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VZV infection of primary keratinocytes

ABSTRACT: Our aim was to investigate the interaction between epidermal differentiation and VZV infection. By means of a calcium-induced keratinocyte differentiation model and RNA-seq we show VZV infection has a profound effect on differentiating keratinocytes and hijacks the normal process of epidermal gene expression to generate a signature resembling patterns of gene expression seen in both heritable and acquired skin-blistering disorders. Analysis of the viral transcriptome provides evidence that VZV replication in skin is tightly linked to differentiation and critically, that late viral gene expression is associated with cellular differentiation. The experiment was performed on human primary keratinocytes under four conditions: undifferentiated/uninfected, uninfected/differentiated, VZV-infected/undifferentiated and VZV-infected/differentiated.

INSTRUMENT(S): Illumina Genome Analyzer IIx

ORGANISM(S): Homo sapiens

SUBMITTER: Dan Frampton 

PROVIDER: E-MTAB-1717 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

RNA-seq analysis of host and viral gene expression highlights interaction between varicella zoster virus and keratinocyte differentiation.

Jones Meleri M   Dry Inga R IR   Frampton Dan D   Singh Manuraj M   Kanda Ravinder K RK   Yee Michael B MB   Kellam Paul P   Hollinshead Michael M   Kinchington Paul R PR   O'Toole Edel A EA   Breuer Judith J  

PLoS pathogens 20140130 1

Varicella zoster virus (VZV) is the etiological agent of chickenpox and shingles, diseases characterized by epidermal skin blistering. Using a calcium-induced keratinocyte differentiation model we investigated the interaction between epidermal differentiation and VZV infection. RNA-seq analysis showed that VZV infection has a profound effect on differentiating keratinocytes, altering the normal process of epidermal gene expression to generate a signature that resembles patterns of gene expressio  ...[more]

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