Characterization of high-risk HIV-1 seronegative hemophiliacs. Clin Immunol 2001 Feb;98(2):200-11
Date
02/13/2001Pubmed ID
11161976DOI
10.1006/clim.2000.4969Scopus ID
2-s2.0-0035126472 (requires institutional sign-in at Scopus site) 55 CitationsAbstract
Mechanisms that protect most high-risk HIV-1 seronegative (HRSN) persons are not well understood. Among hemophiliacs from the Multicenter Hemophilia Cohort Study who remained HIV-1 seronegative despite a high (94%) risk for acquisition of HIV-1 infection, only 7/43 were homozygous for the protective CCR5 Delta32 polymorphism. Among the remainder, neither CCR5 density nor beta-chemokine production, nor in vitro susceptibility to infection with the HIV-1 isolate JR-FL could distinguish HRSN hemophiliacs from healthy controls. When compared to lymphocytes of healthy controls not at risk for HIV-1 infection, diminished spontaneous lymphocyte proliferation was seen in lymphocytes of HRSN hemophiliacs as well as in lymphocytes of hemophiliacs not at risk for HIV-1 infection. Surprisingly sera/plasmas obtained from high-risk HIV-1 seropositve hemophiliacs prior to seroconversion more often contained alloreactive antibodies than date-matched sera/plasmas obtained from HRSN hemophiliacs. Thus alloreactivity may predispose to acquisition of HIV-1 infection after parenteral exposure.
Author List
Salkowitz JR, Purvis SF, Meyerson H, Zimmerman P, O'Brien TR, Aledort L, Eyster ME, Hilgartner M, Kessler C, Konkle BA, White GC 2nd, Goedert JJ, Lederman MMAuthor
Gilbert C. White MD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AdolescentAdult
Chemokine CCL4
Chemokine CCL5
Child
Cohort Studies
Drug Contamination
Factor VIII
Female
Genetic Predisposition to Disease
Genotype
HIV Infections
HIV Seronegativity
HIV Seropositivity
HIV-1
Hemophilia A
Hot Temperature
Humans
Immunity, Innate
Isoantibodies
Lymphocyte Activation
Macrophage Inflammatory Proteins
Male
Polymorphism, Genetic
Receptors, CCR5
Risk
