Arrest of Daudi cell growth by inactive influenza virus in-vitro.

We investigated the destructive capability of three influenza A strains, Victoria, PR8, and their recombinant X47, against the human lymphoma cell line Daudi. Both Victoria and X47 strains share the same envelope glycoproteins (H3N2), while PR8, the second parental strain of X47, differs in its envelope glycoproteins (HON1). The H3N2 strains and particularly the X47 recombinant were cytotoxic to Daudi cells while the HON1 strain was not. To reduce the virulence of the oncolytic viruses, we inactivated them either with heat (56 degrees C/45 min) or with formalin. Both treatments significantly reduced the infectivity of the viruses. The X47 virus treated with formalin retained its hemagglutinin (HA) and neuraminidase (NA) activities but lost its cytotoxic potential. On the other hand, the heat-treated X47 virus retained its HA activity, lost its NA activity, but preserved its cytotoxic potential. Thus, the heat-inactivated X47 virus (X56) was the most effective non-virulent oncolytic agent we tested. The X56 virus arrested Daudi cell multiplication in-vitro by inhibiting cellular DNA synthesis. The mechanism by which X56 inhibited Daudi cell DNA synthesis was not related to interferon induction in Daudi cells, and did not necessarily involve the activation of the Epstein-Barr virus (EBV) genome present in Daudi cells. Although the mechanism remains unclear, the oncolytic potential of the X56 virus on Daudi cells was demonstrated.