4.7 Article

Lipoprotein Profile in Immunological Non-Responders PLHIV after Antiretroviral Therapy Initiation

期刊

出版社

MDPI
DOI: 10.3390/ijms23158071

关键词

antiretroviral therapy; cardiovascular risk; immunological non-responder; lipoproteins; longitudinal analysis; nuclear magnetic resonance; people living with HIV

资金

  1. Fondo de Investigacion Sanitaria (European Regional Development Fund/European Social Fund
  2. A way to make Europe/Investing in your future) [PI16/00503, PI19/01337, PI20/00326]
  3. Programa de Suport als Grups de Recerca AGAUR [2017SGR948]
  4. SPANISH AIDS Research Network-ISCIIIFEDER (Spain) [RD16/0025/0006]
  5. Centro de Investigacion Biomedica en Red de Enfermedades Infecciosas-ISCIII (CIBERINFEC), Madrid, Spain [CB21/13/00020]
  6. Universitat Rovira I Virgili [2019PMF-PIPF-18]
  7. Programa de Intensificacion de Investigadores-ISCIII [INT20/00031]
  8. Premi a la Trajectoria Investigadora dels Hospitals de l'ICS 2018
  9. IISPV [2019/IISPV/05]
  10. GeSIDA through the III Premio para Jovenes Investigadores 2019
  11. Instituto de Salud Carlos III (ISCIII) through the Miguel Servet Program [CP19/00146]

向作者/读者索取更多资源

Nuclear magnetic resonance (NMR)-based lipoprotein tests have shown that LDL-P and HDL-P are better predictors of cardiovascular risk than traditional cholesterol markers. In people with HIV, impaired immune function may be associated with preclinical atherosclerosis and vascular dysfunction. Starting antiretroviral therapy (ART) can equalize the lipoprotein-based cardiovascular risk markers between individuals with poor immunological response (INR) and good immunological response (IR).
Nuclear magnetic resonance (NMR)-based advanced lipoprotein tests have demonstrated that LDL and HDL particle numbers (LDL-P and HDL-P) are more powerful cardiovascular (CV) risk biomarkers than conventional cholesterol markers. Of interest, in people living with HIV (PLHIV), predictors of preclinical atherosclerosis and vascular dysfunction may be associated with impaired immune function. We previously stated that immunological non-responders (INR) were at higher CV risk than immunological responders (IR) before starting antiretroviral therapy (ART). Using Liposcale (R) tests, we characterized the lipoprotein profile from the same cohort of PLHIV at month 12 and month 36 after starting ART, intending to explore what happened with these indicators of CV risk during viral suppression. ART initiation dissipates the differences in lipoprotein-based CV risk markers between INR and IR, and only an increase in the number of HDL-P was found in INR + IR when compared to controls (p = 0.047). Interestingly, CD4(+) T-cell counts negatively correlated with medium HDL-P concentrations at month 12 in all individuals (p = -0.335, p = 0.003). Longitudinal analyses showed an important increase in LDL-P and HDL-P at month 36 when compared to baseline values in both IR and INR. A proper balance between a proatherogenic and atherogenic environment may be related to the reconstitution of CD4(+) T-cell count in PLHIV.

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