Dynamics of virological suppression and systemic immune-inflammatory response following antiretroviral therapy in pediatric HIV infection
Frontiers in cellular and infection microbiology, cilt.16, ss.1918829, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 16
- Basım Tarihi: 2026
- Doi Numarası: 10.3389/fcimb.2026.1918829
- Dergi Adı: Frontiers in cellular and infection microbiology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE, Directory of Open Access Journals, Zoological Record, Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Health Research Premium Collection (ProQuest)
- Sayfa Sayıları: ss.1918829
- Anahtar Kelimeler: antiretroviral therapy, CD4, CD4/CD8, HIV, immune activation, inflammation, pediatric, systemic immune-inflammation index (SII)
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- İstanbul Üniversitesi Adresli: Evet
Özet
Background: Persistent systemic inflammation remains a hallmark of treated HIV infection and is not reliably resolved by virological suppression alone. The Systemic Immune-Inflammation Index (SII), a composite hematologic index [(neutrophil × platelet)/lymphocyte count], has emerged as a candidate inflammatory biomarker. Longitudinal SII data following antiretroviral therapy (ART) initiation in pediatric HIV are lacking. Methods: This single-center retrospective paired longitudinal study included 30 pediatric patients with HIV with laboratory data at baseline and 12 months post-ART. The primary outcome was change in SII; secondary outcomes included CD4%, HIV RNA, and double-negative T-cell percentage (DNT%). Non-improvers were characterized by age, sex, ART regimen, nutritional status, and co-infection status. Paired comparisons used the Wilcoxon signed-rank test; Spearman correlation was the primary inferential method, with Pearson as a sensitivity analysis. Results: Median SII declined numerically (342,637 to 250,527) but did not reach significance (p = 0.428), despite significant improvement in CD4% (p < 0.001) and HIV RNA (p < 0.001). SII failed to improve in 13/30 patients (43.3%). The baseline inverse correlation between SII and CD4% (r = -0.450, p = 0.013) was substantially attenuated at month 12 (r = -0.004, p = 0.985). A parametric correlation between ΔSII and ΔHIV RNA (r = +0.534, p = 0.002) was not confirmed on rank-based testing (ρ = +0.004), reflecting leverage from two extreme-viremia patients. The 1-2-year age group had the highest rate of SII non-improvement (75.0%); an unadjusted post-hoc comparison with the 6-11-year group yielded a nominal p value of 0.038. Female sex was more frequent among non-improvers (53.8% vs. 17.6%; p = 0.056), although the difference was not statistically significant. Genvoya® use showed a similar non-significant trend (p = 0.132). Nutritional status, herpesvirus co-infection, and virological suppression at month 12 were not significantly associated with SII trajectory. Conclusion: In this pediatric HIV cohort, SII failed to improve in nearly half of patients despite successful ART, dissociating from both CD4 reconstitution and HIV RNA suppression. These findings suggest SII reflects a residual inflammatory state driven by mechanisms beyond viral replication, including ART class-specific, sex-related, and developmental factors. Routine SII monitoring may identify patients at ongoing inflammatory risk despite virological success; larger prospective studies are needed.