(HOME) Subject: Hiv/iron

   
   J Clin Virol 2001 Feb;20(3):111-5
   
Iron status and the outcome of HIV infection: an overview.

    Gordeuk VR, Delanghe JR, Langlois MR, Boelaert JR
    
   Center for Sickle Cell Disease and Department of Medicine, Howard
   University College of Medicine, 20059, Washington, DC, USA
   
   [Medline record in process]
   
   Background: Theoretical considerations and experiments in the
   laboratory suggest that excessive iron stores may have an adverse
   effect on immunity. If so, high iron stores might be especially a
   problem in patients with human immunodeficiency virus (HIV) infection.
   Objective and study design: Review published clinical studies that
   provide information regarding the effect of iron status on the outcome
   of HIV infection. Results: Four clinical observations have provided
   some perspective on the effect of iron status on the outcome of HIV-1
   infection. First, in a restrospective study of HIV-positive
   thalassemia major patients, the rate of progression of HIV disease was
   significantly faster in patients with lower doses of desferrioxamine
   and higher serum ferritin concentrations. Second, the inadvertent
   simultaneous administration of low doses of oral iron with dapsone for
   the prophylaxis of Pneumocystis carinii pneumonia in HIV-positive
   patients may have been associated with excess mortality. Third, a
   study of haptoglobin polymorphisms in HIV-positive subjects indicated
   that the haptoglobin 2-2 polymorphism is associated with higher iron
   stores and shortened survival as compared with the haptoglobin 1-1 or
   2-1 phenotypes. Fourth, a retrospective study of bone marrow
   macrophage iron in HIV-positive patients suggested that survival is
   shorter with high iron stores. Conclusion: These four observations
   raise the possibility that high iron status may adversely influence
   the outcome of HIV-1 infection.
   
   PMID: 11166657, UI: 21112136
     _________________________________________________________________
   
Subject: aids/hiv/chelators

   
   J Infect Dis 2000 Feb;181(2):484-90
   
Inhibition of human immunodeficiency virus type 1 replication in human
mononuclear blood cells by the iron chelators deferoxamine, deferiprone, and
bleomycin.

    Georgiou NA, van der Bruggen T, Oudshoorn M, Nottet HS, Marx JJ, van Asbeck
    BS
    
   Department of Internal Medicine, University Medical Center Utrecht,
   Utrecht, The Netherlands. n.georgiou@lab.azu.nl
   
   Replication of human immunodeficiency virus type 1 (HIV-1) can be
   influenced by iron. Hence, decreasing the availability of iron may
   inhibit HIV-1 replication. Deferoxamine and deferiprone, both forming
   catalytically inactive iron-chelator complexes, and bleomycin, by use
   of which iron catalyzes oxidative nucleic acid destruction, were
   investigated. Expression of p24 antigen in human monocyte-derived
   macrophages and peripheral blood lymphocytes (PBL) was reduced by all
   3 iron chelators. In PBL, p24 reduction was mirrored by a decrease in
   proliferation after incubation with deferoxamine or deferiprone,
   suggesting that viral inhibition is closely linked to a decrease in
   cellular proliferation. In contrast, clinically relevant bleomycin
   concentrations reduced p24 levels by approximately 50% without
   affecting proliferation. When deferoxamine and the nucleoside analogue
   dideoxyinosine were used in combination, they acted synergistically in
   inhibiting HIV-1 replication. These observations suggest that iron
   chelators with different mechanisms of action could be of additional
   benefit in antiretroviral combination therapy.
   
   PMID: 10669330, UI: 20134572
     _________________________________________________________________
   
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Subject: HIV and iron

   
   Cell Biochem Funct 1999 Dec;17(4):279-287
   
Iron metabolism and HIV infection: reciprocal interactions with potentially
harmful consequences?

    Savarino A, Pescarmona GP, Boelaert JR
    
   Departiment of Medical and Surgical Sciences, University of Turin,
   Turin, Italy.
   
   [Record supplied by publisher]
   
   Humans with advanced human immunodeficiency virus (HIV) infection
   present some evidence suggestive of iron accumulation. Ferritin
   concentrations increase with HIV disease progression, and iron
   accumulates in several tissues. Iron excess may exert negative effects
   in individuals with HIV. Indeed, iron accumulation seems to be
   associated with shorter survival, and a number of investigations point
   to an iron-mediated oxidative stress in subjects with HIV infection.
   The observations on humans infected with HIV are in part supported by
   in-vitro findings. Indeed, in-vitro HIV infection is associated with
   changes in iron metabolism, and an iron-mediated oxidative stress is
   likely to contribute to viral cytopathogenicity. Furthermore, it is
   interesting to point out that the interaction between iron and HIV may
   be reciprocal, since viruses with a life-cycle involving a DNA phase
   require chelatable iron for optimum replication. This combined
   evidence suggests that iron metabolism is an important area for
   virus/host interaction. These observations may be relevant to both
   laboratory monitoring and clinical treatment of individuals with HIV.
   Copyright 1999 John Wiley & Sons, Ltd.
   
