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SUMMARYThe specificity of serum anti-HA antibody from children immunized or infected with A/Victoria/75 (H3N2) or A/Texas/77 (H3N2) virus was examined using the single radial haemolysis test together with adsorption of antibody with three antigenic variants A/Hong Kong/68 (H3N2), A/Port Chalmers/73 (H3N2) and A/Victoria/75 (H3N2). The majority of young children reacted to vaccination or infection by producing strain-specific (SS) antibody to the homologous virus. A small proportion of children's sera contained cross-reacting (CR) antibodies capable of reacting with the haemagglutinins of all antigenic variants of the subtype including A/HK/1/68. In contrast, most adults reacted immunologically to either vaccination or infection by producing CR antibody, reacting with all variants of the antigenic subtype including the prototype virus A/HK/1/68 (H3N2).

Goose erythrocytes were agglutinated by five strains of rabies virus grown in monolayer cell cultures at pH 6.4 and at 0 to 4 C. Hemagglutination was not affected by the cell type in which the virus was grown. Prerequisites for occurrence of hemagglutination are absence of hemagglutination inhibitors (such as those contained in bovine serum) and a relatively high virus concentration (> 105 plaqueforming units of virus per ml). "Soluble" hemagglutinin was not present in crude preparations of extracellular virus. Treatment of purified preparations of extracellular virus with Tween 80 and ether did not result in release of a "soluble" hemagglutinin. The hemagglutinating property of extracellular virus seemed to be conditioned by the integrity of its coat. Preparations of infectious intracellular virus exhibited about 15 times lower hemagglutinating activity than extracellular virus. This decreased hemagglutinating activity did not seem to be caused by binding of hemagglutination inhibitors to the virus particles. Rabies virus can be quantitatively adsorbed onto and eluted from erythrocytes. Erythrocytes pretreated with rabies virus retained their ability to be agglutinated by the same virus strain. The reaction with rabies virus of erythrocytes treated with the receptor-destroying enzyme or K104 was the same as that of nontreated erythrocytes. The hemagglutinating component of rabies virus, therefore, does not exhibit neuraminidase activity. Treatment of extracellular virus by various agents indicated that the hemagglutinating component consists of protein or lipoprotein. Sulfhydryl groups present in the viral hemagglutinin are essential for hemagglutination. Until recently, only three methods for the assay of rabies virus were available: titration of infectivity in animals, plaque assay in cell cultures (36), and complement fixation (CF). The latter method (24) measures both infectious virus and all noninfectious viral antigens. In 1968, Halonen et al. (12) reported that rabies virus exhibits hemagglutinating activity (HA). This paper deals with the characterization and mechanism of this phenomenon. MATERIALS AND METHODS Virus strainis. The Pitman-Moore (PM), Pasteur, and Flury high egg passage (HEP) strains of rabies virus adapted to growth in human diploid cell strain WI-38 (42) were clone-purified three times in agarosesuspended BHK/13S cells (36). The CVS-11 strain of rabies virus propagated in primary hamster kidney cell cultures (22; obtained through the courtesy of P. E. Halonen, National Communicable Disease Center, Atlanta, Ga.) was also purified by cloning three times in BHK/13S cells. The ERA strain of rabies virus (1) was isolated from the attenuated rabies vaccine lot serial no. 128-2 (Connaught Laboratories, Toronto, Canada) and was propagated for two passages in BHK-21 cell cultures. Seed pools of these virus strains were prepared in BHK-21 cultures. 1381

Twenty histocompatibility antigens of the 1^st and the 2nd HL-A series have been determined in 200 MS patients and 255 randomly-selected healthy individuals of West Germany. Both groups differed significantly in 2 antigens of the 1st, and 2 of the 2nd HL-A series. Whereas the antigens HL-A3,HL-A10 and W5 were found more frequently in multiple sclerosis (MS) patients than in controls, the opposite was true for the antigen HL-A12. Brief comments as to the possible biological meaning of these findings are given.

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The intracytoplasmic ground substance, or matrix, associated with the development of rabies virus and the nucleocapsid of the virus were investigated. The filaments of the matrix were identified as virus-specific by means of ferritin-labeled antibodies. In thin sections, the diameter was 15 nm and the strands seemed to be incorporated into virions during morphogenesis of the virus. The nucleocapsid was isolated from purified virus preparations and was studied in negative contrast. The rabies nucleocapsid appeared as a single-stranded helix with a diameter of 16 nm and a periodicity of 7.5 nm; its length was in excess of I ,im.

The histocompatibility pattern of 160 patients with multiple sclerosis (MS) living in the epidemiological area of Southern Lower Saxony was determined and compared to a control population. The only significant difference was the more frequent occurrence of DW2 in the patient group (44% vs. 21%). Taking a progression index (grade of disability divided by the duration of the disease) as a measure for prognosis no difference could be found between the DW2 positive and the DW2 negative patients. The reason why we could not confirm the worse prognosis for DW2 positive patients found by Jersild et al. (1973) and Raun et al. (1980) remains to be investigated.

Studies on leukocyte antibodies in multiple sclerosis (MS) yielded positive results in 34% of 462 MS patients who were in the chronic stage of the disease, when the sera were tested at 15 °C against homologous lymphocytes of 10 cell donors bearing different HL-A antigens. The corresponding value in healthy controls was 7%. When autologous cells were used for demonstration of complement-dependant cold-reacting cytotoxins (auto-CoCoCy) the percentage of positive reactions rose up to 75%. No correlation of iso-CoCoCy with the HL-A antigens could be demonstrated. CoCoCy-positive sera did not react either with homologous or autologous lymphocytes at 37 °C. CoCoCy activity in sera was destroyed by means of 2-mercaptoethanol. The biological significance of CoCoCy in MS remains unclear.