Differences in the proliferative capacities of 2014 Epidemic and Fermon EV-D68 Strains
Monday, March 5, 2018
South Hall A2 (Convention Center)
Nicholas Klaiber, MD, Michael Mcvoy, PhD, Wei Zhao, MD PhD FAAAAI
RATIONALE: Enterovirus D68 (EV-D68), first isolated in 1962, caused an epidemic of pediatric respiratory disease in 2014. Genomic analysis of EV-D68 strains from this epidemic revealed point mutations not present in the fermon (1962) strain. Such mutations are thought to facilitate EV-D68 replication due to the proximity of these polymorphisms to viral protease cleavage sites. We sought to assess whether the 2014 EV-D68 strain possesses an increased proliferative capacity when compared to the 1962 fermon strain.

METHODS: Using an established rhabdomyosarcoma based model of EV-D68 infection we directly compared proliferative capacity of ATCC VR-1826 EV-D68 (fermon) virus to that of VR-1823 (epidemic) EV-D68. RT-PCR utilizing EV-D68 specific primers and probes was used to compare delta Ct values of the two EV-D68 strains at different time points following inoculation. Indirect immunofluorescence was employed to compare the time course of VP2 protein appearance on rhabdomyosarcoma cells following infection. Graphpad Prism software was utilized to perform student t-test on PCR data and assess statistical significance between groups with significance set at p<0.05

RESULTS: EV-D68 virus derived from the 2014 epidemic was able to proliferate with a 1.6 fold increase in genome copy number over 24 hours compared to an increase of 1.09 in the fermon strain by RT-PCR (p<0.001). VP2 protein of EV-D68 was first detected at 7 hours post-infection compared with 10 hours for the fermon strain.

CONCLUSIONS: The 2014 epidemic EV-D68 strain displays an increased proliferative capacity when compared to the 1962 fermon strain, probably attributed to the previously described point mutations.