ArticleThe American journal of tropical medicine and hygiene2013
Influence of the CCR-5/MIP-1 α axis in the pathogenesis of Rocio virus encephalitis in a mouse model.
Article in The American journal of tropical medicine and hygiene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- A Pocket Guide to CCR5-Neurotropic Flavivirus Edition.Viruses · 2023Review
- Novel small synthetic HIV-1 V3 crown variants: CCR5 targeting ligands.Journal of biochemistry · 2022Article
- Article
- Rocio Virus: An Updated View on an Elusive Flavivirus.Viruses · 2021Review
- CCR5Δ32 in Brazil: Impacts of a European Genetic Variant on a Highly Admixed Population.Frontiers in immunology · 2021Review
- Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.Virus research · 2020Review
- Historical Perspective and Biotechnological Trends to Block Arboviruses Transmission by ControllingFrontiers in medicine · 2020Review
- IL-33 signaling is essential to attenuate viral-induced encephalitis development by downregulating iNOS expression in the central nervous system.Journal of neuroinflammation · 2016Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
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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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