Type I interferons are essential while type II interferon is dispensable for protection against St. Louis encephalitis virus infection in the mouse brain

Author(s)

Rocha, Rebeca Froes ^{[1, 2, 3]} ; Del Sarto, Juliana L. ^[3] ; Gomes, Giovanni F. ^[4] ; Goncalves, Mariana P. ^{[1, 2]} ; Rachid, Milene A. ^[5] ; Smetana, Juliana H. C. ^[1] ; Souza, Daniele G. ^[6] ; Teixeira, Mauro Martins ^[3] ; Marques, Rafael Elias ^[1]

Affiliation

^[1] Brazilian Ctr Res Energy & Mat CNPEM, Brazilian Biosci Natl Lab LNBio, Campinas - Brazil

^[2] State Univ Campinas UNICAMP, Grad Program Genet & Mol Biol, Campinas - Brazil

^[3] Fed Univ Minas Gerais UFMG, Inst Biol Sci, Dept Biochem & Immunol, Immunopharmacol Lab, Belo Horizonte, MG - Brazil

^[4] Fed Univ Minas Gerais UFMG, Inst Biol Sci, Lab Neurofarmacol, Belo Horizonte, MG - Brazil

^[5] Fed Univ Minas Gerais UFMG, Inst Biol Sci, Lab Apoptose, Belo Horizonte, MG - Brazil

^[6] Fed Univ Minas Gerais UFMG, Inst Biol Sci, Lab Interacao Microrganismo Hospedeiro, Belo Horizonte, MG - Brazil

• Document type: Journal article
• Source: VIRULENCE; v. 12, n. 1, p. 244-259, JAN 1 2021.
• Web of Science Citations: 2

Abstract

St. Louis encephalitis virus (SLEV) is a neglected mosquito-borne flavivirus that causes severe neurological disease in humans. SLEV replication in the central nervous system (CNS) induces the local production of interferons (IFNs), which are attributed to host protection. The antiviral response to SLEV infection in the CNS is not completely understood, which led us to characterize the roles of IFNs using mouse models of St. Louis encephalitis. We infected mice deficient in type I IFN receptor (ABR(-/-)) or deficient in Type II IFN (IFN gamma(-/-)) and assessed the contribution of each pathway to disease development. We found that type I and II IFNs play different roles in SLEV infection. Deficiency in type I IFN signaling was associated to an early and increased mortality, uncontrolled SLEV replication and impaired ISG expression, leading to increased proinflammatory cytokine production and brain pathology. Conversely, IFN gamma(-/-) mice were moderately resistant to SLEV infection. IFN gamma deficiency caused no changes to viral load or SLEV-induced encephalitis and did not change the expression of ISGs in the brain. We found that type I IFN is essential for the control of SLEV replication whereas type II IFN was not associated with protection in this model. (AU)

• FAPESP's process: 18/03917-6 - Mechanisms of disease susceptibility and resistance in experimental Mayaro fever in mice
• Grantee: Rafael Elias Marques Pereira Silva
• Support Opportunities: Regular Research Grants
• FAPESP's process: 18/10990-1 - Characterization and therapeutic potential of chemokine action in sepsis and Flavivirus-induced encephalitis
• Grantee: Rafael Elias Marques Pereira Silva
• Support Opportunities: Regular Research Grants