Table 1.

HHV-6 infection of SupT1 cells induces and inhibits multiple genesa

Gene type and Z ratioGene productDescriptionFunction(s)
HHV-6A/controlHHV-6B/control
Up-regulated
 2.472.66PFKPPhosphofructokinaseGlycolytic pathway
 1.552.62PRKM1Protein kinaseMAPS kinase 1 activation
 2.782.46WSX-1Class 1 cytokine receptorProinflammation signaling
 1.602.44SSI-1JAK binding proteinTyrosine kinase signaling
 1.731.91BCL6B-cell CLL/lymphoma 6B-cell signaling, chemokine regulation
 1.581.73HLA-DQB1MHCb class II, DQ beta 1Antigen presentation
 2.121.63HLA-AMHC class IAAntigen presentation
Down-regulated
 −3.02−3.41RYKRYKR-like tyrosine kinaseTyrosine kinase
 −1.83−3.40APPBP1Amyloid precursor protein 1Amyloid processing
 −2.76−3.34ATF2Activating transcription factor 4Transcription regulation
 −3.56−3.23MDM2p53 binding proteinp53 regulation
 −2.94−2.92APLP1Amyloid beta precursor proteinAmyloid beta processing
 −2.89−2.76PSEN2Presenilin 2ERd protein chaperone/amyloid processing
 −2.27−2.74PSEN1Presenilin 1ER protein chaperone/amyloid processing
 −2.98−3.23CXCR5CXC chemokine receptorChemokine signaling
 −1.66−2.25SLAMLymphocytic activation moleculeLymphocyte activation/viral receptor
 −2.13−2.06APLP2Amyloid precursor protein 2Amyloid beta processing
  • a The Z ratios shown represent genes with the greatest changes in expression and are averages from two independent experiments performed in duplicate. The data were sorted based on high Z ratios comparing SupT1 cells infected with HHV-6B (Z29) or variant HHV-6A (GS) and uninfected cells (control). Genes with a variance between experiments of greater than 0.2 were not analyzed.

  • b MHC, major histocompatibility complex.

  • c MAP, mitogen-activated protein.

  • d ER, endoplasmic reticulum.