MERS-CoV mutations in South Korea

Middle East respiratory syndrome coronavirus or MERS-CoV was first reported in September 2012 in Saudi Arabia. Investigations later identified that the first known cases of MERS occurred in Jordan in April 2012. MERS causes a severe respiratory infection with a high case mortality rate (~35%). To clarify: MERS-CoV causes MERS.

So far, all cases of MERS have been linked through travel to or residence in countries in and near the Arabian Peninsula. From May to July 2015, a large outbreak initiated by an infected traveler from the Arabian peninsula swept South Korea and resulted in 186 confirmed cases with 38 deaths (case mortality rate: 20.4%).

Korean Researchers detected a mutant MERS-CoV during that outbreak[1]. They isolated 13 new viral genomes from infected patients and found that 12 of these genomes possessed a mutation in the receptor-binding domain (RBD) of viral spike (S) protein.

Strikingly, these mutations result in reduced affinity. This unexpected finding suggest that the virus adaptation during human-to-human spread may be driven by host immunological pressure such as neutralizing antibodies, resulting in reduced affinity to host receptor, and thereby impairs viral fitness and virulence, rather than positive selection for a better affinity to CD26.

In short, the human immune system may work so effectively that the Middle East respiratory syndrome coronavirus has been forced to adapt itself to survive. In doing so, it made itself less fit to infect humans. It's a strategy that was very effective in the past for the Influenza virus, because it was a sort of 'stepping stone' to become more virulent in the next phase of the process of mutation.

[1] Kim et al: Spread of Mutant Middle East Respiratory Syndrome Coronavirus with Reduced Affinity to Human CD26 during the South Korean Outbreak in mBio – 2016