AI Article Synopsis
- The Rocio virus (ROCV) caused a human encephalitis outbreak in Brazil during the 1970s, but its mechanisms are still not fully understood.
- Researchers discovered that the chemokine receptor CCR5 and its associated molecule MIP-1 α play significant roles in the severity of ROCV-induced encephalitis in mice.
- Knockout mice lacking CCR5 and MIP-1 α showed longer survival and less brain inflammation compared to wild-type mice, indicating that these molecules contribute to the migration of infected cells and influence the disease's progression after ROCV infection.
Article Abstract
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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820313 | PMC |
| http://dx.doi.org/10.4269/ajtmh.12-0591 | DOI Listing |
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