| Abstract: | Adenovirus internalization generally has been accepted to involve an interaction of the adenoviral penton base protein with alpha(v)beta3 and alpha(v)beta5 cell surface integrins. In this study we show that exposure of a panel of melanoma cells to the beta1-activating antibody TS2/16 rendered such cells more susceptible to adenovirus infection. This increase in adenoviral infectivity paralleled effects on cell adhesion, and both these characteristics were mediated, in part, by the alpha5beta1 integrin. These observations suggest that alpha5beta1 may act as an alternative adenovirus receptor and that integrin-activating strategies may improve the efficacy of recombinant adenoviruses as vectors for gene therapy. |
