation declaring a worldwide pandemic on March 11th.
What does coronavirus do in the body?
Figure 2: Spike proteins of a coronavirus
The spike proteins projecting outwards from the viral envelope are used to attach to and infect ACE2 receptors in human cells.
Like a lock and key mechanism, the coronavirus spike proteins lock onto the ACE2 receptors in human tissue, which then allows the viral RNA (its genetic material) to enter our cells. Once inside, the coronavirus RNA effectively hijacks the protein manufacturing machines in your cells and uses this machinery to make thousands of copies of itself. These new viral particles are then released from the cell back into the body where they can go on to infect thousands of new cells. Because viral replication can occur very efficiently in the lungs, the effects of virus are most noticeable and severe in the lower respiratory tract.
How does it manifest?
As with most infections, coronavirus infection usually begins with a mild fever and fatigue as the immune system rallies into action against the invader. Symptoms such as a sore throat and dry cough (no mucous) may also be present, reflecting the fact that some upper as well as lower respiratory tract tissues can be infected(7). In a mild infection, these symptoms may all the patient feels. However in more severe cases, viral replication in lung tissue occurs at a much higher rate, resulting in symptoms such as shortness of breath and chest pain. Over time, patients may go on to develop bilateral pneumonia, where alveolar lung lesions (caused by the virus) and fluid accumulation occur as a result of the inflammatory response from the body. This kind of pneumonia typically affects both lungs and is visible on a CT scan, showing a ‘ground glass’ or consolidated appearance(8). At this point, the oxygen exchange capacity of the lungs becomes severely compromised, which means the patient requires extra oxygen for support, and in critical cases, mechanical ventilation in order to survive.
The replication of viral particles and the associated damage generated in the alveolar regions (oxygen exchange tissues) of the lungs is a distinguishing feature in severe cases of coronavirus. This is in contrast to influenza, where pneumonia of the lung is typically caused by an opportunistic secondary bacterial infection, which occurs due to a weakened immune function. A bad bout of influenza may or may not result in pneumonia, and when it does, the infection is seldom spread symmetrically across both lobes(9). In more severe coronavirus infections, bilateral viral pneumonia is an integral part of the disease process, which is why it has a much higher fatality rate than flu (see figure 3).
Figure 3: Comparison of influenza and coronavirus case fatality rates by age*
The fatality rate of coronavirus is between 10 and 30 times that of flu (which in itself is a serious enough illness). The epidemiological data clearly shows that risk increases drastically with age, but apart from children under 10 years of age, it appears that no age group is immune from this risk. *Data from Chinese Centre for Disease Control 2020.
Why is coronavirus causing so much concern?
As we have seen above, coronavirus infection can cause extensive lung damage in severe cases, which can be fatal. Because novel coronavirus is a new virus and we’re currently undergoing a pandemic, it’s not possible to accurate determine the case fatality rate (CFR) – this is something that can only be done retrospectively. However, the studies conducted to date from the Chinese data have estimated a CFR of anything from 2.2%(10) to 4.01%(11). But even this is hard to determine as many epidemiologists have expressed concerns that the Chinese data may have been incomplete. What we can say is that this novel coronavirus is less fatal that SARS (10.9% CFR) and MERS (CFR 34.7%)(12).
Another reason for concern lies in the infectivity of coronavirus. SARS and MERS both novel (at the time) types of coronavirus were brought under control and contained without causing a worldwide pandemic because their ability to spread was far more limited than coronavirus. In short, SARS/MERS cases were isolated and the spread of outbreaks contained fairly rapidly. However, novel coronavirus is not being contained and is spreading extremely rapidly because of it high transmission rate and infectivity.
Understanding reproduction numbers (R0)
A virus that can easily infect others will obviously spread more rapidly than one that does not easily cause infection. The measure of infectivity is known as the ‘basic reproduction number’ or ‘R0’ for short. The R0 value predicts how many other people an infected person will pass the virus onto. So with a virus with an R0 value of 2, each person will go on to infect on average two other people. The R0 value is incredibly important in determining the speed of spread of a virus. That’s because of its chain reaction effect. For example, take a virus with an R0 of 2. One person will infect two, those two people will infect four, those four will infect eight and so on. With an R0 of 3, the chain will be one person infecting three, three people infecting nine and so on. Now take a chain of ten successive transmissions. Starting with one person, the virus with an R0 of 2 will infect 512 people after ten transmissions. But if the virus has an R0 of 3, after ten transmissions, there will be 19,683 people infected!
As a rule of thumb, a virus needs an R0 significantly over 1.0 to propagate and spread. An R0 of near to 1.0 will mean it won’t infect enough people to sustain its transmission for any length of time. And once R0 drops below 1.0, the number of cases reduces and the chain of infection is broken. Research suggests that the basic reproductive number (R0) of novel coronavirus ranges from 2.0-3.5 during its early phase of spread, regardless of different prediction models(13). However, mathematical modelling conducted on coronavirus at the US Los Alamos Laboratory has suggested the R0 could be as high as 4.7-6.6(14). This is far higher than SARS and MERS(13), and also much higher than most common strains of influenza, which, depending on strain, have an R0 of around 1.4-1.8(15).
