Virus-induced Cytolysis Research Articles

Deficient cytidine monophospho-N-acetylneuraminic acid: glycoprotein sialyltransferase activity in a clone of KB cells with altered cell fusion ability.

Lines of KB cells resistant to Sendai virus-induced cytolysis have been isolated and characterized (Toyama, S., Toyama, Su., and Uetake, H. (1977) Virology 76, 503-515). This study is concerned with the nature of this mutation. Plasma membrane fractions from Sil cells were found to have decreased amount of sialic acid and the same amount of galactose as compared to the membranes from parental KB cells. Sil cells exhibited an increase in sensitivity to toxic effects of ricin and a decrease in sensitivity to wheat germ agglutinin. Binding of wheat germ agglutinin to Sil cells was markedly decreased. Several membrane glycoproteins of Sil cells migrated slightly faster than the corresponding bands of wild type membrane when examined by gel electrophoresis in sodium dodecyl sulfate. Sil cells had decreased sialyltransferase activity that catalyzed the transfer of sialic acid residues from CMP-N-acetylneuraminic acid to glycoprotein acceptors containing Gal beta 1 leads to 3GalNAc alpha 1 leads to O-Ser(Thr) chain. The decreased enzyme activity could not be accounted for by the presence of inhibitors, altered pH optimum, or increased sialidase or CMP-sialic acid hydrolase activities. These results indicate that a molecular basis for the Sil cell phenotype might be the deficiency of sialyltransferase.

Inhibition by interferon of Sendai virus cytolysis.

Treatment of HeLa cells with human interferons inhibited 51Cr release from cells induced by ultraviolet-inactivated Sendai virus. The inhibitory effect became apparent about 6 h after interferon treatment and persisted for 24 to 48 h. In the interferon-treated cells, the cytolysis was inhibited within 10 min after adding virus and the inhibitory action was suppressed by the treatment of the cells with cycloheximide. Mock interferon and mouse interferon did not inhibit the cytolysis and antiinterferon serum neutralized the effect of interferon. All these findings indicate that Sendai virus-induced cytolysis is inhibited by interferon per se. However, interferon did not have any influence on Sendai virus hemolysis.

Altered cell-fusion capacity in lines of KB cells resistant to Sendai virus-induced cytolysis

Lines of KB cells resistant to Sendai virus-induced cytolysis ( sil cells) have been isolated and characterized. Acquisition of resistance to the cytolysis was found to be associated with changes in the cell fusion capacity. The ability of sil cells to adsorb Sendai virus was essentially the same as that of KB cells, although they were found to have a decreased amount of sialic acid compared to KB cells. The elution of adsorbed virus from sil cells was increased over that from KB cells. The penetration of the virus was markedly reduced at high multiplicities of infection, while it proceeded normally at low multiplicities of infection. The consequences of these results are discussed.

Cellular changes attending mengovirus-induced cytolysis of mouse L-cells.

Abstract 1. 1. Mengovirus-induced cytopathology in L-929 cell is shown to be moderated by the host-cell's stage. Late S and G2-M cells resist both artificial lysis with deoxycholate and virus-induced cytolysis. 2. 2. Nuclear lesions are found to precede lysosomal damage as measured by acridine orange vital staining and direct measurement of enzyme release. 3. 3. Nuclear protein alterations whic occur during development of mengovirus-induced cytopathology include leakage to the cytoplasm and extracellular fluids and an oxidation-polymerization of certain non-histone proteins. The synthetic rate of major acid-soluble proteins does not increase during the early hours of infection. 4. 4. These results are considered with respect to the question of the primary event leading to mengovirus-induced cytolysis. The primary role of lysosomes is questioned.