Selenium and interleukins in persons infected with human immunodeficiency virus type 1

被引:59
作者
Baum, MK [1 ]
Miguez-Burbano, MJ [1 ]
Campa, A [1 ]
Shor-Posner, G [1 ]
机构
[1] Univ Miami, Sch Med, Dept Psychiat & Behav Sci, Div Metab & Dis Prevent, Miami, FL 33136 USA
关键词
D O I
10.1086/315911
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
An important role for selenium in human immunodeficiency virus (HIV) disease has been proposed. Decreased selenium levels, as found in persons with HIV infection or AIDS, are sensitive markers of disease progression. Selenium deficiency, an independent predictor of mortality in both HIV-l-infected adults and children, is an essential micronutrient that is associated with an improvement of T cell function and reduced apoptosis in animal models. In addition, adequate selenium may enhance resistance to infections through modulation of interleukin (IL) production and subsequently the Th1/Th2 response. Selenium supplementation up-regulates IL-2 and increases activation, proliferation, differentiation, and programmed cell death of T helper cells. Moreover, selenium supplementation may down-regulate the abnormally high levels of IL-8 and tumor necrosis factor-or observed in HIV disease, which has been associated with neurologic damage, Kaposi's sarcoma, wasting syndrome, and increased viral replication. Together, these findings suggest a new mechanism through which selenium may affect HIV-1 disease progression.
引用
收藏
页码:S69 / S73
页数:5
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共 38 条
  • [1] ABOULAFIA D, 1989, J ACQ IMMUN DEF SYND, V2, P54
  • [2] AUSTRAN B, 1997, SCIENCE, V277, P112
  • [3] Dietary oxidative stress and the potentiation of viral infection
    Beck, MA
    Levander, OA
    [J]. ANNUAL REVIEW OF NUTRITION, 1998, 18 : 93 - 116
  • [4] SERUM SELENIUM CONCENTRATION AND DISEASE PROGRESS IN PATIENTS WITH HIV-INFECTION
    CIRELLI, A
    CIARDI, M
    DESIMONE, C
    SORICE, F
    GIORDANO, R
    CIARALLI, L
    COSTANTINI, S
    [J]. CLINICAL BIOCHEMISTRY, 1991, 24 (02) : 211 - 214
  • [5] Oxidized low-density lipoprotein induces the production of interleukin-8 by endothelial cells
    Claise, C
    Edeas, M
    Chalas, J
    Cockx, A
    Abella, A
    Capel, L
    Lindenbaum, A
    [J]. FEBS LETTERS, 1996, 398 (2-3) : 223 - 227
  • [6] THE TH1-TH2 HYPOTHESIS OF HIV-INFECTION - NEW INSIGHTS
    CLERICI, M
    SHEARER, GM
    [J]. IMMUNOLOGY TODAY, 1994, 15 (12): : 575 - 581
  • [7] HIV infection induces changes in CD4(+) T-cell phenotype and depletions within the CD4(+) T-cell repertoire that are not immediately restored by antiviral or immune-based therapies
    Connors, M
    Kovacs, JA
    Krevat, S
    GeaBanacloche, JC
    Sneller, MC
    Flanigan, M
    Metcalf, JA
    Walker, RE
    Falloon, J
    Baseler, M
    Stevens, R
    Feuerstein, I
    Masur, H
    Lane, HC
    [J]. NATURE MEDICINE, 1997, 3 (05) : 533 - 540
  • [8] TUMOR NECROSIS FACTOR A ACTIVATES HUMAN IMMUNODEFICIENCY VIRUS TYPE-1 THROUGH INDUCTION OF NUCLEAR FACTOR BINDING TO THE NF-KAPPA-B SITES IN THE LONG TERMINAL REPEAT
    DUH, EJ
    MAURY, WJ
    FOLKS, TM
    FAUCI, AS
    RABSON, AB
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (15) : 5974 - 5978
  • [9] ABNORMALITIES OF BLOOD SELENIUM AND GLUTATHIONE-PEROXIDASE ACTIVITY IN PATIENTS WITH ACQUIRED IMMUNODEFICIENCY SYNDROME AND AIDS-RELATED COMPLEX
    DWORKIN, BM
    ROSENTHAL, WS
    WORMSER, GP
    WEISS, L
    NUNEZ, M
    JOLINE, C
    HERP, A
    [J]. BIOLOGICAL TRACE ELEMENT RESEARCH, 1988, 15 : 167 - 177
  • [10] TUMOR NECROSIS FACTOR-ALPHA INDUCES EXPRESSION OF HUMAN IMMUNODEFICIENCY VIRUS IN A CHRONICALLY INFECTED T-CELL CLONE
    FOLKS, TM
    CLOUSE, KA
    JUSTEMENT, J
    RABSON, A
    DUH, E
    KEHRL, JH
    FAUCI, AS
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (07) : 2365 - 2368