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.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-014-0082-y) contains supplementary material, which is available to authorized users.

Highlights

  • Equine infectious anemia virus (EIAV) is an equine lentivirus with a tropism primary for monocyte/macrophage lineage in vivo [1,2]

  • EIAVFDDV13 induced strong resistance to the infection of EIAVUK3 on equine monocyte-derived macrophages (eMDM) To examine the ability of EIAVFDDV13 to interfere with the infection of EIAVUK3, a pathogenic EIAV strain, EIAVFDDV13 and EIAVUK3 viruses at the same infectious titer were first used to infect equal numbers of eMDM The infection and replication patterns of the two strains were analyzed with qRT-PCR

  • This observation is consistent with previous reports that the amount of membrane-bound ELR1 was not reduced by EIAV infection [8,9]

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Summary

Introduction

Equine infectious anemia virus (EIAV) is an equine lentivirus with a tropism primary for monocyte/macrophage lineage in vivo [1,2]. The clinical manifestation of equine infectious anemia (EIA), which is caused by EIAV infection, can be divided into an acute phase, a chronic phase, and an asymptomatic phase. EIAVFDDV13 is an attenuated EIAV vaccine strain that induces immune protection in approximately 80% of vaccinated animals in laboratory and clinical studies [6,7]. An understanding of the mechanism that underlies the induction of immune protection imparted by this attenuated vaccine strain will be useful for elucidating the immune protective mechanism that is responsible for lentivirus infection. The cellular responses of equine macrophages, the primary target cells of EIAV in vivo, should be evaluated after being infected by EIAV

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