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Haemolysis by Sendai Virus: Lack of Requirement for Neuraminidase

Department of Research and Development Wyeth Laboratories, Inc. Box 8299 Philadelphia, Pennsylvania 19101 U.S.A.

Since both neuraminidase and the haemolytic activity of Sendai virus were inhibited by Cu²⁺ ions, it was suggested that neuraminidase was essential for haemolysis (Howe & Morgan, 1969). Haemolysis by Newcastle disease virus (NDV) appeared to be intimately associated with the capacity of the virus to become irreversibly attached to the cell (Burnet, 1950), indicating that neuraminidase, responsible for elution of the virus from red blood cells (RBC), was perhaps not required for, or may even have hindered haemolysis.

The results of this study, aimed at the elucidation of the role of neuraminidase in Sendai virus-induced haemolysis, show that: (1) treatment of the virus by disodium ethylenedi-aminetetraacetate (EDTA) or hydroxyethylethylenediaminetriacetate (HEDTA) causes a simultaneous decrease in neuramininidase activity and an increase in haemolytic activity of the virus. (2) 2-deoxy-2,3-dehydro-N-acetylneuraminic acid (DDANA), a reversible inhibitor of neuraminidase (Meindl & Tuppy, 1969; Meindl et al. 1971), does not interfere with, but augments haemolysis.

Received 6 April 1972; accepted 17 May 1972.