Abstract

Author:
jNdukwe Arua Kalu, Mathew Folarami Olaniyan, Plus Omoruyi Omosigho, Bukhari Isah Shuib, Ewean Chukwuma Omoruyi, Isah Sadiq Yelwa, Iyare Godfrey Innocent, Chinedu Udeckukwu Aka Okeke, Aliyu Mohammed Abdullahi, Ibrahim Alhaji Adamu

Doi: 10.26480/jhcdc.01.2025.51.58

This is an open access article distributed under the Creative Commons Attribution License CC BY 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Despite effective combination antiretroviral therapy (cART), persistent inflammation in individuals with HIV-1 contributes to various comorbidities and treatment failure. This study explores how baseline immune function, disease stage at treatment initiation, and demographic factors influence cART success by comparing inflammatory markers, interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP) between virologically suppressed and virological failure groups. A mixed cross-sectional and longitudinal study was conducted on 93 HIV-1-infected adults receiving cART at IBB Specialist Hospital, Minna (September 2024 – February 2025). Participants were divided into two groups: 50 with viral suppression (<1000 copies/mL) and 43 with virological failure (>1000 copies/mL). HIV-1 RNA levels were measured using COBAS® Taqman®, CD4 counts with Partec™ Cyflow, and plasma IL-6 and hs-CRP via ELISA. Results showed that the Suppressed group had lower systemic inflammation, with 28% exhibiting reduced IL-6 levels and 48% showing hs-CRP <1 mg/L. In contrast, the Virological Failure group had significantly elevated IL-6 (100%) and hs-CRP >3 mg/L (69.76%), indicating heightened immune activation. Additionally, the Virological Failure group was older, had lower CD4 counts, and maintained higher viral loads at both enrollment and six months. A significant correlation was observed between hs-CRP levels and viral load at six months, suggesting inflammation may sustain high viral replication. However, IL-6 and hs-CRP did not strongly correlate with each other or consistently associate with CD4 counts or viral load over time. These findings underscore the importance of addressing inflammation and immune activation in managing HIV, particularly in patients experiencing virological failure.