文摘
Bats are known to harbour a number of emerging and re-emerging zoonotic viruses, many of which are highly pathogenic in other mammals (Rabies, Ebola among others) but result in no clinical symptoms in bats. The ability of bats to coexist with viruses may be the result of rapid control of viral replication early in the immune response. Type I (IFN-¦Á and ¦Â) and type III (¦Ë) interferons (IFNs) provide the first line of defense against viral infection in vertebrates. Using qPCR on primary cell lines from our model bat species, the Australian black flying fox we show that bat IFN-¦Á is expressed at a higher baseline level compared to IFN- ¦Â or ¦Ë in all nine cell lines tested. Stimulation with the TLR3 ligand, pIC resulted in high induction of IFNb and IFNl but very little IFNa upregulation. This unusual expression pattern prompted us to ask the question: which bat IFN-¦Á is responsible for this pattern and what are the mechanisms involved? Genomic analysis has resulted in the identification of fewer bat IFN-¦Á genes (one identified so far) compared to other species (13 in humans). Analysis of the putative promoter regions of the bat IFN-¦Á gene has revealed that the three IRF binding modules (conserved in human/mouse IFN-¦Á) are totally disrupted in the identified bat IFN-¦Á, which makes it totally unresponsive to SeV stimulation. These discoveries are consistent with differences in the IFN-¦Á system of bats compared with other mammals and may have important implications for the role of type I IFNs in the ability of bats to coexist with viruses.