title: Abnormalities in apolipoprotein and lipid levels in an HIV-infected Brazilian population under different treatment profiles: the relevance of apolipoprotein E genotypes and immunological status.
abstract: HIV infection is associated with disturbances in lipid metabolism due to a host's response mechanism and the current antiretroviral therapy. The pathological appearance and progression of atherosclerosis is dependent on the presence of injurious agents in the vascular endothelium and variations in different subsets of candidate genes. Therefore, the Hha I polymorphism in the apolipoprotein E gene was evaluated in addition to triglycerides, total cholesterol, very low-density lipoprotein (VLDL), LDL, high-density lipoprotein (HDL), and apolipoprotein (apo) Al, B and E levels in 86 Brazilian HIV-infected patients and 29 healthy controls. The allele frequency for apoE in the HIV-infected group and controls was in agreement with data on the Brazilian population. Dyslipidemia was observed in the HIV group and verified by increased levels of triglycerides, VLDL and apoE, and decreased levels of HDL and apoAl. The greatest abnormalities in these biochemical variables were shown in the HIV-infected individuals whose immune function was more compromised. The effect of the genetic variation at the APOE gene on biochemical variables was more pronounced in the HIV-infected individuals who carried the apoE2/3 genotype. The highly active anti-retroviral therapy (HAART)-receiving group presented increased levels of total cholesterol and apoE. Dyslipidemia was a predictable consequence of HIV infection and the protease inhibitors intensified the increase in apoE values.
authors.affiliation: Institute of Chemistry, Faculty of Pharmaceutical Sciences, São Paulo State University - UNESP, Araraquara, Brazil. iranmalavazi@bol.com.br
authors.forename: Iran
authors.initials: I
authors.lastname: Malavazi
authors.forename: Emiliana P
authors.initials: EP
authors.lastname: Abrão
authors.forename: Angela Y
authors.initials: AY
authors.lastname: Mikawa
authors.forename: Viviane O
authors.initials: VO
authors.lastname: Landgraf
authors.forename: Paulo I
authors.initials: PI
authors.lastname: da Costa
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D016632:Apolipoprotein A-I / Q000097:blood / Q000235:genetics; D001053:Apolipoproteins / Q000097:blood* / Q000235:genetics; D001055:Apolipoproteins B / Q000097:blood / Q000235:genetics; D001057:Apolipoproteins E / Q000097:blood / Q000235:genetics; D001938:Brazil; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology; D002784:Cholesterol / Q000097:blood; D002985:Clinical Protocols; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D005838:Genotype; D015658:HIV Infections / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood* / Q000209:etiology / Q000235:genetics; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000097:blood; D008297:Male; D011110:Polymorphism, Genetic / Q000235:genetics; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D001053:Apolipoproteins; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D008055:Lipids; D008074:Lipoproteins; D018894:Reverse Transcriptase Inhibitors; D014280:Triglycerides; D002784:Cholesterol