title: Antibody response to human immunodeficiency virus type 1 protease according to risk group and disease stage.
abstract: Three groups with different routes of human immunodeficiency virus type 1 (HIV-1) transmission (homosexual men, hemophiliacs, and children) were studied for serum antibodies to a recombinant form of the HIV-1 protease using an enzyme-linked immunoassay. At 1 year after seroconversion, defined as the moment antibodies to HIV-1 proteins were first detected, 56% (34/61) of the homosexual men had antibodies to protease, and 2 years after seroconversion this percentage was 63% (24/38). Within this 2-year period these antibodies were no longer detected in 16% (9/56). A similar pattern was observed in 20 hemophiliacs who seroconverted after exposure to HIV-1-contaminated blood products. We found that 63% (160/255) of homosexual men in Centers for Disease Control stage II or III, 60% (9/15) of patients with acquired immunodeficiency syndrome (AIDS)-related complex, and 36% (14/39) of patients with AIDS had antibodies to protease. In 255 homosexual men in Centers for Disease Control stage II or III, antibodies to protease were significantly more frequently found in samples lacking HIV-1 antigen (P less than 0.001) and possessing antibodies to HIV-1 core proteins (P less than 0.001). Twenty-four persons who developed AIDS were studied longitudinally: 58% (14/24) had antibodies to protease 1 year before developing symptoms; 29% (7/24) showed a decline and 29% (7/24) showed a loss of antibodies to protease at the onset of symptoms. Within a group of 47 HIV-1-infected children, 90% (18/20) with a stable disease course were persistently protease antibody positive, versus 4 of 27 children (15%) with an unstable disease course (P = 0.0001). These data indicate that HIV-1 protease is expressed and antigenic in most HIV-1-infected individuals and that a decline or absence of antibodies to protease is strongly associated with unstable disease in children and AIDS in adults.
authors.affiliation: Human Retrovirus Laboratory, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: C A
authors.initials: CA
authors.lastname: Boucher
authors.forename: M H
authors.initials: MH
authors.lastname: de Jager
authors.forename: C
authors.initials: C
authors.lastname: Debouck
authors.forename: L G
authors.initials: LG
authors.lastname: Epstein
authors.forename: F
authors.initials: F
authors.lastname: de Wolf
authors.forename: T F
authors.initials: TF
authors.lastname: Wolfs
authors.forename: J
authors.initials: J
authors.lastname: Goudsmit
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000150:complications / Q000276:immunology*; D000328:Adult; D002648:Child; D015331:Cohort Studies; D004797:Enzyme-Linked Immunosorbent Assay; D015483:HIV Antibodies / Q000096:biosynthesis*; D015497:HIV-1 / Q000201:enzymology*; D006467:Hemophilia A / Q000150:complications; D006716:Homosexuality; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D010447:Peptide Hydrolases / Q000276:immunology*; D011379:Prognosis; D011446:Prospective Studies; D011994:Recombinant Proteins / Q000276:immunology; D012307:Risk Factors
chemical_list: D015483:HIV Antibodies; D011994:Recombinant Proteins; D010447:Peptide Hydrolases