1. Virology Laboratory, National Institute for Research and Development, Ministry of Health, Indonesia.
2. Plum Island Animal Disease Center, USDA, Agricultural Research Service, North Atlantic Area, Greenport, New York 11944, USA.
Background: Viral infections induce expression of type I interferons (IFNα/β) which result in an antiviral state within cells or animals. However, some viruses, notably influenza viruses (IV), have evolved mechanisms of evasion and blocking of IFN to survive in nature. Swine influenza virus (SIV) can inhibit IFN and as with other IV does it through its NS1 protein, identified as a virulence factor in pigs.
Methods: To determine whether different SIV strains varied in their ability to induce IFNβ in cell culture and the relative sensitivity of these strains to exogenous IFNβ, three strains were tested in SJPL cells originally deposited as epithelial-like cell line of swine lung origin (ATCC, Richmond, MD) but later characterized as cells of monkey origin.
Results: The SIV strains tested here induced significant synthesis of IFNβ in SJPL cells, with levels that were higher to those induced by poly I:C. The induction of IFNβ by SIV peaked at three days post-infection and was not dependent on the infectious virus dose. Interestingly, priming the cells with exogenous recombinant swine IFNβ had no significant inhibitory effect on the replication of these SIV strains. NS1- antagonistic compounds did not change IFNβ induction and had variable and unexpected effects on virus replication of the three SIV strains tested.
Conclusions: Our study showed that while the SIV strains tested here were capable to induce IFNβ in SJPL cells these were relatively resistant to the antiviral effects of exogenous IFNβ. NS1-antagonistic compounds did not affect IFNβ induction and had variable effects on the replication of the SIV strains tested. These seemingly contradicting results suggest virus evasion by mechanisms other than NS1.
Keywords: Swine influenza virus, interferon β, SJPL cells, NS1 protein