' ^/ t! K3 @! n+ f, }Abstract: Bats are natural reservoir hosts for many viruses that produce no clinical symptoms in bats.1 f8 U2 J6 d8 k7 X
Therefore, bats may have evolved effective mechanisms to control viral replication. However, little* k7 V2 r3 Q% n( C9 |' V# f: D
information is available on bat immune responses to viral infection. Type I interferon (IFN) plays a2 o/ V, c/ `/ v( u7 o$ R. Q
key role in controlling viral infections. In this study, we report the cloning, expression, and / _+ d5 [2 d/ z x, D9 Q: O7 gbiological activity of interferon β (IFNβ) from the Chinese microbat species, Myotis davidii. We% c7 {7 r* o) ~" p& D
demonstrated the upregulation of IFNB and IFN-stimulated genes in a kidney cell line derived from, C: S9 W% d! i( J) G5 L4 ?( ?
M. davidii after treatment with polyI:C or infection with Sendai virus. Furthermore, the recombinant - o* s$ |7 I4 t" u+ [5 F$ \IFNβ inhibited vesicular stomatitis virus and bat adenovirus replication in cell lines from two bat 6 J) R8 ~! b6 d4 j3 h8 Wspecies, M. davidii and Rhinolophus sinicus. We provide the first in vitro evidence of IFNβ antiviral4 w9 ~ v/ M, Q F, z* f, y
activity in microbats, which has important implications for virus interactions with these hosts.3 r6 N4 d3 k( ~8 e. d