Given the modest proportion of cells expressing elevated HLA-I after viral infection, the paucity of response to either human IFNα (monitored by Western blotting) or human IFNγ (using reporter assays) and the lack of immunoreactivity of human proteins exported from 1.1B4 cells in exosomes, we were drawn towards the possibility that the cultures may have become contaminated and that human cells were present in the minority. The gene discussed is IFNG; the disease is viral infectious disease.