   PMID: 10587615
     _________________________________________________________________
   
Subject: iron and immune

   
   Ann Clin Lab Sci 2000 Oct;30(4):354-65
   
Effects of iron overload on the immune system.

    Walker EM Jr, Walker SM
    
   Department of Pathology, Marshall University and Huntington DVA
   Medical Center, West Virginia, 25704, USA. walkere@marshall.edu
   
   [Medline record in process]
   
   Iron and its binding proteins have immunoregulatory properties, and
   shifting of immunoregulatory balances by iron excess or deficiency may
   produce severe, deleterious physiological effects. Effects of iron
   overload include decreased antibody-mediated and mitogen-stimulated
   phagocytosis by monocytes and macrophages, alterations in T-lymphocyte
   subsets, and modification of lymphocyte distribution in different
   compartments of the immune system. The importance of iron in
   regulating the expression of T-lymphocyte cell surface markers,
   influencing the expansion of different T-cell subsets, and affecting
   immune cell functions can be demonstrated in vitro and in vivo. The
   poor ability of lymphocytes to sequester excess iron in ferritin may
   help to explain the immune system abnormalities in iron-overloaded
   patients. Iron overload as seen in hereditary hemochromatosis patients
   enhances suppressor T-cell (CD8) numbers and activity, decreases the
   proliferative capacity, numbers, and activity of helper T cells (CD4)
   with increases in CD8/CD4 ratios, impairs the generation of cytotoxic
   T cells, and alters immunoglobulin secretion when compared to treated
   hereditary hemochromatosis patients or controls. A correlation has
   recently been found between low CD8+ lymphocyte numbers, liver damage
   associated with HCV positivity, and severity of iron overload in
   beta-thalassemia major patients. Iron overload, with its associated
   increases of serum iron levels and transferrin saturation, may cause a
   poor response to interferon therapy. Iron overload with hyperferremia
   is associated with suppressed functions of the complement system
   (classic or alternative types). High plasma ferritin content in
   patients with chronic, diffuse diseases of the liver (cirrhosis,
   chronic hepatitis), beta-thalassemia major, dyserythropoiesis, and
   hereditary hemochromatosis may induce the development of anti-ferritin
   antibodies with the production of circulating immune complexes.
   Increased body stores of iron in various clinical situations may tip
   the immunoregulatory balance unfavorably to allow increased growth
   rates of cancer cells and infectious organisms, and complicate the
   clinical management of preexisting acute and chronic diseases.
   
   PMID: 11045759, UI: 20498458
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   [Inhibitory effect of inositol hexasulfate and inositol hexaphosphoric
   acid (phytic acid) on the proliferation of the human immunodeficiency
   virus (HIV) in vitro]
   
   Kansenshogaku Zasshi. 1989 Jul;63(7):676-83. Unique Identifier :
   AIDSLINE MED/90131940
   Otake T; Shimonaka H; Kanai M; Miyano K; Ueba N; Kunita N; Kurimura T
     _________________________________________________________________
   
   Abstract: The monosaccharide substances inositol hexasulfate (IHS) and
   inositol hexaphosphoric acid (Phytic acid, IHP) were investigated for
   their antiviral effect on the human immunodeficiency virus (HIV) in
   vitro. In MT-4 cells IHS completely inhibited the cytopathic effect of
   HIV and the HIV specific antigen expression at a concentration of 1.67
   mg/ml. IHP moderately inhibited both of HIV effects as mentioned
   above.
     _________________________________________________________________
   
   Keywords: *Antiviral Agents English Abstract Human HIV/*DRUG
   EFFECTS/GROWTH & DEVELOPMENT HTLV-I Infections/PATHOLOGY
   Inositol/*ANALOGS & DERIVATIVES/PHARMACOLOGY Monocytes/DRUG
   EFFECTS/MICROBIOLOGY Phytic Acid/*PHARMACOLOGY JOURNAL ARTICLE
   
   SOURCE: National Library of Medicine. NOTICE: This material may be
   protected by Copyright Law (Title 17, U.S.Code).
   


Subject: malaria/Hiv

> Malaria Twice As Likely Among HIV-1-Positive People
http://www.docguide.com/dgc.nsf/news/D85CAFF138D59BFC85256962004B2E90

People who are infected with the human immunodeficiency
1 (HIV-1) virus positive may be twice as likely to develop
malaria as are HIV-1-negative people, research in Uganda
has found.

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