TABLE 2.
Strongest network of inflammatory markers contributing to Combinatory Immune Signature that were common between HIV-uninfected (HIV-) women and virally suppressed women with HIV (HIV+VS).
| Combinatory immune signature | HIV-serostatus |
|
| HIV- (n = 56) | HIV+VS (n = 49) | |
| 1 | Immune activation & vascular dysfunction | Immune activation & vascular dysfunction |
| Beta-2 microglobulin, Clusterin, Cystatin C, sCD14, sVEGFR2 | Beta-2 microglobulin, Clusterin, Cystatin C, sCD14, sVEGFR2 | |
| 2 | T Cell-dependent antiviral response | T Cell-dependent antiviral response |
| TRAIL/CD253, IL-10, FGF-2, Fractalkine/CX3CL1, SDF-1a + b/CXCL12, ITAC/CXCL11 | TRAIL/CD253, IL-10, BCA-1/CXCL13, 6CKINE/CCL21 | |
| 3 | Neuroinflammatory signaling | Neuroinflammatory signaling |
| Fractalkine/CX3CL1, FGF-2, serum amyloid A, CRP | TRAIL/CD253, serum amyloid A, CRP, IL-10, Adiponectin | |
Markers in italics were negatively associated with the profile; otherwise, the markers were positively associated with the profile. Our analyses focused on how the interrelated networks of inflammatory mediators cooperated together. As such, the same categorical description could be assigned for Combinatory Immune Signatures, despite having non-identical composition of individual immune markers.