Production of β‐Chemokines in Human Immunodeficiency Virus (HIV) Infection: Evidence that High Levels of Macrophage Inflammatory Protein‐1β Are Associated with a Decreased Risk of HIV Disease Progression

ABSTRACT Macrophage inflammatory protein-1α (MIP-1α) and MIP-1β play an important role in modulating immune responses. To understand their importance in immunity to placental malaria (PM) and in human immunodeficiency virus (HIV)-PM coinfection, we investigated levels of these chemokines in the placental intervillous blood plasma (IVB plasma) and cord blood plasma of HIV-negative PM-negative, HIV-negative PM-positive, HIV-positive PM-negative, and HIV-positive PM-positive women. Compared to HIV-negative PM-negative women, the MIP-1β concentration in IVB plasma was significantly elevated in HIV-negative PM-positive women and HIV-positive PM-positive women, but it was unaltered in HIV-positive PM-negative women. Also, PM-infected women, irrespective of their HIV status, had significantly higher levels of MIP-1β than HIV-positive PM-negative women. The MIP-1α level was not altered in association with either infection. The IVB plasma levels of MIP-1α and MIP-1β positively correlated with the cord blood plasma levels of these chemokines. As with IVB plasma, only cord plasma from PM-infected mothers had significantly elevated levels of MIP-1β compared to PM-negative mothers, irrespective of their HIV infection status. MIP-1β and MIP-1α levels in PM-positive women were positively associated with parasite density and malaria pigment levels. Regardless of HIV serostatus, the IVB MIP-1β level was significantly lower in women with PM-associated anemia. In summary, an elevated level of MIP-1β was associated with PM. HIV infection did not significantly alter these two chemokine levels in IVB plasma.

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Markers predicting progression of human immunodeficiency virus-related disease.

Clinical Microbiology Reviews ◽

10.1128/cmr.7.1.14 ◽

1994 ◽

Vol 7 (1) ◽

pp. 14-28 ◽

Cited By ~ 62

Author(s):

C M Tsoukas ◽

N F Bernard

Keyword(s):

Human Immunodeficiency Virus ◽

Immune System ◽

Hiv Infection ◽

Disease Progression ◽

Opportunistic Infections ◽

Surrogate Marker ◽

Disease Process ◽

Surrogate Markers ◽

Hiv Disease ◽

Immunodeficiency Virus

Human immunodeficiency virus (HIV) interacts with the immune system throughout the course of infection. For most of the disease process, HIV activates the immune system, and the degree of activation can be assessed by measuring serum levels of molecules such as beta 2-microglobulin and neopterin, as well as other serum and cell surface phenotype markers. The levels of some of these markers correlate with clinical progression of HIV disease, and these markers may be useful as surrogate markers for development of clinical AIDS. Because the likelihood and timing of development of clinical AIDS following seroconversion, for any particular individual, are not readily predictable, the use of nonclinical disease markers has become critically important to patient management. Surrogate markers of HIV infection are, by definition, measurable traits that correlate with disease progression. An ideal marker should identify patients at highest risk of disease progression, provide information on how long an individual has been infected, help in staging HIV disease, predict development of opportunistic infections associated with AIDS, monitor the therapeutic efficacy of immunomodulating or antiviral treatments, and the easily quantifiable, reliable, clinically available, and affordable. This review examines the current state of knowledge and the role of surrogate markers in the natural history and treatment of HIV infection. The clinical usefulness of each marker is assessed with respect to the criteria outlined for the ideal surrogate marker for HIV disease progression.

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HLA-B63 Presents HLA-B57/B58-Restricted Cytotoxic T-Lymphocyte Epitopes and Is Associated with Low Human Immunodeficiency Virus Load

Journal of Virology ◽

10.1128/jvi.79.16.10218-10225.2005 ◽

2005 ◽

Vol 79 (16) ◽

pp. 10218-10225 ◽

Cited By ~ 58

Author(s):

Nicole Frahm ◽

Sharon Adams ◽

Photini Kiepiela ◽

Caitlyn H. Linde ◽

Hannah S. Hewitt ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

Hiv Infection ◽

Disease Progression ◽

Hla Class I ◽

Class I ◽

Binding Motif ◽

Hiv Disease ◽

Hiv Replication ◽

Immune Correlates ◽

Immunodeficiency Virus

ABSTRACT Several HLA class I alleles have been associated with slow human immunodeficiency virus (HIV) disease progression, supporting the important role HLA class I-restricted cytotoxic T lymphocytes (CTL) play in controlling HIV infection. HLA-B63, the serological marker for the closely related HLA-B*1516 and HLA-B*1517 alleles, shares the epitope binding motif of HLA-B57 and HLA-B58, two alleles that have been associated with slow HIV disease progression. We investigated whether HIV-infected individuals who express HLA-B63 generate CTL responses that are comparable in breadth and specificity to those of HLA-B57/58-positive subjects and whether HLA-B63-positive individuals would also present with lower viral set points than the general population. The data show that HLA-B63-positive individuals indeed mounted responses to previously identified HLA-B57-restricted epitopes as well as towards novel, HLA-B63-restricted CTL targets that, in turn, can be presented by HLA-B57 and HLA-B58. HLA-B63-positive subjects generated these responses early in acute HIV infection and were able to control HIV replication in the absence of antiretroviral treatment with a median viral load of 3,280 RNA copies/ml. The data support an important role of the presented epitope in mediating relative control of HIV replication and help to better define immune correlates of controlled HIV infection.

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Activation of NF-κB by R5 and X4 Human Immunodeficiency Virus Type 1 Induces Macrophage Inflammatory Protein 1α and Tumor Necrosis Factor Alpha in Macrophages

Journal of Virology ◽

10.1128/jvi.76.14.7363.2002 ◽

2002 ◽

Vol 76 (14) ◽

pp. 7363-7363

Author(s):

Wonkyu Choe ◽

David J. Volsky ◽

Mary Jane Potash

Keyword(s):

Human Immunodeficiency Virus ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Necrosis Factor Alpha ◽

Inflammatory Protein ◽

Immunodeficiency Virus ◽

Factor Alpha ◽

Macrophage Inflammatory Protein ◽

Necrosis Factor

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Human immunodeficiency virus (HIV) infection

Oxford Handbook of Nutrition and Dietetics ◽

10.1093/med/9780199585823.003.0031 ◽

2011 ◽

pp. 663-669

Keyword(s):

Human Immunodeficiency Virus ◽

Hiv Infection ◽

Opportunistic Infections ◽

Tissue Loss ◽

Atherosclerotic Cardiovascular Disease ◽

Hiv Disease ◽

Hiv Replication ◽

Pharmacological Management ◽

Nutritional Conditions ◽

Immunodeficiency Virus

Introduction, nutritional goals, and assessment 664 Unintentional weight and lean tissue loss 666 Cardiovascular risk and complications associated with HIV disease and treatment 667 Additional dietary issues 668 Untreated human immunodeficiency virus (HIV) infection leads to progressive suppression of immune function, eventually rendering the body susceptible to opportunistic infections and tumours. While there is no cure, antiretroviral therapy (ART) is highly effective in suppressing HIV replication. HIV disease is now a chronic condition and causes of death in this population have shifted from traditional AIDS-related illnesses to non-AIDS (Acquired Immune Deficiency Syndrome) events, the most common being atherosclerotic cardiovascular disease, liver disease, end-stage renal disease and non-AIDS–defining malignancies. There are a diverse range of nutritional conditions associated with HIV, reflecting the complexity of the disease and pharmacological management....

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