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Alteration of type I interferon response is associated with subclinical atherosclerosis in virologically suppressed HIV‐1‐infected male patients
Author(s) -
Santinelli Letizia,
De Girolamo Gabriella,
Borrazzo Cristian,
Vassalini Paolo,
Pinacchio Claudia,
Cavallari Eugenio Nelson,
Statzu Maura,
Frasca Federica,
Scordio Mirko,
Bitossi Camilla,
Viscido Agnese,
Ceccarelli Giancarlo,
Mancone Massimo,
Mastroianni Claudio Maria,
Antonelli Guido,
d'Ettorre Gabriella,
Scagnolari Carolina
Publication year - 2021
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.27028
Subject(s) - medicine , asymptomatic , framingham risk score , subclinical infection , interferon , pathogenesis , peripheral blood mononuclear cell , gastroenterology , immunology , disease , biology , biochemistry , in vitro
Given human immunodeficiency virus‐1 (HIV‐1)‐infected patients have alterations in the type I interferon (IFN‐I) pathway and are also at elevated risk of atherosclerosis, we evaluated IFN‐I response and subclinical cardiovascular disease (CVD) association in HIV‐1‐infected patients. Transcript levels of IFN‐α/β and IFN‐stimulated gene 56 (ISG56) were evaluated by RT/real‐time PCR in peripheral blood mononuclear cells collected from asymptomatic HIV‐1‐positive male patients at high risk of developing CVD ( n  = 34) and healthy subjects ( n  = 21). Stenosis degree (≥ or <50%), calcium volume score, calcium Agatston score, and myocardial extracellular volume were examined by coronary computerized tomography scan. Carotid intima‐media thickness (cIMT), Framingham risk score, atherosclerotic cardiovascular disease (ASCVD) score, and risk score developed by data collection on adverse effects of anti‐HIV drugs (D:A:D) were also measured. Increased IFN‐α, IFN‐β, and ISG56 levels were observed in all HIV‐1‐infected males compared to healthy controls ( p  < .001 for all genes analyzed). HIV‐1‐infected patients with a stenosis degree ≥50% showed a higher Framingham risk score ( p  = .019), which was correlated with IFN‐β and ISG56 levels. HIV‐1‐infected males with enhanced IFN‐I levels and stenosis displayed a higher ASCVD calculated risk ( p  = .011) and D:A:D score ( p  = .004). Also, there was a trend toward higher IFN‐α and ISG56 mRNA levels in HIV‐1‐positive patients with an increased cIMT ( p  > .05). Dysregulation of IFN‐I response might participate in the pathogenesis of HIV‐1‐associated CVD.

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