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RIIa (CD32) Polymorphism and Onchocercal Skin Disease: Implications for the Development of Severe Reactive Onchodermatitis (ROD)
The pathologic manifestations of Onchocerca volvulus infection depend on the interplay between the host and the parasite. A genetic single nucleotide polymorphism in the Fc
RIIa gene, resulting in arginine (R) or histidine (H) at position 131, affects the binding to the different IgG subclasses and may influence the clinical variations seen in onchocerciasis. This study investigated the relationship between this polymorphism and disease outcome. FcRIIa genotyping was performed on clinically characterized onchocerciasis patients (N = 100) and healthy controls (N = 74). FcRIIa genotype R/R131 frequencies were significantly higher among patients with severe dermatopathology (P < 0.001). Increased risk of developing this form was mostly associated with one tribe (Masalit) (OR = 3.2, 95% CI 1–9.9, P = 0.042). The H131 allele was found to be significantly associated with a reduced risk of having the severe form of the disease (adjusted OR = 0.26, 95% CI = 0.13–0.46, P < 0.001). Our findings suggest that the polymorphism influences the clinical outcome of onchocerciasis.
Received March 13, 2007. Accepted for publication July 2, 2007.
Acknowledgments: We are indebted to all the villagers who willingly participated in this study and to the health personnel in the medical centers in the villages in Sundus area. We are also thankful to administrative staff at Doka locality, Gedarif state. Our thanks also extend to the staff at the National Onchocerciasis Control Program, Tropical Medicine Research Institute, Khartoum, Sudan. Special thanks go to Alex Szalai, The University of Alabama, USA, for the fruitful discussion and comments. Our thanks extend to Tom Nutman, Laboratory of Parasitic Diseases, National Institute of Health, USA, for the critical reading of the manuscript.
Financial support: This work was supported by the Tropical Medicine Research Institute-National, Centre for Research, Academy of Medical Sciences and Technology, Sudan and by grants from the Swedish Medical Research Council (VR) and SIDA/SAREC. This work is part of the activities of the BioMalPar European Network of Excellence supported by a European grant (LSHP-CT-2004-503578) from the Priority 1 " Life Sciences, Genomics and Biotechnology for Health" in the 6th Framework Programme.
Disclosure: The authors have no conflict of interest concerning the work reported in this article.
* Address correspondence to Klavs Berzins, Wenner-Gren Institute, Department of Immunology, Stockholm University, Svante Arrhenius väg 16, SE-106 91 Stockholm, Sweden. E-mail: klavs{at}imun.su.se
Authors’ addresses: Magdi M.M. Ali, Tropical Medicine Research Institute, National Centre for Research, P.O. Box 1304, Khartoum, Sudan. Magdi M.M. Ali, Salah E. Farouk, Amre Nasr, and Klavs Berzins, Department of Immunology, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, Sweden. Telephone: 46-8-164170, Fax: 46-8-157356, E-mail: klavs{at}imun.su.se. Gehad ElGhazali, Department of Microbiology and Immunology, Faculty of Medicine, University of Khartoum and Faculty of Medicine, King Fahad Medical City, Riyadh, Saudia Arabia. Scott M. Montgomery, Department of Clinical Epidemiology Karolinska Hospital, Karolinska Institute M9:01, SE-171 76 Stockholm, Sweden and Clinical Research Centre, Örebro University Hospital, Sweden. Suzan I. A. Noori, Department of Neurology, Khartoum Teaching Hospital, Sudan; Current address: Department of Neurology Rashid Hospital, Dubai, UAE. Mahadi M. Shamad and Omar E. Fadlelseed, Departments of Dermatology and of Biochemistry, Faculty of Medicine, University of Juba, Sudan.
The first two authors contributed equally to this study.
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