Cyclophilin B facilitates the replication of Orf virus
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RESEARCH
Open Access
Cyclophilin B facilitates the replication of Orf virus Kui Zhao1, Jida Li2, Wenqi He1, Deguang Song1, Ximu Zhang3, Di Zhang1, Yanlong Zhou1 and Feng Gao1,4*
Abstract Background: Viruses interact with host cellular factors to construct a more favourable environment for their efficient replication. Expression of cyclophilin B (CypB), a cellular peptidyl-prolyl cis-trans isomerase (PPIase), was found to be significantly up-regulated. Recently, a number of studies have shown that CypB is important in the replication of several viruses, including Japanese encephalitis virus (JEV), hepatitis C virus (HCV) and human papillomavirus type 16 (HPV 16). However, the function of cellular CypB in ORFV replication has not yet been explored. Methods: Suppression subtractive hybridization (SSH) technique was applied to identify genes differentially expressed in the ORFV-infected MDBK cells at an early phase of infection. Cellular CypB was confirmed to be significantly upregulated by quantitative reverse transcription-PCR (qRT-PCR) analysis and Western blotting. The role of CypB in ORFV infection was further determined using Cyclosporin A (CsA) and RNA interference (RNAi). Effect of CypB gene silencing on ORFV replication by 50% tissue culture infectious dose (TCID50) assay and qRT-PCR detection. Results: In the present study, CypB was found to be significantly up-regulated in the ORFV-infected MDBK cells at an early phase of infection. Cyclosporin A (CsA) exhibited suppressive effects on ORFV replication through the inhibition of CypB. Silencing of CypB gene inhibited the replication of ORFV in MDBK cells. In conclusion, these data suggest that CypB is critical for the efficient replication of the ORFV genome. Conclusions: Cellular CypB was confirmed to be significantly up-regulated in the ORFV-infected MDBK cells at an early phase of infection, which could effectively facilitate the replication of ORFV. Keywords: ORFV, Cellular cyclophilin B, Cyclosporine A, RNA interference, Replication
Background Orf virus (ORFV) is the type species of the genus Parapoxvirus, which has a worldwide distribution and is the causative agent of Orf, a contagious debilitating skin disease of sheep and goats also known as contagious ecthyma, contagious pustular dermatitis, infectious labial dermatitis, scabby mouth or sore mouth [1]. Primary infections are usually resolved within 1–2 months, however repeated and persistent infections can occur in the presence of an intensive inflammatory host antivirus immune response [2, 3]. The mechanisms that establish the repeated and persistent infections in vivo are almost * Correspondence: [email protected] 1 College of Veterinary Medicine, Jilin University, 5333 Xi’an Road, Changchun 130062, China 4 Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, 5333 Xi’an Road, Changchun 130062, China Full list of author information is available at the end of the article
completely unknown. Currently, the host immune response to ORFV has been exte
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