Title Mutations in VP1 and 3A proteins improve binding and replication of rhinovirus C15 in HeLa-E8 cells.
Author Bochkov, Yury A; Watters, Kelly; Basnet, Sarmila; Sijapati, Shakher; Hill, Marchel; Palmenberg, Ann C; Gern, James E
Journal Virology Publication Year/Month 2016-Dec
PMID 27743961 PMCID PMC5110265
Affiliation + expend 1.Department of Pediatrics, University of Wisconsin-Madison, Madison, WI, USA. Electronic address: yabochkov@wisc.edu.

Viruses in the rhinovirus C species (RV-C) can cause severe respiratory illnesses in children including pneumonia and asthma exacerbations. A transduced cell line (HeLa-E8) stably expressing the CDHR3-Y529 receptor variant, supports propagation of RV-C after infection. C15 clinical or recombinant isolates replicate in HeLa-E8, however progeny yields are lower than those of related strains of RV-A and RV-B. Serial passaging of C15 in HeLa-E8 resulted in stronger cytopathic effects and increased (>/=10-fold) virus binding to cells and progeny yields. The adaptation was acquired by two mutations which increased binding (VP1 T125K) and replication (3A E41K), respectively. A similar 3A mutation engineered into C2 and C41 cDNAs also improved viral replication (2-8 fold) in HeLa but the heparan sulfate mediated cell-binding enhancement by the VP1 change was C15-specific. The findings now enable large-scale cost-effective C15 production by infection and the testing of RV-C infectivity by plaque assay.

StrainID RV Species Serotype Length(nt) Country Year Strain Name
ANZ04536 A 16 7116 USA 1985 KC939
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