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Effect of Respiratory Syncytial Virus Infection of HeLa-Cell Macromolecular Synthesis

Ramon Hamilton

^* Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan 48201
Department of Experimental Biology, The Upjohn Company, Kalamazoo, Michigan 49001, U.S.A.

Cells infected with respiratory syncytial (RS) virus eventually die but there appears to be no specific mechanism for shutting off cellular synthesis of macromolecules. DNA and RNA synthesis, as measured by the incorporation of labelled thymidine or uridine, do not begin to shut down until some time between 11 and 18 h after infection. By 18 h their rates of synthesis are reduced to approx. 50% for DNA and 35% for RNA.

Protein synthesis continues throughout the course of infection at approximately the same rate. Synthesis of most of the cellular polypeptides also continues, but the distribution of polypeptides of high and low mol. wt. shifts. The increase in the proportion of those of high mol. wt. includes a peak that represents one of the seven previously identified virion polypeptides.

Another consequence of RS virus infection is an increase in glucosamine incorporation, beginning near the end of the virus eclipse period (12 h after infection), which may be associated with virion glycoprotein synthesis. Polyacrylamide-gel electrophoresis of glucosamine-labelled cells reveals that at 18 h after infection two of the three previously identified virion glycoproteins are present.

Received 26 January 1977; accepted 22 April 1977.