Le SIDA au Ghana (serveur d'exploration)

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Sustained plasma TNF-α and HIV-1 load despite resolution of other parameters of immune activation during treatment of tuberculosis in Africans

Identifieur interne : 001207 ( Main/Exploration ); précédent : 001206; suivant : 001208

Sustained plasma TNF-α and HIV-1 load despite resolution of other parameters of immune activation during treatment of tuberculosis in Africans

Auteurs : S. D. Lawn [États-Unis, Royaume-Uni] ; R. J. Shattock [Royaume-Uni] ; J. W. Acheampong [Ghana] ; R. B. Lal [États-Unis] ; T. M. Folks [États-Unis] ; G. E. Griffin [Royaume-Uni] ; S. T. Butera [États-Unis]

Source :

RBID : Pascal:00-0065196

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English descriptors

Abstract

Objective: To determine the impact of treatment of tuberculosis on plasma HIV-1 load in African subjects and to correlate viral load with response to treatment and changes in immune activation. Design: Clinical and microbiological responses, immune activation parameters and plasma HIV-1 load were determined in 20 patients with pulmonary tuberculosis and HIV-1 coinfection in Ghana, West Africa during the first 3 months of anti-tuberculosis treatment. Methods: Plasma HIV-1 load and markers of immune activation were determined by commercially available assays. Human leukocyte antigen (HLA)-DR incorporation into the HIV-1 envelope was measured by using an immunomagnetic capture technique. Results: Treatment of tuberculosis resulted in significant improvements in weight and haemoglobin, a high sputum smear conversion rate and marked reductions in mean plasma tumour necrosis factor (TNF) receptor-1, interleukin-6 and C-reactive protein. Furthermore, incorporation of host HLA-DR into the HIV-1 envelope decreased; this also suggested a reduction in immune activation of the cells supporting viral replication. However, of importance with regard to AIDS pathogenesis, neither mean plasma TNF-α nor HIV-1 load decreased significantly. Conclusions: The failure of HIV-1 plasma load to decline significantly during the initial months of anti-tuberculosis treatment is associated with high, sustained systemic levels of TNF-α. The dissociation between the sustained levels of plasma TNF-α and the major reductions in other, diverse immune activation parameters may represent dysregulation of cytokine production in these African patients.


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Le document en format XML

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<term>AIDS-Related Opportunistic Infections (virology)</term>
<term>Antibacterial agent</term>
<term>Antitubercular Agents (therapeutic use)</term>
<term>Antituberculous agent</term>
<term>Blood plasma</term>
<term>Chemotherapy</term>
<term>Complication</term>
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<term>Human</term>
<term>Humans</term>
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<term>Immunological investigation</term>
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<term>Tuberculosis (drug therapy)</term>
<term>Tuberculosis (immunology)</term>
<term>Tuberculosis (virology)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
<term>Tumor necrosis factor α</term>
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<term>Viral load</term>
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<term>Antigènes HLA-DR (immunologie)</term>
<term>Antituberculeux (usage thérapeutique)</term>
<term>Charge virale</term>
<term>Facteur de nécrose tumorale alpha (métabolisme)</term>
<term>Ghana</term>
<term>Humains</term>
<term>Infections opportunistes liées au SIDA (immunologie)</term>
<term>Infections opportunistes liées au SIDA (traitement médicamenteux)</term>
<term>Infections opportunistes liées au SIDA (virologie)</term>
<term>Tuberculose ()</term>
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<term>Tuberculose (traitement médicamenteux)</term>
<term>Tuberculose (virologie)</term>
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<term>HLA-DR Antigens</term>
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<term>Tumor Necrosis Factor-alpha</term>
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<term>Antitubercular Agents</term>
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<term>Ghana</term>
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<term>Tuberculosis</term>
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<term>AIDS-Related Opportunistic Infections</term>
<term>Tuberculosis</term>
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<term>Antigènes HLA-DR</term>
<term>Infections opportunistes liées au SIDA</term>
<term>Tuberculose</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>AIDS-Related Opportunistic Infections</term>
<term>Tuberculosis</term>
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<term>HIV-1</term>
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<keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr">
<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Facteur de nécrose tumorale alpha</term>
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<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr">
<term>Infections opportunistes liées au SIDA</term>
<term>Tuberculose</term>
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<term>Antituberculeux</term>
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<term>Infections opportunistes liées au SIDA</term>
<term>Tuberculose</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en">
<term>AIDS-Related Opportunistic Infections</term>
<term>Tuberculosis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Humans</term>
<term>Viral Load</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Charge virale</term>
<term>Ghana</term>
<term>Humains</term>
<term>SIDA</term>
<term>Tuberculose</term>
<term>Virus HIV1</term>
<term>Infection opportuniste</term>
<term>Tuberculose</term>
<term>Complication</term>
<term>Chimiothérapie</term>
<term>Traitement</term>
<term>Plasma sanguin</term>
<term>Facteur nécrose tumorale α</term>
<term>Efficacité traitement</term>
<term>Immunorestauration</term>
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<term>Ghana</term>
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<front>
<div type="abstract" xml:lang="en">Objective: To determine the impact of treatment of tuberculosis on plasma HIV-1 load in African subjects and to correlate viral load with response to treatment and changes in immune activation. Design: Clinical and microbiological responses, immune activation parameters and plasma HIV-1 load were determined in 20 patients with pulmonary tuberculosis and HIV-1 coinfection in Ghana, West Africa during the first 3 months of anti-tuberculosis treatment. Methods: Plasma HIV-1 load and markers of immune activation were determined by commercially available assays. Human leukocyte antigen (HLA)-DR incorporation into the HIV-1 envelope was measured by using an immunomagnetic capture technique. Results: Treatment of tuberculosis resulted in significant improvements in weight and haemoglobin, a high sputum smear conversion rate and marked reductions in mean plasma tumour necrosis factor (TNF) receptor-1, interleukin-6 and C-reactive protein. Furthermore, incorporation of host HLA-DR into the HIV-1 envelope decreased; this also suggested a reduction in immune activation of the cells supporting viral replication. However, of importance with regard to AIDS pathogenesis, neither mean plasma TNF-α nor HIV-1 load decreased significantly. Conclusions: The failure of HIV-1 plasma load to decline significantly during the initial months of anti-tuberculosis treatment is associated with high, sustained systemic levels of TNF-α. The dissociation between the sustained levels of plasma TNF-α and the major reductions in other, diverse immune activation parameters may represent dysregulation of cytokine production in these African patients.</div>
</front>
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<li>Royaume-Uni</li>
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<name sortKey="Lal, R B" sort="Lal, R B" uniqKey="Lal R" first="R. B." last="Lal">R. B. Lal</name>
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<name sortKey="Griffin, G E" sort="Griffin, G E" uniqKey="Griffin G" first="G. E." last="Griffin">G. E. Griffin</name>
<name sortKey="Shattock, R J" sort="Shattock, R J" uniqKey="Shattock R" first="R. J." last="Shattock">R. J. Shattock</name>
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