Inhibition of the IFN Response by Bluetongue Virus: The Story So Far

Rojas, José M.; Avia, Miguel; Martı́n, Verónica; Sevilla, Noemı́

doi:10.3389/fmicb.2021.692069

Cited by 8 publications

(8 citation statements)

References 124 publications

(242 reference statements)

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“…NS1 promotes viral protein expression [ 25 ]; NS2 is an RNA binding protein which is the main component of viral inclusion bodies [ 26 ]; while NS3 is involved in virion egress [ 27 , 28 , 29 ]. VP3, NS3, NS4, and the putative NS5 are involved in impairing the host cellular response to BTV by acting as interferon antagonist and/or by promoting cellular shut-off [ 30 , 31 , 32 , 33 , 34 , 35 ].…”

Section: Bluetongue Virus: the Prototypical Orbivirusmentioning

confidence: 99%

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The Interplay between Bluetongue Virus Infections and Adaptive Immunity

Rodríguez-Martín

Louloudes-Lázaro

Avia

et al. 2021

Viruses

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Viral infections have long provided a platform to understand the workings of immunity. For instance, great strides towards defining basic immunology concepts, such as MHC restriction of antigen presentation or T-cell memory development and maintenance, have been achieved thanks to the study of lymphocytic choriomeningitis virus (LCMV) infections. These studies have also shaped our understanding of antiviral immunity, and in particular T-cell responses. In the present review, we discuss how bluetongue virus (BTV), an economically important arbovirus from the Reoviridae family that affects ruminants, affects adaptive immunity in the natural hosts. During the initial stages of infection, BTV triggers leucopenia in the hosts. The host then mounts an adaptive immune response that controls the disease. In this work, we discuss how BTV triggers CD8+ T-cell expansion and neutralizing antibody responses, yet in some individuals viremia remains detectable after these adaptive immune mechanisms are active. We present some unpublished data showing that BTV infection also affects other T cell populations such as CD4+ T-cells or γδ T-cells, as well as B-cell numbers in the periphery. This review also discusses how BTV evades these adaptive immune mechanisms so that it can be transmitted back to the arthropod host. Understanding the interaction of BTV with immunity could ultimately define the correlates of protection with immune mechanisms that would improve our knowledge of ruminant immunology.

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Section: Bluetongue Virus: the Prototypical Orbivirusmentioning

confidence: 99%

“…Once BTV reaches the LN, it can disrupt follicular DC activity [ 94 ]. BTV has the capacity to replicate in ruminants in presence of a concomitant antiviral IFN response (reviewed in [ 34 ]). We have shown that BTV presence in the LN triggered the expression of the IFN-stimulated gene Mx1 [ 94 ].…”

Section: Btv Disruption Of Adaptive Immunitymentioning

confidence: 99%

The Interplay between Bluetongue Virus Infections and Adaptive Immunity

Rodríguez-Martín

Louloudes-Lázaro

Avia

et al. 2021

Viruses

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“…43 The reason for the stunted response is unclear. In sheep, BTV has been reported to antagonize interferon synthesis and might be able to downregulate the innate immune response, 46 possibly interfering with the synthesis of SAA. African horse sickness virus nonstructural protein 4 has recently been demonstrated to contribute to potential mechanisms to overcome the host's antiviral response by colocalization with promyelocytic leukemia nuclear bodies 47 and interference with the JAK-STAT pathway that is instrumental in the interferon pathway.…”

Section: Discussionmentioning

confidence: 99%

Experimental infection with African Horse Sickness Virus in horses induces only mild temporal hematologic changes and acute phase reactant response

Schliewert

Hooijberg

Steyn

et al. 2022

ajvr

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OBJECTIVE African Horse Sickness (AHS) is a vector-borne disease endemic to sub-Saharan Africa caused by African Horse Sickness Virus (AHVS). Infections in naïve horses have high morbidity and mortality rates. AHS pathogenesis is not well understood; neither the hematologic changes nor acute phase response occurring during infection has been fully evaluated. The study’s objective was to characterize the hematologic changes and acute phase response during experimental infection with AHSV. ANIMALS 4 horses negative for AHSV group-specific antibodies. PROCEDURES In this prospective, longitudinal study conducted between November 23 and December 2, 2020, horses were experimentally infected with AHSV, and blood samples were obtained before inoculation and then every 12 hours until euthanasia. Hematologic changes and changes for serum amyloid A (SAA) and iron concentration were evaluated over time using a general linear model including natural logarithm of sampling time. RESULTS All horses were humanely euthanized due to severe clinical signs typical of AHS. Median Hct increased significantly, and the median WBC count, monocyte count, eosinophil count, and myeloperoxidase index changed significantly in all horses over time. Horses developed marked thrombocytopenia (median, 48 X 103 cells/µL; range, 21 X 103 to 58 X 103 cells/µL) while markers of platelet activation also changed significantly. Median SAA increased and serum iron concentration decreased significantly over time. CLINICAL RELEVANCE Results indicated severe thrombocytopenia with platelet activation occurs during infection with AHSV. Changes in acute phase reactants SAA and iron, while significant, were unexpectedly mild and might not be useful clinical markers.

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“…VP3, NS3, NS4 and the putative NS5 are involved in countering the antiviral cell response. VP3, NS3 and NS4 can act as IFN antagonists (reviewed in [34]). VP3 can impair IFN induction [35], while NS3 and NS4 can counter IFN induction as well as type I and type II IFN signaling [36][37][38][39][40].…”

Section: Figure 1 Schematic Representation Of Bluetongue Virus (Btv) (A)mentioning

confidence: 99%

Vaccination as a Strategy to Prevent Bluetongue Virus Vertical Transmission

2021

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Bluetongue virus (BTV) produces an economically important disease in ruminants of compulsory notification to the OIE. BTV is typically transmitted by the bite of Culicoides spp., however, some BTV strains can be transmitted vertically, and this is associated with fetus malformations and abortions. The viral factors associated with the virus potency to cross the placental barrier are not well defined. The potency of vertical transmission is retained and sometimes even increased in live attenuated BTV vaccine strains. Because BTV possesses a segmented genome, the possibility of reassortment of vaccination strains with wild-type virus could even favor the transmission of this phenotype. In the present review, we will describe the non-vector-based BTV infection routes and discuss the experimental vaccination strategies that offer advantages over this drawback of some live attenuated BTV vaccines.

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Inhibition of the IFN Response by Bluetongue Virus: The Story So Far

Cited by 8 publications

References 124 publications

The Interplay between Bluetongue Virus Infections and Adaptive Immunity

The Interplay between Bluetongue Virus Infections and Adaptive Immunity

Experimental infection with African Horse Sickness Virus in horses induces only mild temporal hematologic changes and acute phase reactant response

Vaccination as a Strategy to Prevent Bluetongue Virus Vertical Transmission

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