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Influence of the CCR-5/MIP-1 α Axis in the Pathogenesis of Rocio Virus Encephalitis in a Mouse Model

2013; American Society of Tropical Medicine and Hygiene; Volume: 89; Issue: 5 Linguagem: Inglês

10.4269/ajtmh.12-0591

1476-1645

Juliana Helena Chávez, Rafael Freitas de Oliveira França, Carlo José Freire Oliveira, Maria Teresa P. de Aquino, Kléber Juvenal Silva Farias, Paula Renata Lima Machado, Thelma Fátima Mattos Oliveira, Jonny Yokosawa, Edson García Soares, João S. Silva, Benedito Antônio Lopes da Fonseca, Luíz Tadeu Moraes Figueiredo,

interferon and immune responses

Rocio virus (ROCV) caused an outbreak of human encephalitis during the 1970s in Brazil and its immunopathogenesis remains poorly understood. CC-chemokine receptor 5 (CCR5) is a chemokine receptor that binds to macrophage inflammatory protein (MIP-1 α). Both molecules are associated with inflammatory cells migration during infections. In this study, we demonstrated the importance of the CCR5 and MIP-1 α, in the outcome of viral encephalitis of ROCV-infected mice. CCR5 and MIP-1 α knockout mice survived longer than wild-type (WT) ROCV-infected animals. In addition, knockout mice had reduced inflammation in the brain. Assessment of brain viral load showed mice virus detection five days post-infection in wild-type and CCR5-/- mice, while MIP-1 α-/- mice had lower viral loads seven days post-infection. Knockout mice required a higher lethal dose than wild-type mice as well. The CCR5/MIP-1 α axis may contribute to migration of infected cells to the brain and consequently affect the pathogenesis during ROCV infection.