Coronavirus – some information

Coronavirus – some information

A The virus

  • COVID-19 is the name of the disease. The name of the virus is SARS-CoV-2. Not very snappy, but it identifies its relationship to the virus (SARS-CoV) that caused the SARS outbreak in 2002. The virus that caused the MERS outbreak in 2012 (MERS-CoV) was also a coronavirus, although a different type. (see below for more about these diseases).
  • It is a virus, not a bacterium. Therefore antibacterial disinfectants will (probably) not be effective. Alcohol (70%) and hypochlorite (bleach) will kill it.
  • Coronaviruses in general are not uncommon – for example, they are estimated to cause about 10% of colds.
  • The genetic material of coronaviruses is RNA, not DNA. This is significant because RNA genomes tend to mutate more rapidly.
  • The RNA is contained in an envelope, which is surrounded by an array of spikes. These are glycoproteins (proteins with sugar molecules attached). The spikes are necessary for attachment to human cells, by binding to specific receptors. The spikes are the likely target for an immune response,
  • After attachment of the virus, the RNA enters the host cell and uses the protein synthesis machinery of the cell to produce the proteins needed for copying the RNA and formation of new virus particles.
  • The cell then dies and releases the new virus particles which go on to infect other cells.

B. COVID-19 and other coronavirus diseases

  • When you cough or sneeze, or, to a lesser extent, speak or just breathe, you shed droplets of various sizes. If you are infected, these will contain virus particles, depending on their size. Bigger droplets are more likely to contain virus.
  • The larger droplets will fall quite quickly (and may contaminate surfaces); smaller ones may remain airborne for some time. These droplets are mainly water. Because of the large surface-volume ratio, the water evaporates readily, forming tiny ‘droplet nuclei’ which can consist of a virus particle and not much else. They may remain airborne for a long time.
  • Incidentally, those droplet nuclei are too small to be intercepted by a mask, so even a well-fitting mask will offer imperfect protection against infection. However, the particles emitted by an infected person are larger, and can be intercepted by a mask. So wearing a mask will reduce the infectivity of someone with the disease.
  • For most respiratory pathogens, it is these droplet nuclei that are the problem, as they are small enough to bypass the mechanical barriers in the respiratory tract and penetrate right into the lungs. SARS-CoV-2 seems to be unusual in that picking it up from contaminated surfaces seems to be more common, and also in that it can infect through the eyes. Hence the advice to decontaminate surfaces and wash your hands frequently
  • The vast majority of infected people show few if any symptoms. This may be due to a level of non-specific immunity to coronaviruses, from previous infections with other coronaviruses, and/or the body’s natural resistance to infection.
  • A small proportion develop severe disease, and some die. In part this it thought to be due to an over-reaction by the immune system. Most of those who die have some underlying health condition, including reduced immunity and pre-existing respiratory tract conditions.
  • There is uncertainty about the real mortality rate (primarily because of uncertainty about the actual number of infections), but the general consensus is that it is about 1%. The mortality rate increases with age, from 50 onwards. This could be due not to age itself but the higher prevalence of underlying conditions, especially the reduction in immunity as you get older.
  • SARS (Severe Acute Respiratory Disease) started in China in 2002. There were over 8000 cases, mainly in China and Hong Kong, plus a number in other countries in the region (e.g., Taiwan, Singapore, Vietnam.) Apart from an outbreak in Canada (257 cases, traced to a traveller from Hong Kong), there was only a sprinkling of cases in the rest of the world. The apparent mortality was quite high (about 10%).
  • MERS (Middle East Respiratory Syndrome). The first case was identified in Saudi Arabia in 2012. Most subsequent cases were in Saudi Arabia, plus smaller numbers in other middle-Eastern countries. There were few cases elsewhere in the world. The disease has reappeared repeatedly in Saudi Arabia, and there was an outbreak in South Korea in 2015 (traced to a man who had visited Saudi Arabia). MERS appears to be more severe, with mortality rates estimated as high as 40%.
  • Why have SARS and MERS (in contrast to COVID-19) not spread more widely? That is a very interesting question, and I wish I knew the answer!

