By Thomas M. Bell (Auth.)
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30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 45 Porterfield, J. S. (1962) Advances in Virus Research, 9, 127. Hirst, G. K. (1941) Science, 94, 22. , Hare, R. (1941) Canad. Pub. Health J. 32, 530. Horsfall, F. L. (1954) / . Exper. Med. 100, 135. , Fox, J. P. (1957) Proc. Soc. Exp. Biol. Med. 96, 788. Lerner, A. ML, Cherry, J. , Finland, M. (1963) Virology, 19, 58. , Burnet, F. M. (1957) Virology, 4, 305. Pereira, H. , Figueiredo, M. V. T. (1962) Virology, 18, 1. Burnet, F. , Stone, J. (1947) Aust.
Cells treated in this way are unable to synthesise infectious virus, viral haemagglutinin or viral nucleic acid, but they produce more interferon. 19'20 Since cancer cells are wholly or partially independent of oxidative pathways for their metabolism21 this suggests VIRAL INTERFERENCE AND ANTI-VIRAL SUBSTANCES 49 that interferon acts as an inhibitor of an energy providing oxidative process and subsequent work has tended to confirm this hypothesis. Interferon-treated cells show increased glycolysis, increased oxygen uptake, decreased uptake of inorganic phosphate and decreased oxidation of glucose via the pentose cycle.
24 However, the haemagglutinin, whether it is virus particle or soluble antigen adsorbs to a specific site on the cell wall of erythrocytes. This erythrocyte-virus complex then agglutinates a second cell by joining it to the original complex. 20 The types of haemagglutinin vary with the site of attachment to the erythrocyte and the spontaneous disassociation of the virus from the cells. There are several methods of defining the site of attachment. 25 Once treated with RDE the erythrocytes can no longer be agglutinated by the Myxoviruses although they are still agglutinable by Picornaviruses and Reoviruses.