Infectious bursal disease virus (IBDV) causes an important disease in young chickens. Chicken heat-shock protein 90 (cHsp90) has been shown to be a functional component of the cellular receptor complex for IBDV infection. This study demonstrates the inhibitory effect of vectorexpressed anti-cHsp90a microRNA (miRNA) on IBDV infection. The reporter vectors pcHsp90a-EGFP and pcHsp90b-EGFP were constructed to facilitate effective miRNA selection. Two anticHsp90a and one anti-cHsp90b miRNA-expression vectors were constructed for a stable transfection study. Poly(A)-tailed RT-PCR detected sequence-specific miRNA transcription in transfected cells. Semiquantitative RT-PCR showed inhibition of cHsp90 transcription in transfected cells. A virus-titration assay showed that the anti-cHsp90a miRNA, but not the anticHsp90b miRNA, had inhibitory effects on IBDV infection. These results suggest that cHsp90a is a functional component of the cellular receptor complex for IBDV infection, and that anti-cHsp90a miRNA could be used as an anti-IBDV reagent.Infectious bursal disease (IBD) is a highly contagious and immunosuppressive disease in young chickens (Sharma et al., 2000). The causative agent, infectious bursal disease virus (IBDV), is a dsRNA virus belonging to the genus Avibirnavirus of the family Birnaviridae (Dobos et al., 1995). IBDV targets the precursors of antibody-producing B-lymphocytes in the bursa of Fabricius (BF), leading to depletion of B-lymphocytes in the BF (Becht, 1980). IBDV infection can cause different mortalities in young chickens, as well as increased susceptibility to other infectious diseases and poor immune response to vaccines (Lukert & Saif, 1997;Van Den Berg, 2000). Despite widely used vaccination programmes, IBD remains one of the major economically important diseases of poultry and thus the development of new strategies for efficient control of the disease is essential (Sharma et al., 2000).RNA interference (RNAi) is a post-transcriptional genesilencing mechanism conserved in eukaryotes ranging from worms to humans (Fire et al., 1998;Meister & Tuschl, 2004). Since its discovery in 1994 as an innate antiviral mechanism, RNAi has become a powerful strategy against a variety of virus infections (Zhou & Rossi, 2011). RNAi has also been used as an in vitro strategy against IBDV, including small interfering RNA (siRNA) against the viral structural protein genes (Gao et al., 2008;Sajjanar et al., 2011) and artificial microRNA (miRNA) targeting VP1 or VP2 transcription (Wang et al., 2009(Wang et al., , 2010. However, IBDV is antigenically variable and undergoing rapid mutation (Müller et al., 2003), which must be addressed in order to establish a viable RNAi approach.IBDV enters the host cell by binding to cellular receptors; several different membrane proteins have been shown to interact with IBDV of different virulence (Delgui et al., 2009; Luo et al., 2010). Lin et al. (2007) demonstrated that chicken heat-shock protein 90 (cHsp90) is a functional component of the cellular receptor complex essential...