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Войти в исследования International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2025
Intensification with a CCR5 inhibitor at antiretroviral therapy initiation modulates interleukin-18 and inflammation-driven immune pathways in people with HIV.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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De La Torre Tarazona Erick, Calderón-Vicente Sergio, Fons-Contreras María, Rava Marta, Ruiz-Sancho Andrés Luis, Rivero Antonio, Macías Juan, Olalla Julián, Alcaraz Vidal Begoña, Rodríguez Díaz Daniel, Alcamí José, Muriel Alfonso, Serrano-Villar Sergio, Moreno Santiago, CoRIS cohort
Аннотация
OBJECTIVES: Persistent inflammation in people with HIV (PWH) on antiretroviral therapy (ART) may drive comorbidities and disease progression. Because CCR5 signaling regulates viral entry and immune activation, maraviroc (MVC) may contribute to attenuate inflammation, although previous findings have been inconsistent. This study evaluated a broad panel of markers to assess the long-term immunomodulatory effects of MVC when added at ART initiation.
METHODS: We conducted a longitudinal observational study including PWH starting ART with MVC (MVC group, n = 14) or without MVC (non-MVC group, n = 28), matched by sex, age, and ART regimen. Plasma markers were quantified by proximity extension assay (PEA) and enzyme-linked immunosorbent assay methods. Mixed multivariate models analyzed marker dynamics, and functional analyses identified enriched biological pathways.
RESULTS: PEA showed significant variation in up to 15 inflammatory markers (e.g. CXCL9, CXCL10, interferon-γ, CCL19) in both groups over ART initiation. Moreover, interleukin-18 declined significantly only in the MVC group (17.6% per year by PEA, and 35.5% by enzyme-linked immunosorbent assay, P <0.05). Functional Enrichment analyses showed a stronger downregulation of inflammation-related pathways, particularly, the chemokine signaling, in the MVC group (q <0.05).
CONCLUSIONS: Our results suggest that MVC intensification at ART initiation might contribute to reducing interleukin-18 levels and inflammation-driven immune pathways, providing insights for strategies to mitigate persistent inflammation in PWH.
METHODS: We conducted a longitudinal observational study including PWH starting ART with MVC (MVC group, n = 14) or without MVC (non-MVC group, n = 28), matched by sex, age, and ART regimen. Plasma markers were quantified by proximity extension assay (PEA) and enzyme-linked immunosorbent assay methods. Mixed multivariate models analyzed marker dynamics, and functional analyses identified enriched biological pathways.
RESULTS: PEA showed significant variation in up to 15 inflammatory markers (e.g. CXCL9, CXCL10, interferon-γ, CCL19) in both groups over ART initiation. Moreover, interleukin-18 declined significantly only in the MVC group (17.6% per year by PEA, and 35.5% by enzyme-linked immunosorbent assay, P <0.05). Functional Enrichment analyses showed a stronger downregulation of inflammation-related pathways, particularly, the chemokine signaling, in the MVC group (q <0.05).
CONCLUSIONS: Our results suggest that MVC intensification at ART initiation might contribute to reducing interleukin-18 levels and inflammation-driven immune pathways, providing insights for strategies to mitigate persistent inflammation in PWH.