Based on 3 genome sequences from 30 samples that Prof Drosten has been working with, no significant changes in the genome of Jeddah variants could be seen compared to previous sequences. The spike gene, a likely indicator of viral change, is "100 percent identical" to key regions from earlier MERS-CoV genome sequences.
This swings the focus for finding a reason for the outbreak in Jeddah, Kingdom of Saudi Arabia (KSA) and the cluster in Abu Dhabi, the United Arab Emirates (UAE) back onto asking about:
- What happened to infection prevention and control?
And why does this seem to happen in April (2013 and 2014) in particular?
- Has recent increased testing simply uncovered that which was already happening?
Perhaps there have always been more MERS-CoV infected people and a slightly better efficiency of transmission than we expected based on past efforts which mainly tested the sickest and most obvious of cases of MERS.
I'm also wonder a couple of other things.
As I've asked before, how were these samples selected? In a ProMED announcement a short time ago (thanks to Crawford Kilian/@Crof for pointing it out) we learned that the 3 complete genomes are from early on in the outbreak. So that raises the question of whether the virus has remained identical to earlier strains, later on in the outbreak?
Also, what do other seasonal human endemic respiratory viruses do in the Arabian peninsula? Are these sorts of outbreaks, but due to other viruses like influenzaviruses, parainfluenzaviruses, rhinoviruses, respiratory syncytial virus, metapneumoviruses or other coronaviruses etc also happen to this extent and with similar clinical impact? What is the occurrence of acute pneumonia like in the KSA and UAE?
I thank Prof Drosten for his efforts, efficiency and rapid (sample were only dispatched to Germany 14-Apr and we have 3 complete genomes already!) and open communication. And I take special note of his comments...
"In light of some of the recent comments implicating delays in following up on the outbreak it is worth considering the timing and the workload associated with careful testing and internal confirmation done in Jeddah. It is also worth mentioning that samples were already dispatched from KSA MOH Riyadh to Germany on [14 Apr 2014] -- just about a week after receipt of samples in Jeddah regional laboratory, testing, internal confirmatory testing, and transport to Riyadh. After dispatch from Riyadh, samples were not successfully delivered through customs in Germany with an administrative process that took 3 days (17 Apr 2014). The sequencing work in Bonn started only on [22 Apr 2014] for the simple reason that most of the laboratory staff (including myself) have been on Easter holidays. Sequencing of further samples taken at later time points in Jeddah is underway."
For my own part in communicating a message of delay, I'd like to add that, in my opinion, there really should be some local viral genotyping in place by now and that should have been producing 2014 MERS-CoV variant sequences all year. A great deal of fuss might have been side-stepped if we new the virus wasn't a factor in the outbreak.
For now, based on these 3 complete genomes and Prtof Drosten's 25 other partial spike gene sequences, there is no indication that viral change occurred early on in the Jeddah outbreak. No MERS-CoV v2.0 in town. No "mutant killer virus" headlines that can withstand scrutiny. We next await some detailed evolutionary analyses from Prof Andrew Rambaut who has these sequences. They are also available at http://www.virology-bonn.de
- ProMED post.