Journal
PROGRESS IN NEUROBIOLOGY
Volume 91, Issue 2, Pages 121-129Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2009.12.006
Keywords
Alphavirus; Neuroinfection; Innate immunity; Neurodegeneration
Categories
Funding
- University of La Reunion
- French Ministry of Health [PRHC 2006-2009]
- French overseas Ministry (MOM)
- CRVOI (centre de recherche et de veille de l'Ocean Indien)
- Regional council of La Reunion
- Europe (CPER/FEDER/GRII)
- University of La Reunion
- French Ministry of Health [PRHC 2006-2009]
- French overseas Ministry (MOM)
- CRVOI (centre de recherche et de veille de l'Ocean Indien)
- Regional council of La Reunion
- Europe (CPER/FEDER/GRII)
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Chikungunya virus (CHIN) is transmitted by Aedes mosquitoes and causes an acute symptomatic illness with fever, skin rash, and incapacitating arthralgia, which can evolve into chronic rheumatoid arthritis in elderly patients. This is a tropical disease originally described in central/east Africa in the 1960s, but its 2004 re-emergence in Africa and rapid spread in lands in and around the Indian Ocean (Reunion island, India, Malaysia) as well as Europe (Italy) led to almost 6 million cases worldwide. The risk of importation and spreading diseases with long-term sequelae is even greater today given the global distribution of the vectors (including in the Americas), increased tourism and the apparent capacity of CHIKV to produce high levels of viremia (10(9)-10(12) virus/ml of blood) and new mutants. CHIKV-associated neuropathology was described early in the 1960s, but it is the unprecedented incidence rate in Indian Ocean areas with efficient clinical facilities that allowed a better description of cases with severe encephalitis, meningoencephalitis, peripheral neuropathies and deaths among newborns (mother-to-child infection), infants and elderly patients. Death rates following CHIKV infection were estimated at 1:1000 cases in la Reunion's outbreak. These clinical observations have been corroborated by experimental infection in several mouse models, leading to CNS pathologies. We further describe in this review the capacity of CHIN to infect neurons and glial cells, delineate the fundamental innate (intrinsic) immune defence mechanisms to protect from infection and argue about the possible mechanisms involved in the encephalopathy. (C) 2010 Elsevier Ltd. All rights reserved.
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