Abstract
Studies carried out by one of us (A. B. S.) since 1944 have established the fact that several immunologically distinct but related types of virus are responsible for the clinically typical and) atypical forms of dengue. 1 Since the adaptation of dengue virus to mice, 2 Sabin and Schlesinger found that the neutralizing antibodies which developed following infection were so highly type-specific, that by means of the neutralization test 3 in mice one could not diagnose infections caused by heterologous immunological types of virus which have not as yet been propagated successfully in mice. Continuous serial, intracerebral passage in mice has increased the titer of our Hawaii strain of virus from 10−1 to about 10−5 or 10−6, and following intracerebral passage in 3- to 4-day-old mice (a procedure suggested by Dr. Gordon Meiklejohn) titers of 10−7 to 10−8 could be achieved. Satisfactory complement-fixing (C-F) antigens could be prepared from the brains of mice which were either 3 to 7 days old or approximately 14 days old at the time of inoculation with virus of highest titer (0.03 × 10−7 −0.03 × 10−8) which could be obtained only from the younger suckling mice. Comparative tests on aliquot portions of 20% aqueous extracts of the infected mouse brains revealed that antigen prepared by benzene extraction of the lyophilized material 4 , 5 was no more potent as regards the number of antigenic units or the titer obtained with dengue antisera than that prepared only by centrifugation at 13,000 r.p.m. in the cold (Type SS-1 Swedish angle centrifuge—Sorvall), and both were equally effective in increasing the titer of complement. The 20% mouse brain suspension prepared by inoculation of 3- to 7-day-old mice contained 16 to 32 units of antigen per 0.25 ml as compared with 4 units (with two exceptions when it was only 1 unit and one when it was 8 units) for the similar suspension prepared in a similar manner from approximately 14-day-old mice.
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