An Equine Infectious Anemia Virus Variant Superinfects Cells through Novel Receptor Interactions

Brindley, Melinda A.; Zhang, Baoshan; Montelaro, Ronald C.; Maury, Wendy

doi:10.1128/jvi.01142-08

Cited by 8 publications

(14 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the present study, only limited up-or down-regulation on the mRNA level of EIAV receptor ELR1 was detected in eMDM infected with either EIAV FDDV13 or EIAV UK3. This observation is consistent with previous reports that the amount of membrane-bound ELR1 was not reduced by EIAV infection [8,9]. In addition, these two EIAV strains acted similarly on ELR1 expression but induced TLR3 expression differently, which implicates that ELR1 does not play an essential role in the resistance to subsequent infection inducted by EIAV FDDV13.…”

Section: Discussionsupporting

confidence: 82%

“…Noticeably, in addition to the previously reported mechanism, i.e. masking viral receptor ELR1 by the SU protein of EIAV [8,9], our results revealed that up-regulation of the soluble EIAV receptor and interferonβ (IFNβ) by activated Tolllike receptor 3 (TLR3) are also largely involved in the resistance to EIAV UK3 infection induced by EIAV FDDV13 .…”

Section: Introductionmentioning

confidence: 67%

“…On the contrary, our results also show that the resistance to subsequent infected EIA-V UK3 induced by a TLR3 ligand, poly I:C, was noticeably lower than that induced by EIAV FDDV13 (90% vs 98% of inhibition), and the knockdown of TLR3 expression by siRNA only reversed 10-20% resistance to the subsequently infected virus. Even though the incomplete interference of TLR3 expression (about 65%) partially counts for the incomplete reverse of the EIAV FDDV13 -induced SIR, other mechanisms may also be involved in, such as interfering viral entrance by the binding of EIAV gp90 surface protein to the membrane-bound receptor ELR1 [8,9].…”

Section: Discussionmentioning

confidence: 99%

“…The EIAV receptor ELR1 has been shown to play an important role in induction of superinfection resistance (SIR) [9]. To investigate the role of ELR1 in the infection resistance induced in eMDM by EIAV FDDV13 , a quantitative analysis of ELR1 mRNA levels in eMDM up to 36 hpi with EIAV FDDV13 was performed.…”

Section: Eiav Fddv13 Induced Strong Resistance To the Infection Of Eimentioning

confidence: 99%

See 3 more Smart Citations

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

Wang

Lin

et al. 2014

Vet Res

View full text Add to dashboard Cite

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 EIAV FDDV13 , a Chinese attenuated EIAV strain, induced a strong resistance to subsequent infection by a pathogenic strain, EIAV UK3 . 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 EIAV FDDV13 compared with eMDM infected with EIAV UK3 . Stimulating eMDM with poly I:C resulted in similar resistance to EIAV infection as induced by EIAV FDDV13 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 EIAV FDDV13 . These results indicate that the induction of restraining infection by EIAV FDDV13 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.

show abstract

Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Eiav Fddv13 Induced Strong Resistance To the Infection Of Eimentioning

confidence: 99%

See 2 more Smart Citations

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

Wang

Lin

et al. 2014

Vet Res

View full text Add to dashboard Cite

show abstract

“…A third type of direct VVI is viral superinfection exclusion, which occurs when a primary viral infection induces resistance to subsequent infections by similar viruses. Superinfection exclusion is known to occur among bacteriophage, retroviruses, hepadnaviruses, arboviruses, and plant viruses (Brindley et al, 2008;Geib et al, 2003;McAllister and Barrett, 1977;Nethe et al, 2005;Saumet and Lecellier, 2006). Mechanisms of exclusion are diverse and have not been determined in all cases, but all mechanisms described so far depend on direct interaction of products of the primary infection with the secondary infecting virus.…”

Section: Superinfection Exclusionmentioning

confidence: 99%

A systematic approach to virus–virus interactions

et al. 2010

View full text Add to dashboard Cite

A virus-virus interaction is a measurable difference in the course of infection of one virus as a result of a concurrent or prior infection by a different species or strain of virus. Many such interactions have been discovered by chance, yet they have rarely been studied systematically. Increasing evidence suggests that virus-virus interactions are common and may be critical to understanding viral pathogenesis in natural hosts. In this review we propose a system for classifying virus-virus interactions by organizing them into three main categories: (1) direct interactions of viral genes or gene products, (2) indirect interactions that result from alterations in the host environment, and (3) immunological interactions. We have so far identified 15 subtypes of interaction and assigned each to one of these categories. It is anticipated that this framework will provide for a more systematic approach to investigating virus-virus interactions, both at the cellular and organismal levels.

show abstract