Systems immunology approach for resolving the mechanisms of vaccine-induced classical swine fever protection

• Grant number: 19/16444-1
• Support Opportunities: Regular Research Grants
• Duration: December 01, 2019 - November 30, 2022
• Field of knowledge: Biological Sciences - Immunology - Immunogenetics
• Convênio/Acordo: University of Surrey
• Mobility Program: SPRINT - Projetos de pesquisa - Mobilidade
• Principal Investigator: Helder Takashi Imoto Nakaya
• Grantee: Helder Takashi Imoto Nakaya
• Principal researcher abroad: Falko Steinbach
• Institution abroad: University of Surrey, England
• Host Institution: Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE). Sociedade Beneficente Israelita Brasileira Albert Einstein (SBIBAE). São Paulo , SP, Brazil
• Associated research grant: 18/14933-2 - Integrative biology applied to human health, AP.JP2

Abstract

Classical Swine Fever (CSF) is a contagious, hemorrhagic and often fatal disease of Suidae, such as pigs and wild boar, caused by the classical swine fever virus (CSFV). CSFV is an enveloped, single-stranded RNA virus that belongs to the Flaviviridae family (Moennig, 2000), distantly related for example to Zika and Yellow Fever virus. CSFV can be controlled by vaccination particularly using the C strain vaccine. The vaccine provides rapid and complete protection of pigs against infection and also prevents viral transmission within 5 days of vaccination. The immunological signaling cascades behind the early protection afforded by C Strain are poorly understood but precede the adaptive response, where IFN³+ CD8+ cells arrive before the detection of a virus-neutralizing antibody response. Interferon is a key component of how the innate immune system responds to challenge with CSFV. System Immunology approaches have been carried out in humans for example on the highly efficacious Yellow Fever vaccine. Deciphering the immune signaling pathways underpinning the effectiveness of the C strain vaccine can shape and optimize the next generation of marker and subunit vaccines well beyond CSFV as access to material including post-mortem tissues where required is not limited. Previous work has indicated a key role of the interferon system if stimulated prior to the challenge. The team at UoS has already carried out studies further to the one mentioned above to characterize the action of the CSFV C strain vaccine upon vaccination. In particular, we have carried out one study sampling tonsils at various time points in the first 90 hours, comparing C-strain and a virulent challenge virus to baseline. Samples have been stored for subsequent analysis by deep sequencing, which will be carried out in 2019. For early 2020 another such study is planned into the design of which the team at USP will provide input. The project is specifically designed to foster the collaboration between Prof Nakaya's team at USP and Prof Steinbach's team in Surrey through collaborative visits in particular. The aim is to generate data in collaboration from which publications and further grant applications will be generated in the course of the project. (AU)