Talía Sainz1, María Álvarez-Fuente, María Luisa Navarro, Laura Díaz, Pablo Rojo, Daniel Blázquez, María Isabel de José, José Tomás Ramos, Sergio Serrano-Villar, Jorge Martínez, Constancio Medrano, María Ángeles Muñoz-Fernández, María José Mellado. 1. *Laboratorio de InmunoBiología Molecular, Hospital General Universitario Gregorio Marañón e Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain; †Unidad de Enfermedades Infecciosas, Servicio de Pediatría, Hospital General Universitario Gregorio Marañón, Madrid, Spain; ‡Unidad de Cardiología Infantil, Hospital General Universitario Gregorio Marañón, Madrid, Spain; §Unidad de Inmunodeficiencias, Servicio de Pediatría, Hospital Universitario Doce de Octubre, Madrid, Spain; ‖Servicio de Pediatría, Hospital Universitario La Paz, Madrid, Spain; ¶Servicio de Pediatría, Hospital de Getafe, Madrid, Spain; #Servicio de Enfermedades Infecciosas, Hospital Universitario Ramón y Cajal, and IRYCIS, Madrid, Spain; **Servicio de Pediatría, Hospital Universitario Niño Jesús, Madrid, Spain; and ††Servicio de Pediatría, Hospital Carlos III, Madrid, Spain.
Abstract
BACKGROUND: HIV-infected adults display increased cardiovascular disease, probably driven by inflammation and immune activation. These relationships have not been addressed in vertically HIV-infected children and adolescents, a population at very high risk for long-term non-AIDS complications. METHODS: Carotid intima media thickness (IMT) was measured in a cohort of HIV-infected children and adolescents and healthy controls. C-reactive protein and markers of immune activation (CD38⁺HLA-DR⁺) and immune senescence (CD28⁻CD57⁺) were determined. RESULTS: One hundred fifty HIV-infected patients and 150 controls were included, 64.8% female. IMT was thicker in HIV-infected patients (0.434 mm ± 0.025 vs. 0.424 mm ± 0.018, P < 0.001). After adjustment by age, sex, body mass index, and smoking status, HIV infection was independently associated with thicker IMT (odds ratio, 2.28; 95% confidence interval: 1.25 to 4.13; P = 0.007). Among HIV-related variables, a low CD4 nadir was related to an increased IMT. Although HIV-infected subjects presented higher frequencies of activated CD4⁺ and CD8⁺ T cells (P = 0.002 and P = 0.087, respectively), no relation was found between IMT and inflammation, immune activation, or senescence. CONCLUSIONS: Structural changes of the vasculature present early in vertically HIV-infected subjects as well as immune activation and senescence. These patients should be carefully monitored for the prompt detection and early treatment of cardiovascular disease.
BACKGROUND:HIV-infected adults display increased cardiovascular disease, probably driven by inflammation and immune activation. These relationships have not been addressed in vertically HIV-infectedchildren and adolescents, a population at very high risk for long-term non-AIDS complications. METHODS: Carotid intima media thickness (IMT) was measured in a cohort of HIV-infectedchildren and adolescents and healthy controls. C-reactive protein and markers of immune activation (CD38⁺HLA-DR⁺) and immune senescence (CD28⁻CD57⁺) were determined. RESULTS: One hundred fifty HIV-infectedpatients and 150 controls were included, 64.8% female. IMT was thicker in HIV-infectedpatients (0.434 mm ± 0.025 vs. 0.424 mm ± 0.018, P < 0.001). After adjustment by age, sex, body mass index, and smoking status, HIV infection was independently associated with thicker IMT (odds ratio, 2.28; 95% confidence interval: 1.25 to 4.13; P = 0.007). Among HIV-related variables, a low CD4 nadir was related to an increased IMT. Although HIV-infected subjects presented higher frequencies of activated CD4⁺ and CD8⁺ T cells (P = 0.002 and P = 0.087, respectively), no relation was found between IMT and inflammation, immune activation, or senescence. CONCLUSIONS: Structural changes of the vasculature present early in vertically HIV-infected subjects as well as immune activation and senescence. These patients should be carefully monitored for the prompt detection and early treatment of cardiovascular disease.
Authors: Khaled Z Abd-Elmoniem; Aylin B Unsal; Sarah Eshera; Jatin R Matta; Nancy Muldoon; Dorothea McAreavey; Julia B Purdy; Rohan Hazra; Colleen Hadigan; Ahmed M Gharib Journal: Clin Infect Dis Date: 2014-08-25 Impact factor: 9.079
Authors: A Bamford; A Turkova; H Lyall; C Foster; N Klein; D Bastiaans; D Burger; S Bernadi; K Butler; E Chiappini; P Clayden; M Della Negra; V Giacomet; C Giaquinto; D Gibb; L Galli; M Hainaut; M Koros; L Marques; E Nastouli; T Niehues; A Noguera-Julian; P Rojo; C Rudin; H J Scherpbier; G Tudor-Williams; S B Welch Journal: HIV Med Date: 2015-02-03 Impact factor: 3.180
Authors: Lisa J Frigati; Jennifer Jao; Sana Mahtab; Nana-Akua Asafu Agyei; Mark F Cotton; Landon Myer; Heather J Zar Journal: AIDS Res Hum Retroviruses Date: 2018-09-25 Impact factor: 2.205
Authors: Lukasz D Weiner; Mauricio Retuerto; Christopher L Hager; Vanessa El Kamari; Lingpeng Shan; Abdus Sattar; Manjusha Kulkarni; Nicholas Funderburg; Mahmoud A Ghannoum; Sahera Dirajlal-Fargo; Grace A McComsey Journal: AIDS Res Hum Retroviruses Date: 2019-04-04 Impact factor: 2.205
Authors: Allison Ross Eckard; Julia C Rosebush; S Thera Lee; Mary Ann O'Riordan; Jakob G Habib; Julie E Daniels; Danielle Labbato; Monika Uribe-Leitz; Ann Chahroudi; Grace A McComsey Journal: Pediatr Infect Dis J Date: 2016-12 Impact factor: 2.129
Authors: David B Hanna; Mengye Guo; Petra Bůžková; Tracie L Miller; Wendy S Post; James H Stein; Judith S Currier; Richard A Kronmal; Matthew S Freiberg; Siiri N Bennett; Cecilia M Shikuma; Kathryn Anastos; Yanjie Li; Russell P Tracy; Howard N Hodis; Joseph A Delaney; Robert C Kaplan Journal: Clin Infect Dis Date: 2016-04-26 Impact factor: 9.079