MERS-CoV – Will the time-bomb explode?

Transmission Electron Micrograph of MERS-CoV. Credit: NIAID
Transmission Electron Micrograph of MERS-CoV. Credit: NIAID

Over the last few weeks, the media have been particularly interested in covering the Ebola outbreak in West Africa (see my previous post, ‘Ebola – Time to Panic?‘), and this has resulted in rumours and scares about it spreading slightly closer to home. However, in my opinion, there is a virus which the developed world should be considerably more concerned about.

Middle East Respiratory Syndrome Coronavirus (MERS-CoV) is a virus very similar to the virus which caused the Severe Acute Respiratory Syndrome (SARS) outbreak in 2002/3, which resulted in 8,273 confirmed cases in 37 different countries, killing 775 (9%) (1).  As the name suggests (scientists can be an incredibly imaginative bunch), MERS-CoV has been circulating mainly in Middle Eastern regions, including the Kingdom  of Saudi Arabia, Qatar, and the United Arab Emirates (UAE) (2).  The World Health Organisation (WHO) received reports of 254 laboratory-confirmed cases of MERS-CoV infection between September 2012 and the 24th of April, including 93 deaths (a fatality rate of over 35%)(3). There have been confirmed cases in people travelling to the Arabian Peninsula who have then brought the disease back to their home countries, in cluding the United Kingdom, France and, most recently, the USA, although no further infection is thought to have come from these (4).  Symptoms include cough, fever, and shortness of breath (5), although there have also been links with side-effects such as stillbirths (6). There is currently no vaccine.

To understand these viruses a little better, we’re going to have to delve into their biology. Both MERS-CoV and SARS-CoV have genetic material made of a molecule known as RNA (ribonucleic acid). This is a molecule like DNA (deoxyribonucleic acid – our own genetic material), but it is less stable and more prone to mutation. This increased likelihood of mutation can be bad for the virus (much like mutations can be bad for humans), but some mutations will change the virus in a way which might make it more successful or able to do new things.

This mutation is important because both SARS-CoV and MERS-CoV are zoonotic viruses (transmitted from animals to humans) thought to originate in bats. However, the strain of the viruses found in bats are actually unable to infect humans. This is because the virus needs to be able to bind to certain molecules which vary between host species; think of a lock and a key – a key (virus molecules) to one door (host cells) will not open another (i.e. a different host species). However, by mutating the virus can change to allow it to bind the human molecules, and therefore infect humans – the key has changed to fit a new lock (although it probably can’t infect bats anymore!).

However, it is likely that a single mutation is not enough for the virus to be transmitted directly to humans (in this case think of the locks being so different that the keys have to change twice). This means that it is likely that there was an intermediate step, something where the locks are similar to both bats and humans which can act as a stepping stone. It has been suggested that  SARS was passed from bats to civets (small carnivorous mammals), where it mutated again into a form able to infect humans (7).  In a similar fashion, it is thought that camels act as a similar intermediate between the bat reservoir and human population for MERS-CoV.

Thankfully, although now able to infect humans, MERS-CoV is not well enough adapted to humans to be transmitted between humans multiple times. This is very similar to what we’ve seen before with different influenza strains, like bird flu. Although transmission may be possible, on average each infected person will infect less than one other person, meaning that the outbreak will die-out. However, the more people that are infected, the higher the chances that the virus will adapt to be spread between humans. If this happens, the average number of new infections from an infected individual may become greater than one – and then the virus will spread through the population.

It’s important to point out at this point that the virus doesn’t ‘want’ or ‘try’ to mutate – mutations are random events. Think of it in exactly the same way as animal evolution because exactly the same processes are involved; mutations are most likely to be deleterious, but once in a while they’ll make the individual more successful. The giraffe ancestors didn’t ‘want’ to grow longer necks, and lions didn’t ‘try’ to grow sharp teeth, random mutations slowly made these changes which made the individuals more successful. Remember, evolution is all about the survival of the fittest. It’s exactly the same with the virus – there’s no intention or fore-thought, but if it does evolve to infect humans, it has a whole new range of hosts it can infect!

So, should we be worried? As noted in the introduction, this virus almost certainly poses more of a threat globally than Ebola. My reasoning for this assertion lies within the routes of transmission – Ebola requires direct contact in order to spread, while MERS-CoV is thought to spread via droplets. At the moment, MERS-CoV is poorly adapted to humans, and so the only instances of transmission so far have been following lengthy contact with ill individuals, with small clusters within hospitals (8). However, as discussed above, there is the continual threat that it will become better adapted, and better at spreading. The question is, will it? The very nature of mutation is unpredictable, but the odds are probably in our favour (look at the history of these scares – there were more near-misses than real pandemics). That said, no one can truly say. Indeed, MERS-CoV may well be the time-bomb that we fear.

Amongst all of the uncertainty, what is certain is that if MERS-CoV doesn’t prove to be a global threat, there will soon be another virus which emerges to replace it. We must increase surveillance of potential reservoirs of these viruses, such as bats, so that we can better predict and prepare for the next outbreak. In my next post I shall address how we should go about this surveillance, whether or not we can predict the mutations required for human transmission of these viruses, and the biosecurity issues surrounding such research.

 

  1. Coleman, C, and Frieman, M; Journal of Virology (2014), volume 88 no. 10; ‘Coronaviruses: Important Emerging Human Pathogens
  2. WHO – Middle East respiratory syndrome coronavirus (MERS‐CoV), Summary and literature update – as of 27 March 2014
  3. Middle East respiratory syndrome coronavirus (MERS-CoV) – update as of 24th April
  4. MERS in the Arabian Peninsula (CDC)
  5. Centers for Disease Control and Prevention (CDC) – MERS-CoV
  6. Payne, D, et al. (2014). Journal of Infectious Diseases (10.1093/infdis/jiu068); Stillbirth During Infection with Middle East respiratory syndrome coronavirus
  7. Li, W, Wong, S-K, Li, F, Kuhn, J H, Huang, I-C, Choe, H, and Farzan, M; Journal of Virology (2006), volume 80 no. 9; ‘Animal Origins of the Severe Acute Reespiratory Syndrome Coronavirus: Insight from ACE2-S-Protein Interactions
  8. Assiri, A, et al. (2013) N Engl J Med 2013; 369:407-416, Hospital Outbreak of Middle East Respiratory Syndrome
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