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FILARIAL-SPECIFIC ANTIBODY RESPONSE IN EAST AFRICAN BANCROFTIAN FILARIASIS: EFFECTS OF HOST INFECTION, CLINICAL DISEASE, AND FILARIAL ENDEMICITY

The effect of host infection, chronic clinical disease, and transmission intensity on the patterns of specific antibody responses in Bancroftian filariasis was assessed by analyzing specific IgG1, IgG2, IgG3, IgG4, and IgE profiles among adults from two communities with high and low Wuchereria bancrofti endemicity. In the high endemicity community, intensities of the measured antibodies were significantly associated with infection status. IgG1, IgG2, and IgE were negatively associated with microfilaria (MF) status, IgG3 was negatively associated with circulating filarial antigen (CFA) status, and IgG4 was positively associated with CFA status. None of the associations were significantly influenced by chronic lymphatic disease status. In contrast, IgG1, IgG2, and IgG4 responses were less vigorous in the low endemicity community and, except for IgG4, did not show any significant associations with MF or CFA status. The IgG3 responses were considerably more vigorous in the low endemicity community than in the high endemicity one. Only IgG4 responses exhibited a rather similar pattern in the two communities, being significantly positively associated with CFA status in both communities. The IgG4:IgE ratios were higher in infection-positive individuals than in infection-negative ones, and higher in the high endemicity community than in the low endemicity one. Overall, these results indicate that specific antibody responses in Bancroftian filariasis are more related to infection status than to chronic lymphatic disease status. They also suggest that community transmission intensity play a dominant but subtle role in shaping the observed response patterns.

Received January 5, 2006. Accepted for publication February 28, 2006.

Acknowledgments: We are grateful to the villagers and village helpers of Masaika (Tanzania) and Kingwede (Kenya) for their cooperation, and for the dedicated and skilled assistance provided by staff from the Bombo Field Station (Tanzania) and Msambweni Field Station (Kenya), as well as for the technical assistance provided in the immunological laboratory at the DBL–Institute for Health Research and Development (Denmark).

Financial support: The work was supported by the International Cooperation with Developing Countries Program of the European Communities (contract no. ERBIC18CT970257) and the DBL–Institute for Health Research and Development (Denmark). Edwin Michael was supported by a Medical Research Council Fellowship (United Kingdom), and Walter G. Jaoko was supported by a Fellowship from the Danish Agency for Development Assistance.

^* Address correspondence to Paul E. Simonsen, DBL–Institute for Health Research and Development, Jaegersborg Alle 1D, 2920 Charlottenlund, Denmark. E-mail: pesimonsen{at}dblnet.dk

Authors’ addresses: Walter G. Jaoko, Department of Medical Microbiology, University of Nairobi, PO Box 19676, Nairobi, Kenya, E-mail: wjaoko{at}kaviuon.org. Paul E. Simonsen, DBL–Institute for Health Research and Development, Jaegersborg Alle 1 D, 2920 Charlottenlund, Denmark, Telephone: 45-77-32-77-32, Fax: 45-77-32-77-33, E-mail: pesimonsen{at}dblnet.dk. Dan W. Meyrowitsch, Department of Epidemiology, Institute of Public Health, University of Copenhagen, Blegdamsvej 2, 2200 Copenhagen N, Denmark, E-mail: d.meyrowitsch{at}pubhealth.ku.dk. Benson B. A. Estambale, Institute of Tropical and Infectious Diseases, University of Nairobi, PO Box 19676, Nairobi, Kenya, E-mail: bestambale{at}unobi.ac.ke. Mwele N. Malecela-Lazaro, National Institute for Medical Research, PO Box 9653, Dar es Salaam, Tanzania, E-mail: mmalecela{at}nimr.or.tz. Edwin Michael, Department of Infectious Diseases Epidemiology, Imperial College School of Medicine, Norfolk Place, London W2 1PG, United Kingdom, E-mail: e.michael{at}ic.ac.uk.

Reprint requests: Paul E. Simonsen, DBL–Institute for Health Research and Development, Jaegersborg Alle 1 D, 2920 Charlottenlund, Denmark.

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