Authors: K M Rogers D H Black R Eberle
Publish Date: 2006/11/23
Volume: 152, Issue: 3, Pages: 543-552
Abstract
Infection of mice with herpesvirus papio 2 HVP2 parallels zoonotic monkey B virus infections A major benefit of the HVP2/mouse model is the existence of two HVP2 subtypes HVP2nv rapidly invades and destroys the CNS while HVP2ap produces no clinical signs and mild histopathological lesions However in the natural baboon host no difference in pathogenicity of HVP2 subtypes is evident Primary dermal fibroblast cells were evaluated as a model system for defining virushost interactions that influence the outcome of a crossspecies infection No differences in plaque formation or virus replication were observed between HVP2 subtypes in primary baboon dermal fibroblast cultures In contrast when primary mouse dermal fibroblasts PMDF were infected HVP2nv replicated to higher titers and was more efficient at shutting down hostcell protein synthesis compared to HVP2ap HVP2apinfected PMDF cells produced more IFNβ compared to HVP2nv and IFNβ pretreatment of PMDF cultures inhibited HVP2ap replication but did not affect HVP2nv The differential pathogenicity of HVP2 subtypes in mice and the lack of such differences in the natural baboon host are recapitulated in the primary dermal fibroblast cell culture system This model may prove useful in examining early local host responses that influence the outcome of crossspecies infections
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