title: Plasma platelet-activating factor acetylhydrolase activity in human immunodeficiency virus infection and the acquired immunodeficiency syndrome.
abstract: Platelet-activating factor (PAF) acetylhydrolase (PAF-AH) catalyzes the hydrolysis of PAF, a mediator of inflammation, as well as other biologically active oxidized phospholipids. In humans, plasma PAF-AH activity is bound to low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Higher levels of plasma PAF-AH activity have been found in a variety of diseases, and are thought to be a defense mechanism against the toxic effects of PAF and oxidized phospholipids. We studied plasma PAF-AH activity in patients with human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS), a disease characterized by chronic HIV infection and a systemic host response. Plasma PAF-AH activity was significantly greater in AIDS patients compared with control subjects (25.2 +/- 2.0 v 17.0 +/- 0.8 nmol/min/mL, P < .001). The higher levels of plasma PAF-AH activity were found in LDL (28.2 +/- 2.2 v 18.3 +/- 1.0 nmol/min/mL for AIDS v controls, respectively, P = .0005), but not in HDL. Plasma PAF-AH activity in AIDS correlated with circulating interferon alfa (r = .575, P = .005) and plasma triglycerides (r = .556, P < .0025). The presence of secondary infection in AIDS did not significantly change plasma PAF-AH activity. The initiation of a new antiretroviral regimen with either a protease inhibitor or the nucleoside analog lamivudine did not significantly decrease plasma PAF-AH activity, despite successful suppression of HIV RNA levels. Plasma PAF-AH activity may be a sensitive marker of the host response to infection, and the higher levels of plasma and LDL-associated PAF-AH activity in patients with HIV infection and AIDS may be a physiological response to protect the host against oxidative injury from PAF and oxidized phospholipids.
authors.affiliation: Department of Veterans Affairs Medical Center, San Francisco, CA 94121, USA.
authors.forename: W
authors.initials: W
authors.lastname: Khovidhunkit
authors.forename: R A
authors.initials: RA
authors.lastname: Memon
authors.forename: J K
authors.initials: JK
authors.lastname: Shigenaga
authors.forename: M
authors.initials: M
authors.lastname: Pang
authors.forename: M
authors.initials: M
authors.lastname: Schambelan
authors.forename: K
authors.initials: K
authors.lastname: Mulligan
authors.forename: K R
authors.initials: KR
authors.lastname: Feingold
authors.forename: C
authors.initials: C
authors.lastname: Grunfeld
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000163:Acquired Immunodeficiency Syndrome / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D000209:Acute-Phase Proteins / Q000032:analysis; D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use; D016207:Cytokines / Q000097:blood; D005260:Female; D015658:HIV Infections / Q000097:blood* / Q000188:drug therapy; D006801:Humans; D007239:Infections / Q000097:blood / Q000150:complications; D019259:Lamivudine / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D010741:Phospholipases A / Q000097:blood*; D011480:Protease Inhibitors / Q000627:therapeutic use
chemical_list: D000209:Acute-Phase Proteins; D019380:Anti-HIV Agents; D016207:Cytokines; D008055:Lipids; D008074:Lipoproteins; D011480:Protease Inhibitors; D019259:Lamivudine; D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase