title: Infection of equine monocyte-derived macrophages with an attenuated equine infectious anemia virus (EIAV) strain induces a strong resistance to the infection by a virulent EIAV strain.
abstract: The Chinese attenuated equine infectious anemia virus (EIAV) vaccine has successfully protected millions of equine animals from EIA disease in China. Given that the induction of immune protection results from the interactions between viruses and hosts, a better understanding of the characteristics of vaccine strain infection and host responses would be useful for elucidating the mechanism of the induction of immune protection by the Chinese attenuated EIAV strain. In this study, we demonstrate in equine monocyte-derived macrophages (eMDM) that EIAVFDDV13, a Chinese attenuated EIAV strain, induced a strong resistance to subsequent infection by a pathogenic strain, EIAVUK3. Further experiments indicate that the expression of the soluble EIAV receptor sELR1, Toll-like receptor 3 (TLR3) and interferon β (IFNβ) was up-regulated in eMDM infected with EIAVFDDV13 compared with eMDM infected with EIAVUK3. Stimulating eMDM with poly I:C resulted in similar resistance to EIAV infection as induced by EIAVFDDV13 and was correlated with enhanced TLR3, sELR1 and IFNβ expression. The knock down of TLR3 mRNA significantly impaired poly I:C-stimulated resistance to EIAV, greatly reducing the expression of sELR1 and IFNβ and lowered the level of infection resistance induced by EIAVFDDV13. These results indicate that the induction of restraining infection by EIAVFDDV13 in macrophages is partially mediated through the up-regulated expression of the soluble viral receptor and IFNβ, and that the TLR3 pathway activation plays an important role in the development of an EIAV-resistant intracellular environment.
authors.forename: Jian
authors.initials: J
authors.lastname: Ma
authors.forename: Shan-Shan
authors.initials: SS
authors.lastname: Wang
authors.forename: Yue-Zhi
authors.initials: YZ
authors.lastname: Lin
authors.forename: Hai-Fang
authors.initials: HF
authors.lastname: Liu
authors.forename: Qiang
authors.initials: Q
authors.lastname: Liu
authors.forename: Hua-Mian
authors.initials: HM
authors.lastname: Wei
authors.forename: Xue-Feng
authors.initials: XF
authors.lastname: Wang
authors.forename: Yu-Hong
authors.initials: YH
authors.lastname: Wang
authors.forename: Cheng
authors.initials: C
authors.lastname: Du
authors.forename: Xian-Gang
authors.initials: XG
authors.lastname: Kong
authors.affiliation: State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, Heilongjiang, China. Jianhua_uc@126.com.
authors.forename: Jian-Hua
authors.initials: JH
authors.lastname: Zhou
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Wang
mesh_terms: D000818:Animals; D060467:Disease Resistance; D004797:Enzyme-Linked Immunosorbent Assay / Q000662:veterinary; D004859:Equine Infectious Anemia / Q000235:genetics / Q000276:immunology* / Q000821:virology; D005786:Gene Expression Regulation; D006734:Horse Diseases / Q000235:genetics / Q000276:immunology* / Q000821:virology; D006736:Horses; D004860:Infectious Anemia Virus, Equine / Q000235:genetics / Q000502:physiology*; D016899:Interferon-beta / Q000235:genetics / Q000378:metabolism; D008264:Macrophages / Q000276:immunology; D060888:Real-Time Polymerase Chain Reaction / Q000662:veterinary; D011991:Receptors, Virus / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D051196:Toll-Like Receptor 3 / Q000235:genetics / Q000378:metabolism; D014765:Viral Vaccines / Q000276:immunology*
chemical_list: D011991:Receptors, Virus; D051196:Toll-Like Receptor 3; D014765:Viral Vaccines; D016899:Interferon-beta
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