Descriptive modification of inflammatory markers in HIV patients after cART initiation according to gender, smoking habit, CMV infection, BMI and serum lipids

Persistent inflammation, despite anti-retroviral therapy (ART), is an independent predictor of mortality and comorbidities in HIV infection. Multiple factors, including lifestyle and chronic viral coinfections, may contribute. Several of these factors are also associated with a chronic inflammation...

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Veröffentlicht in:Cytokine (Philadelphia, Pa.) Pa.), 2021-07, Vol.143, p.155547-155547, Article 155547
Hauptverfasser: Zanella, Isabella, Biasiotto, Giorgio, Castelli, Francesco, Calza, Stefano, Carriero, Canio, Degli Antoni, Melania, Focà, Emanuele, Quiros-Roldan, Eugenia
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Sprache:eng
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Zusammenfassung:Persistent inflammation, despite anti-retroviral therapy (ART), is an independent predictor of mortality and comorbidities in HIV infection. Multiple factors, including lifestyle and chronic viral coinfections, may contribute. Several of these factors are also associated with a chronic inflammation in the general population. Little is known about the degree to which these factors influence inflammation in HIV infection, particularly within the first year of ART. The purpose of this study was to distinguish the effects of factors (gender, body mass index, cholesterol and triglyceride levels, smoke habit and cytomegalovirus seropositivity), known to contribute to inflammation, on inflammation biomarkers over the first year of ART in HIV-infected patients. Linear mixed model analysis revealed significant biomarker decreases [soluble CD14 (s-CD14), soluble CD163 (s-CD163) and D-dimer (DD)], or increases [C Reactive Protein (CRP) and interleukin-6 (IL-6)] over time in the whole cohort, differences in most categories (genders for IL-6, smoke habit for s-CD14, cytomegalovirus infection for s-CD163 and IL-6) and in some category × time interactions [gender for interleukin-7 (IL-7)], cytomegalovirus infection for s-CD14 and cholesterol levels for s-CD14 and Tumor Necrosis Factor α (TNF-α)]. This explorative longitudinal study suggests further investigations on targeting inflammation pathophysiology in HIV-infected patients on ART.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2021.155547