It’s important to also understand that the R0 of a virus is also determined partly by its intrinsic nature and the environment in which it exists. Therefore, a virus might have an R0 value of 2.5 in a community where no measures such as quarantining, social distancing and movement restrictions are implemented. However, when these measures are introduced, the effective R0 drops significantly – and this has been demonstrated with coronavirus outbreak in China(16).
Asymptomatic transmission and persistence
What is it about the characteristics of coronavirus that confers its high R0 value, and potential to infect many others causing a pandemic? Scientific research on this topic has identified three main factors:
- Asymptomatic transmission during incubation – those infected with coronavirus will experience several days of incubation during which no symptoms are present, but when viral particles can be shed to infect others(17). The typical duration of incubation is around 5 days but can be much longer(18). In short, many infectious individuals are likely to be spreading the virus in their communities before developing any symptoms, making containment extremely difficult.
- Spread via droplet and aerosolised transmission – infected individuals can easily shed viral particles across a wide area by coughing and sneezing. This is via both droplet transmission and aerosolised transmission(19). When viral particles become aerosolised, they can spread over a much wider area than in solely droplet transmission and are therefore more hazardous(20). In a paper published on March 6th in the journal ‘Practical Preventive Medicine, researchers presented evidence that in an enclosed environment such as an air-conditioned bus, coronavirus can become airborne, infect people up to 4.5 metres away, and persist in the for 30 minutes once the infectious person has departed that environment (see figure 4)(21). Although this data was gathered from a single case study rather than a controlled trial, it provides a useful insight into the potential challenges authorities face in slowing down the spread of this disease.
- Persistence on surfaces – the once shed onto surfaces, the coronavirus is remarkably persistent, which means that the likelihood of someone touching the infected surface and transferring virus particles to their eyes or mouth is greatly increased. A new analysis of 22 studies has studied the (structurally very similar) close cousins of novel coronavirus, such as SARS, MERS, and common cold coronaviruses(22). It found that viral particles can survive intact (and thus infectious) on inanimate surfaces like metal, glass or plastic for up to 9 days.
Plan view of the bus. Security camera footage showed patient “A” (in red) did not interact with others throughout the four-hour ride indicating airborne transmission. But by the time the bus stopped at the next city, the virus had already jumped from the carrier to seven other passengers.
Crashing the health care system
At the time of writing, a number of sporting events are being postponed or cancelled in an effort to slow the spread of coronavirus. In Japan, the Tokyo Marathon scheduled for March 1st was cancelled for all non-international runners, and the Boston Marathon looks increasingly in doubt. Meanwhile, the London Marathon has been postponed until October. All UK Premier League Football has been suspended till early April, and there’s also speculation that the 2020 Tokyo Olympics may fall victim too. With mass gatherings, social events and schools closing, many readers may be wondering why such exceptional measures are being taken to slow the spread of the virus? The answer is in the numbers. The high R0 of coronavirus combined with the severity of the illness in a significant number of people could lead large numbers of people needing high levels of medical care, all at the same time – a scenario that even the most advanced healthcare system will not cope with.
Current data on live cases suggests that around 10% of total coronavirus cases are requiring hospitalization – ie needing oxygen, antibiotic therapy etc, and 5% of total cases will require critical care in an ICU bed(23), with mechanical ventilation and intubation to oxygenate patients. Without this critical care, patients will not survive. A large number of cases in any one region therefore has the potential to completely overload even the most advanced healthcare system, drastically increasing the case fatality rate.
Flatten the curve
In England for example, health officials have suggested that in a worst-case scenario, up to 80% of the population might expect to become infected over the next year. That would translate to 48 million cases, or 4 million cases per month. If 5% of those cases need ICU care, that’s 200,000 cases per month. When you consider that there are only around 4,100 ICU beds in total in England, you can imagine the consequences. That’s why the aim of governments and health authorities is (or should be) to ‘flatten the curve’ – ie to lower the peak of cases by slowing down the virus spread (using measures such as extra hygiene precautions, social distancing, school closures, travel restrictions and even quarantines) so that a lower number of cases occur over a much longer time period (see figure 5).
Figure 5: Flattening the curve
Slowing and delaying the spread reduces the magnitude of the peak, reducing the likelihood of crashing the healthcare system.
It’s also worth pointing out at this juncture that while severe cases and fatalities are much more common in the elderly and those with pre-existing health conditions, the data coming in suggests that younger adults are not entirely immune from the worst effects of the virus. Although the large majority of cases in younger people are mild, some individuals have reported much more serious illness, requiring a few weeks to fully recover(24).
Also, using the data summarised in figure 2 above, we can see that the CFR for those in the 20-40 age group is reported to be around 0.2% – or two cases per thousand. If millions of younger adults are infected, the data predicts several thousand of those may result in fatalities. It is therefore incumbent upon all of us to act responsibly, and take whatever measures we can to reduce the spread of this virus, and minimise the effects of it should we become infected – for the good of not just ourselves, but everyone in the community, young or old.
In part two of this article, we’re going to look at how to do just that, starting with measures to prevent infection – particularly those of relevance to athletes in training and competition. Stay safe!
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