AJTMH HINARI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am. J. Trop. Med. Hyg., 74(1), 2006, pp. 41-43
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by EGGENA, M. P.
Right arrow Articles by DORSEY, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by EGGENA, M. P.
Right arrow Articles by DORSEY, G.
Related Collections
Right arrow Immunology
Right arrow Malaria

SHORT REPORT


CD4 T CELL ACTIVATION AS A PREDICTOR FOR TREATMENT FAILURE IN UGANDANS WITH PLASMODIUM FALCIPARUM MALARIA

MARK P. EGGENA, HEIDI HOPKINS, BANSON BARUGAHARE, MARTIN OKELLO, FRANCIS SSALI, PETER MUGYENYI, PHILIP J. ROSENTHAL, HUYEN CAO, AND GRANT DORSEY*
Department of Medicine, San Francisco General Hospital, University of California, San Francisco, California; Joint Clinical Research Centre, Kampala, Uganda; California Department of Health Services, Richmond, California

 

ABSTRACT

Host immunity plays an important role in response to antimalarial therapy but is poorly understood. To test whether T cell activation is a risk factor for antimalarial treatment failure, we studied CD4+ and CD8+ T cell activation in 31 human immunodeficiency virus–negative Ugandan patients 5–37 years of age who were treated for uncomplicated Plasmodium falciparum malaria. Increased CD4+ T cell activation, as indicated by co-expression of HLA-DR and CD38, was an independent risk factor for treatment failure (hazard ratio = 2.45, 95% confidence interval = 1.02–5.89, P = 0.05) in multivariate analysis controlling for age, baseline temperature, and pre-treatment parasite density. The results provide insight into the role of cellular immunity in response to antimalarial therapy and underscore the need to investigate the mechanisms behind immune activation.

Received June 4, 2005. Accepted for publication September 6, 2005.

Acknowledgments: We thank the Makerere University–University of California, San Francisco Kampala staff (Basaliza M. Karakire, Regina Nakafeero, Maxwell B. Kilama, Marx Dongo, William Musoke, Bridget Nzarubara, Anne Gasasira, Denise Njama-Meya, Gertrude Kilama, Christopher Bongole, Mary Kasango, Sara Kibirango, Kenneth Mwebaze and Erika Leemann) for their assistance. We also sincerely thank all study patients for participating in this investigation.

Financial support: This work was supported by National Institutes of Health (NIH) grants AI43754, AI054366, and AI052142, and the Fogarty International Center/NIH (grant TW00007).

Disclosure: None of the authors have any commercial or other associations that might pose a conflict of interest.

* Address correspondence to Grant Dorsey, San Francisco General Hospital, 1001 Potrero, Building 30, Room 408, San Francisco, CA 94110. E-mail: grantd{at}itsa.ucsf.edu

Authors’ addresses: Mark P. Eggena, Heidi Hopkins, Philip J. Rosenthal, and Grant Dorsey, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA 94110, Telephone: 415-206-4680, Fax: 415-648-8425, E-mail: grantd{at}itsa.ucsf.edu. Banson Barugahare, Martin Okello, Francis Ssali, and Peter Mugyenyi, Joint Clinical Research Centre, Kampala, Uganda. Huyen Cao, California Department of Health Services, Richmond, CA 94801.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Society of Tropical Medicine and Hygiene.