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The rapidly sedimenting hemagglutinin (RHA) representing the purified virion and the slower-sedimenting hemagglutinin (SHA) of several flaviviruses were separated and used in hemagglutination inhibition tests with the 19S (immunoglobulin M) and 7S (immunoglobulin G) immunoglobulin fractions of rabbit antisera, prepared against purified viral antigens or against crude virus pools. The antibody specificity in tests with RHA was identical to the specificity in those employing SHA. 7S antibody cross-reacted broadly with all flavivirus antigens, whereas 19S antibodies were relatively specific in cross-reactions among flaviviruses (RHA or SHA). SHA was consistently inhibited by antibody to a greater extent than RHA. Anti-envelope protein, anti-RHA antibodies and anti-SHA antibodies were unable to discriminate between RHA and SHA. It was concluded that the relative amounts of RHA or SHA in crude hemagglutinin preparations have no influence on the result of hemagglutination inhibition tests with flaviviruses.

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Summary. Metal chektes of 1, 10‐phenanthroline bases are lethal to cultured mammalian cells at concentrations as low as 10–7 molar. Chektes of Fe(II), Cu(II), Cd(II) and Ni(II) are more potent than those of Ru(II), which are highly stable and chemically inert. Activity is generally enhanced by increasing the number of methyl substituents in the phenanthroline ring or, in the case of Ru(II) chektes, by replacing one phenanthroline by an acetylacetonato ligand. There are striking differences between the chektes in the rapidity with which they kill cells Compounds containing Fe(II) or Ni(II), and those derived from unsubstituted 1,10‐phenanthroline, take days to initiate lethal changes at limit dilution. On the other hand, chektes containing Cd(II) or Cu(II) and hexamethylphenanthroline ligands, or Ru(II) together with the acetytacetonato ligand, initiate lethal cell damage that cannot be reversed following 2 hours’contact. A number of metal chektes actually prolong the survival of cells in culture at concentrations two to ten times lower than those damaging the cell. At cytocidal concentrations some depress the pH of the culture medium, whereas others increase it. By repeated passage of a mouse leukaemia cell line in the presence of acetykcetonato bis (3, 4, 7, 8‐tetramethyl‐1, 10‐phenanthroline) ruthenium (II) chloride, a stable mutant has been obtained which is resistant to ten times the dose of chekte lethal to the parental line. The correspondence between the cytocidal and virostatic titres of chektes in this and other cell lines suggests that these compounds inhibit virus multiplication by one of the mechanisms whereby they kill the cell.