RESULTS : Three cell lines showed similar results with additive effects of TNF-alpha and radiation in both assays.
Thus , low amounts of LPS , which could easily be present in vivo , may serve as a potent trigger signal for TNF-alpha production from macrophages that have been primed by influenza A virus infection.
Therefore , it has been suggested that cellular cofactors that are essential for influenza virus infection might be better targets for antiviral therapy.
Here we demonstrate that the closely related Hendra virus V protein also inhibits cellular responses to IFN through binding and cytoplasmic sequestration of both STAT1 and STAT2 , but not STAT3.