title: Interleukin-10 blocks in vitro replication of human cytomegalovirus by inhibiting the virus-induced autophagy in MRC5 cells.
abstract: BACKGROUND
  Interleukin-10 is an important cytokine that regulates immune response. Previous studies have shown that human cytomegalovirus can trigger cell autophagy during the early stages of infection. To our knowledge, whether IL-10 inhibits HCMV-induced autophagy and virus replication has not been studied previously.
  
  
  OBJECTIVE
  We investigated whether IL-10 affects cell viability and autophagy under the conditions of starvation and HCMV infection by using the MRC5 cell line. We also explored the role of IL-10-mediated autophagy on HCMV replication.
  
  
  RESULTS
  Our data showed that IL-10 inhibited the autophagic flux of the MRC5 cells irrespective of starvation or HCMV infection, and suppressed HCMV replication. The promotion of autophagy with either a pharmacological inducer (rapamycin), or a technique to over-express the BECN1 gene reversed the effect of IL-10 on virus replication. Furthermore, the PI3K/Akt signal pathway was activated when the cells were pretreated with IL-10.
  
  
  CONCLUSIONS
  Our results indicated that IL-10 can suppress HCMV replication by inhibiting autophagy in host cells during the early stages of infection.
authors.affiliation: Department of Neonatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China. Electronic address: wlsjtu@163.com.
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Neonatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China. Electronic address: zhanghuipingok@163.com.
authors.forename: Huiping
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Neonatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China. Electronic address: qianjh668@126.com.
authors.forename: Jihong
authors.initials: J
authors.lastname: Qian
authors.affiliation: Department of Obstetrics, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China.
authors.forename: Kanqing
authors.initials: K
authors.lastname: Wang
authors.affiliation: Department of Neonatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China.
authors.forename: Jianxing
authors.initials: J
authors.lastname: Zhu
mesh_terms: D001343:Autophagy / Q000235:genetics / Q000276:immunology* / Q000502:physiology*; D002460:Cell Line; D003587:Cytomegalovirus / Q000276:immunology* / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D016753:Interleukin-10 / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D053701:Receptors, Interleukin-10 / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014779:Virus Replication / Q000276:immunology*
chemical_list: C508609:IL10 protein, human; D012333:RNA, Messenger; D053701:Receptors, Interleukin-10; D016753:Interleukin-10; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt
keywords: Autophagy; Cytomegalovirus infection; IL-10; PI3K pathway