Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9289289 | Virus Research | 2005 | 9 Pages |
Abstract
The six coxsackievirus B serotypes (CVB1-6) use the coxsackie- and adenovirus receptor (CAR) for host cell entry. Four of these serotypes, CVB1, 3, 5 and 6, have also shown the capacity to replicate and cause cytolysis in rhabdomyosarcoma (RD) cells, a CAR-deficient cell line. This extended tropism has been associated with an acquired ability to bind decay accelerating factor (DAF). In this study, we have adapted the CVB2 prototype strain Ohio-1 (CVB2/O) to replicate in RD cells. Two types of infection were identified: (I) an enterovirus-typical, lytic infection, and (II) a non-lytic infection. Both CVB2/O-RD variants retained the prototype-ability to cause cytopathic effect in HeLa cells using CAR as receptor. Phenotypic and genotypic changes in the CVB2/O-RD-variants were determined and compared to the prototype cultured in HeLa cells. Inhibition studies using antibodies against CAR and DAF revealed a maintained ability of the CVB2/O-RD-variants to bind CAR, but no binding to DAF was observed. In addition, neither the prototype nor the CVB2/O-RD-variants were able to cause hemagglutination in human red blood cells, an enterovirus feature associated with affinity for DAF. Sequence analysis of the CVB2/O-RD-variants showed acquired mutations in the capsid region, suggesting extended receptor usage towards an alternative, yet unidentified, receptor for CVB2.
Related Topics
Life Sciences
Immunology and Microbiology
Virology
Authors
Charlotta Polacek, Jens-Ola Ekström, Anneli Lundgren, A. Michael Lindberg,