title: Inhibitory effects of lithium chloride on replication of type II porcine reproductive and respiratory syndrome virus in vitro.
abstract: BACKGROUND
  Porcine reproductive and respiratory syndrome (PRRS) is one of the most serious diseases affecting the swine industry worldwide; however, there are no efficient control strategies against PRRS virus (PRRSV) at present. Therefore, development of new antiviral treatment strategies is urgently needed. As reported, lithium chloride (LiCl) can efficiently impair the replication of a variety of viruses, including infectious bronchitis coronavirus (IBV) and transmissible gastroenteritis coronavirus (TGEV). In this report, we explored whether LiCl had the potential to inhibit PRRSV infection.
  
  
  METHODS
  MARC-145 cells were treated with LiCl at various stages of PRRSV life cycle. Virus titration assay was performed to determine the virus infectivity. The expression of viral mRNA and protein was measured by real-time PCR and indirect immunofluorescence assay, respectively. The transcript levels of cytokines were evaluated by real-time PCR.
  
  
  RESULTS
  LiCl significantly suppressed the synthesis of viral RNA and protein; however, it did not block PRRSV binding and entry. Further studies confirmed that LiCl inhibited PRRSV replication at an early stage and TNF-α, an antiviral cytokine, was significantly increased after LiCl treatment. Thus, we suggested that LiCl inhibited PRRSV infection by up-regulating the level of antiviral cytokine TNF-α at an early infection stage.
  
  
  CONCLUSIONS
  Our findings imply that the LiCl has the potential to be used as anti-PRRSV therapy.
authors.affiliation: College of Veterinary and National Engineering Research Center for Breeding Swine Industry, South China Agricultural University, Guangzhou, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Cui
authors.forename: Jiexiong
authors.initials: J
authors.lastname: Xie
authors.forename: Ming
authors.initials: M
authors.lastname: Gao
authors.forename: Han
authors.initials: H
authors.lastname: Zhou
authors.forename: Yao
authors.initials: Y
authors.lastname: Chen
authors.forename: Tiantian
authors.initials: T
authors.lastname: Cui
authors.forename: Xiaolei
authors.initials: X
authors.lastname: Bai
authors.forename: Heng
authors.initials: H
authors.lastname: Wang
authors.forename: Guihong
authors.initials: G
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000998:Antiviral Agents / Q000494:pharmacology*; D002461:Cell Line, Transformed; D002522:Chlorocebus aethiops; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000821:virology; D005786:Gene Expression Regulation; D054884:Host-Pathogen Interactions; D007668:Kidney / Q000187:drug effects / Q000276:immunology / Q000821:virology; D018021:Lithium Chloride / Q000494:pharmacology*; D019316:Porcine respiratory and reproductive syndrome virus / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000819:agonists* / Q000235:genetics / Q000276:immunology; D014764:Viral Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D053585:Virus Attachment; D053586:Virus Internalization; D014779:Virus Replication / Q000187:drug effects / Q000235:genetics
chemical_list: D000998:Antiviral Agents; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D014764:Viral Proteins; D018021:Lithium Chloride