Etiologies of the Experimental Dengues of Siler and Simmons

Scott B. HalsteadDepartment of Tropical Medicine and Medical Microbiology, University of Hawaii, School of Medicine, 3675 Kilauea Avenue, Honolulu, Hawaii 96816

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Four participants in the American Army Philippine dengue (d) studies of Siler (1924–25) and five subjects from the studies of Simmons (1929–30) were bled 42 to 48 years after experimental infection. Sera were studied by hemagglutination-inhibition, complement-fixation and plaque reduction neutralization (PRNT) tests for antibodies to the known viral causes of the dengue syndrome in Asia and to St. Louis encephalitis virus. PRNT tests were done with and without fresh normal human serum (accessory factor). Serum from one of four Siler study volunteers had unequivocal evidence of only a previous d4 infection; the remainder had broadly reactive group B antibodies, including d4, suggesting past infection with two or more different dengue viruses. Sera from four of the Simmons study group had high-titered PRNT antibodies to d1 and the remaining serum had d1 antibody when accessory factor was added. In three sera there was monotypic PRNT antibody to d1. Accessory factor increased PRNT titers, particularly to d1 virus in the Simmons' group. Only sera with antibody patterns suggesting past infections with two or more dengue viruses had high levels of SLE PRNT antibody. It is concluded that d4 was transmitted in the 1924 to 1925 and d1 in the 1929 to 1930 experiments. Notable differences in clinical features of dengue infections in the two studies suggest the possibility of the existence of an unique spectrum of responses to infection with different dengue virus types.