Table 2.
GO and Pathway Analysis of Transcriptional Responses Attributable to Acute and Convalescent iNTS Disease and “Other” Infections
| Datasets compared | DE genes up/down regulated | Gene ontology terms in DE gene datasets (number of genes) | Pathways in DE gene datasets |
| Acute iNTS vs HIV+ (1511 DE genes) | 1075 upregulated | Cell cycle (55); DNA replication (25); DNA translation (18); DNA repair (26); Mitosis (39); Cell division (36) | Viral mRNA translation; Viral replication; Cell cycle; Nucleotide excision repair; Aurora B signalling |
| 436 downregulated | Chemotaxis (10) | None | |
| Acute “other” infections vs HIV+ (1535 DE genes) | 1017 upregulated | Innate immune response (51); Inflammatory response (24) | IL-1 mediated signalling; IL-4 mediated signalling; Complement and coagulation; Atypical NFκB |
| 518 downregulated | Transmembrane receptor activity (13); Immune response (26) | NK cell mediated cytotoxicity; TCR signalling in naive CD4 T-cells; 2nd messenger molecules in TCR signalling; Translocation of ZAP to immonological synapse; Antigen processing and presentation; Cytokine-cytokine receptor interaction | |
| FU early (1–2 months) vs HIV+ (418 DE genes) | 257 upregulated | Cell cycle; Cell division; Translation | Cell cycle; Viral mRNA translation; Influenza life cycle; Influenza infection |
| 161 downregulated | None | None | |
| FU late (3-5 months) vs HIV+ (38 DE genes) | 19 upregulated | None | None |
| 19 downregulated | None | None |
All cases are compared with stage-matched HIV-infected controls in order to demonstrate the transcriptional responses attributable to bacterial infection, against a background of HIV-infection (see Figure 2).
Abbreviations: DE, differentially expressed; FUearly, the 8 convalescent cases in the bacterial infection cluster that were sampled 1–2 months after acute infection; FUlate, the 4/5 convalescent cases in the control cluster that were sampled after 3–5 months; GO, gene ontology.