Every couple of years or so it seems the world is gripped by a new epidemiological scare: CJD, SARS, Avian flu, Swine flu… This year’s new panic seems to be over coronavirus, one of the many viruses that can be responsible for the common cold (or even SARS). The coronaviruses are RNA viruses with a massive genome (26-32kb: which is frankly ridiculous) and a protective envelope, covered in viral spike peplomers which lead to their name. The particular strain of interest right now presents as pneumonia, with renal failure in some patients, and is referrred to as hCoV-EMC.
The key ingredients for a global pandemic are that it occurs across a wide area and that it is able to spread from person to person. Various zoonotic diseases are able to be passed from animals to humans (see rabies, swine flu and bird flu), but this only becomes a global risk when individual humans are seen to pass the disease to one another. In the last two months there have been nine reported infections with a novel strain of coronavirus, in Qatar, Saudi Arabia and Jordan, five of which were fatal. Because three patients in Qatar and two patients in Jordan were closely associated, there is a very real chance that human-to-human transmission has occurred (although they may have simply been exposed to the same source). This, combined with the currently-reported very high death rate (i.e. more than 50%) is really very concerning.
SARS (severe acute respiratory syndrome) is also caused by a coronavirus, and there has been some concern that we could be facing a pandemic of similar size and severity. It was this fear that led to a recent paper in mBio investigating the receptor sites of the virions. The particular receptor utilised by the SARS-causing coronavirus (angiotensis-converting enzyme 2, or ACE2) is limited to humans, meaning that zoonotic transfer was unlikely. It has previously been shown that SARS-CoV infection can be blocked with an anti-ACE2 antibody. What Muller et al have demonstrated in this paper is that the anti-ACE2 antibody works in kidney cells from monkeys, humans and swine to block infection with SARS-CoV, but that the same is not true of the new coronavirus currently making the headlines. This is apparently because the ACE2 enzyme isn’t actually involved in CoV-EMC replication, as it is in the SARS-responsible CoV.
This is actually slightly worrying and depressing news. While it’s interesting that the two viruses are unlikely to utilise the same receptor, and therefore have similar epidemiology, from the point of view of fighting the disease, this makes it an unknown quantity. Given that the Müller et al suggest it may utilise a broadly conserved receptor present across the animal kingdom. From the point of view of preventing repeated infection, or multiple posts, this could be very serious indeed.
Müller, MA et al (2012) mBio 3 (6):e00515-12