Publication: Factors contributing to the development of cerebral malaria. I. Humoral immune responses
Issued Date
1984-01-01
Resource Type
ISSN
00029637
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2-s2.0-0021347245
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Mahidol University
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SCOPUS
Bibliographic Citation
American Journal of Tropical Medicine and Hygiene. Vol.33, No.1 (1984), 1-11
Suggested Citation
S. Tharavanij, M. J. Warrell, S. Tantivanich, P. Tapchaisri, M. Chongsa-Nguan, V. Prasertsiriroj, J. Patarapotikul Factors contributing to the development of cerebral malaria. I. Humoral immune responses. American Journal of Tropical Medicine and Hygiene. Vol.33, No.1 (1984), 1-11. doi:10.4269/ajtmh.1984.33.1 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/30618
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Title
Factors contributing to the development of cerebral malaria. I. Humoral immune responses
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Abstract
Humoral immune responses to malaria were studied in 100 patients with cerebral malaria of whom 53 had added complications, 108 patients with acute malaria, and 100 blood donors. The methods employed were indirect hemagglutination (IHA), indirect fluorescent antibody (IFA), enzyme-linked immunosorbent assay (ELISA), and parasite growth inhibition (PGI) tests. Patients with cerebral malaria, especially those with complications, had histories of fewer attacks of malaria in the previous 5 years than did those with acute malaria, suggesting that the cerebral malaria patients were less immune. The combined cerebral malaria group (complicated and uncomplicated) did not show defective humoral immune responses, since the initial seronegative rate and the mean initial IHA and IFA antibody titers were not significantly different from those of acute malaria patients and the mean initial ELISA titer was even higher than that of the acute malaria group. Reduced humoral responses were found only in complicated cerebral malaria patients, as their mean initial IHA titer was lower and their IHA seronegative rate was higher than those in acute malaria patients and in the uncomplicated cerebral malaria group. The combined cerebral malaria group had greater PGI activity than that of acute malaria patients, but this increased activity was entirely due to the higher results obtained in the complicated cerebral malaria group. The increased PGI activity returned to normal after recovery. An IgG preparation from seven of eight of these sera failed to exert the growth inhibition effect. Factors other than IgG were therefore responsible for the inhibition of parasite growth.