The Interplay between Bluetongue Virus Infections and Adaptive Immunity

Abstract

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 We present some unpublished data showing that BTV infection also affects other T cell populations such as CD4+ T-cells or γδ T-cells, as well as B-cell numbers in the periphery.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.

A Machine Learning Framework to Identify the Correlates of Disease Severity in Acute Arbovirus Infection

“…Notably, two other BTMs associated B-cell enrichment (BTM M47.3 and BTM M47.4) were also identified in the top 35 parameters suggesting a trend in B cell reduction in animals with severe disease. These data are in line with previously published reports showing that BTV causes lymphopenia 41 and a transitory immunosuppression due to inhibition of B-cell division in germinal centres due to infection of follicular dendritic cells 32,42 . Indeed, we detected a reduced number of follicles in the lymph nodes draining the sites of virus inoculation in animals with severe disease (Fig.…”

Unleashing the Immune Arsenal: Development of Broad-spectrum Multiepitope Bluetongue Vaccine Targeting Conserved T Cell Epitopes of Structural Proteins

“…Collectively, the comprehensive profiling of our vaccine constructs underscores their potential as promising candidates for effective BT vaccine development. With a focus on cell-mediated immunity, which has demonstrated its importance in providing cross-protection against various BTV serotypes in prior research (Umeshappa, Singh et al 2010, singh 2011, Umeshappa, Singh et al 2011, Rojas, Rodriguez-Calvo et al 2017, Potter 2019, Evseev and Magor 2021, Rodríguez-Martín D 2021, Wang, Tang et al 2022, Zheng, Guo et al 2022…”

Nanoparticle- and Microparticle-Based Vaccines against Orbiviruses of Veterinary Importance

“…In this sense, MHC class Ipeptide complexes formation yields could differ between the 'phagosome-to-cytosol' and the direct endosomal loading pathways, which could explain the higher efficacy of nanoparticles to induce MHC class I cross-presentation [134][135][136]. Although orbiviruses can transiently impair B-cell responses [137], humoral immunity is also triggered after infection with BTV, AHSV or EHDV, with the most exposed protein of the virion and major determinant of virus serotype, VP2, as the main target of Nabs [138][139][140][141]. Th2 cell development subsequently leads to clonal expansion of B cells and affinity maturation of produced antibodies [142,143].…”

“…Particulate systems, like VLPs, are strong stimulators of B-cell-mediated immune responses. These highly organized and dense antigenic structures prompt direct cross- Although orbiviruses can transiently impair B-cell responses [137], humoral immunity is also triggered after infection with BTV, AHSV or EHDV, with the most exposed protein of the virion and major determinant of virus serotype, VP2, as the main target of Nabs [138][139][140][141]. Th2 cell development subsequently leads to clonal expansion of B cells and affinity maturation of produced antibodies [142,143].…”