C. Testing

  • The commonly used test is a molecular one technically known as RT-PCR (Reverse Transcriptase- Polymerase Chain Reaction). This copies the RNA into DNA and then amplifies it to an extent that it can be detected. It is very sensitive, but it detects the RNA and not the whole virus. So you may remain positive for a short while after the virus has been eliminated, and you are therefore no longer infectious. Conversely, it may not pick up the infection in the very early stages, when only a few cells are infected.
  • This test requires sophisticated materials and equipment, and skilled technicians. All of these are in short supply, which limits the number that can be done. Some countries were better prepared than others and/or were quicker to react and get everything in place.
  • How important is testing? It is useful for essential staff (esp NHS workers) to know whether or not they are infected, so they can continue to work. Widespread testing would be useful, as getting a better handle on the actual number of cases would inform policy decisions, but I’m sceptical as to how important this is. The traditional view, that finding cases enables the identification of contacts who can then be quarantined, becomes untenable with large number of cases, at least without a degree of surveillance that might well be unacceptable except under authoritarian rule.
  • A different test, that relies on the detection of specific antibodies, is much discussed. Such tests are being evaluated. However, they tell you whether someone has had the disease, not whether they are infected.

D. Interpreting the data

  • We are showered with statistics – numbers of cases or deaths, in various countries. These are a few points to consider when we look at those numbers, especially when comparing data from different countries.
  • Are the numbers adjusted for the population size? Very often they are not, or they don’t say one way or the other. Clearly, a large country would expect more cases than a small one.
  • Do they refer to the cumulative number (the total number of cases/deaths during the epidemic) or the number that day/week?
  • If considering the number of cases, the definition of a ‘case’ may vary between countries. In particular, consider the impact of testing. A country like Germany (which is doing a lot of testing) will identify a large number of cases with few if any symptoms that may not be counted by other countries – and hence will be expected to have a large number of ‘cases’.
  • The number of deaths is often regarded as a more reliable comparison, but this may also have problems. Does it include those who die outside hospital? And remember that many who die as a result (probably) of coronavirus infection actually die from e.g., pneumonia, heart failure, multiple organ failure, etc. How are these deaths recorded? Procedures may vary between countries.
  • To overcome these difficulties, it is best to look at the trends in different countries, i.e., the number of cases/deaths over time. This assumes that the practice in each country is consistent, which is not always true – the UK figure of deaths suddenly jumped today (3 April) after a change in reporting procedure.
  • Bear in mind that there is a delay between ‘cases’ and ‘deaths’ – so you might expect the death rate to continue to go up while the infection rate is levelling off.
  • The trend line will also show where the countries are on the epidemic curve. Italy for example had its first case earlier than Germany did, so comparing those two countries needs to take account of that, in effect looking at where Italy was a short while ago.
  • When considering deaths, it is important to remember that many deaths are among the very old or those who have other serious conditions. Trying not to be callous about this, we have to remember that some of them would be expected to die anyway in any given period. To get a true picture of the impact, we should look at excess deaths – i.e., the number of deaths above the number that would be expected to happen anyway. Bear in mind that there are normally about 0.5 million deaths per year (England and Wales).

E. In defence of ‘herd immunity’

  • The course of an epidemic is determined by a parameter known as R, the Reproduction Number, which is the number of people infected by a single case. At the outset, for COVID-19, R has been estimated as about 2.5.
  • R itself depends on a number of factors; I’ll just consider two of them. Firstly, the number of contacts a person has while they are infectious, and secondly how likely it is that those contacts are actually susceptible to the virus.
  • ‘Social distancing’ (or in extreme cases, isolation) is obviously a way of reducing the first of these.
  • The second factor comes into play when a significant number of people have had the disease (and are, we hope, immune to re-infection). This is the natural way in which an epidemic becomes self-limiting. As more people become infected, and hence immune, R falls. When it gets down to less than 1, the epidemic stops, even though there are a number (possibly a large number) of people still susceptible. This is ‘herd immunity’.
  • The point at which herd immunity kicks in (the Herd Immunity Threshold or HIT) is related to the initial value of R (Ro). Mathematically, the proportion still susceptible at the HIT is 1/Ro. So, if Ro is 2.5, we would get herd immunity with 40% still sensitive, or 60% having been infected. That’s a lot of people. But if we combine it with other measures, effectively reducing the value of Ro, say to 1.5, we get herd immunity after 33% have been infected. And if we reduce Ro still further, to 1, then we get herd immunity straightaway.
  • This is all a gross simplification! In particular, it assumes a homogeneous population, which is obviously not true. Someone living in London, especially if they still travel on public transport, will pass on the virus much more often than someone in the Highlands of Scotland. But it demonstrates the principle.

I hope this all makes sense. If you want to ask anything, or disagree with me, feel free to email me. You might also like to read my book Understanding Microbes which amplifies some of the basic issues (although not COVID-19 as it was published in 2013)

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