TABLE 2

HIV viremia results in NK cell downregulation of eIF2 signaling and upregulation of IFN signaling determined using pathway analysis of transcripts obtained from NK cells of HIV- and HCV-infected patientsa

PathwaysbPRatioz-scoreDifferentially expressed genes of interest
HIV
    Interferon signaling2.14E–066/361.63OAS1, JAK1, MX1, STAT2
    NK cell signaling6.93E–0710/120NARAC2, KIR2DS4, LAIR1, CD244, SH2D1B
    Nucleotide excision repair5.24E–044/35NAPOLR2G, POLR2J, POLR2L
    EIF2 signaling7.58E–0814/212−2.45RPL24, RPS7, RPL15, RPL27, EIF3F
    Remodeling of epithelial adherence junctions3.53E–089/66−2.00TUBA1B, ARPC2, RAB7A, ARPC3
    Regulation of actin-based motility by Rho3.94E–057/86−2.65RAC2, ACTR3, CDC42, ARPC2
    FcγR-mediated phagocytosis in macrophages and monocytes6.52E–057/93−2.65RAC2, ACTR3, CDC42, ARPC2
    Glycolysis I4.93E–065/24NAPGK1, TPI1, PGAM1, PKM, PGAM4
    Oxidative phosphorylation1.32E–047/104NAATP5O, NDUFA12, COX7A2L
HCV
    Interferon signaling1.75E–064/362OAS1, IFI6, STAT2, STAT1
    NK cell signaling1.60E–087/120NACD247, KIR2DS4, KIR3DL2, PRKCH
    DNA double-strand break repair by NHEJ5.23E–042/14NAXRCC6, ATM
    GADD45 signaling9.76E–042/19NAGADD45B, ATM
  • a The table presents the results of the pathway analysis of NK cell transcripts derived from 6 HIV- and 8 HCV-infected patients. The significance of modulation, not necessarily up- or downregulation, of each pathway is indicated by the P value. The z-score displays the overall direction, and the degree of overlap with the preset gene lists per pathway is indicated by a ratio. The HBV-infected cohort, regardless of the clinical phase, did not significantly modulate (according to preset criteria of P < 10−4 and minimal overlap of 5%) a single known pathway and was therefore not included in this table.homologous end joining; NA, not applicable.

  • b Only pathways with a ratio of >0.05 and P value of <10−4 are depicted, resulting in the exclusion of HBV-infected cohorts.