title: High-density lipoprotein concentrations relate to the clinical course of HIV viral load in patients undergoing antiretroviral therapy.
abstract: OBJECTIVE
  To determine whether levels of HDL are associated with viral load response in HIV-treated patients, and to seek an explanation based on amino acid sequence similarity between the key apolipoprotein A1 and HIV proteins concerned in viral replication.
  
  
  METHODS
  The major HDL lipoprotein is apolipoprotein A1, which is able to inhibit HIV-induced syncytium formation. This retrospective clinical study assessed the relationship between the response to antiretroviral treatment (time of undetectable viral load/duration of viral suppression below the limit of detection) and HDL-cholesterol levels on commencing antiretroviral treatment.
  
  
  METHODS
  HIV-treated patients with undetectable HIV viral loads were followed every 3 months for 36 months. We measured total cholesterol, HDL-cholesterol, triglycerides, previous responses to antiretroviral treatment, opportunistic infections, sex and age. These variables were assessed in relation to the time of undetectable viral load until viral rebound. Amino acid sequence alignment was performed with HIV proteins and apolipoprotein A1 to detect shared similarity.
  
  
  RESULTS
  The Cox proportional hazards model showed a significant association between HDL-cholesterol and the time of undetectable viral load. The other variables studied were not associated. There was 30% sequence similarity in an area of 50 amino acids shared between apolipoprotein A1 and p17 Gag-HIV protein.
  
  
  CONCLUSIONS
  High levels of HDL-cholesterol are associated with a better viral response in treated HIV patients. This association could be related to the sequence similarity and structure homology between apolipoprotein A1 and p17 Gag-HIV protein, which raises the intriguing clinical possibility that inducing an increase in HDL could assist HIV therapy.
authors.affiliation: Servei de Medicina Interna of the Hospital Universitari de Sant Joan, Universitat Rovira i Virgili, Reus, Spain. cavillaverde@grupsagessa.com
authors.forename: Carlos
authors.initials: C
authors.lastname: Alonso-Villaverde
authors.forename: Teresa
authors.initials: T
authors.lastname: Segues
authors.forename: Blai
authors.initials: B
authors.lastname: Coll-Crespo
authors.forename: Rosa
authors.initials: R
authors.lastname: Pérez-Bernalte
authors.forename: Antoni
authors.initials: A
authors.lastname: Rabassa
authors.forename: Maika
authors.initials: M
authors.lastname: Gomila
authors.forename: Sandra
authors.initials: S
authors.lastname: Parra
authors.forename: M Asunción
authors.initials: MA
authors.lastname: Gozález-Esteban
authors.forename: Ma Jesús
authors.initials: MJ
authors.lastname: Jiménez-Expósito
authors.forename: Lluis
authors.initials: L
authors.lastname: Masana
mesh_terms: D000328:Adult; D000595:Amino Acid Sequence; D023241:Antiretroviral Therapy, Highly Active; D016632:Apolipoprotein A-I / Q000097:blood / Q000737:chemistry; D015415:Biomarkers / Q000097:blood; D005260:Female; D015683:Gene Products, gag / Q000737:chemistry; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy* / Q000821:virology; D015497:HIV-1 / Q000502:physiology; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D016016:Proportional Hazards Models; D012189:Retrospective Studies; D016415:Sequence Alignment; D019562:Viral Load; D014779:Virus Replication
chemical_list: D016632:Apolipoprotein A-I; D015415:Biomarkers; D015683:Gene Products, gag; D008075:Lipoproteins, HDL