A Major Epidemic of Chikungunya Virus Infection on Réunion Island, France, 2005–2006

Renault, Philippe; Solet, Jean-Louis; Sissoko, Daouda; Balleydier, Elsa; Larrieu, Sophie; Filleul, Laurent; Lassalle, Christian; Thiria, J.; Rachou, Emmanuelle; Valk, Henriette de; Ilèf, D.; Ledrans, Martine; Quatresous, I.; Quénel, Philippe; Pierre, V.

doi:10.4269/ajtmh.2007.77.727

Cited by 443 publications

(400 citation statements)

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“…In March 2005, CHIKV emerged for the first time in the southwestern Indian Ocean region in the Comoro Islands, probably introduced from Kenya, where the outbreak started in 2004. The CHIKV rapidly spread to other islands in the region, including Mayotte, the Seychelles, Mauritius and La Réunion, with a major outbreak responsible for at least 266,000 cases (1/3 of the population) from November 2005-June 2006 (Renault et al 2007). Usually considered to be a secondary vector, Ae.…”

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confidence: 99%

Failure to demonstrate experimental vertical transmission of the epidemic strain of Chikungunya virus in Aedes albopictus from La Réunion Island, Indian Ocean

Vazeille

Mousson

Failloux

2009

Mem. Inst. Oswaldo Cruz

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Aedes albopictus was responsible for transmission in the first outbreak of chikungunya (CHIK) on La Réunion Island, Indian Ocean, in 2005-2006. The magnitude of the outbreak on this island, which had been free of arboviral diseases for over 30 years, as well as the efficiency of Ae. albopictus as the main vector, raises questions about the maintenance of the CHIK virus (CHIKV) through vertical transmission mechanisms. Few specimens collected from the field as larvae were found to be infected. In this study, Ae. albopictus originating from La Réunion were orally infected with a blood-meal containing 10 8 pfu/mL of the CHIKV epidemic strain (CHIKV 06.21 Chikungunya virus (CHIKV) is a vector-borne alphavirus transmitted to humans by mosquitoes belonging to the genus Aedes. It was first isolated in 1953 in Tanzania (Ross 1956) and until recently outbreaks had only been observed in Africa, Asia and India. In Africa, CHIKV is maintained within a sylvatic cycle with wild mosquitoes as vectors (Jupp & Kemp 1996, Diallo et al. 1999. In Asia and India, a sylvatic cycle has never been demonstrated and CHIKV is mainly transmitted within an urban cycle primarily involving the human-biting Aedes aegypti and the less anthropophilic Aedes albopictus (Jupp & McIntosh 1988 (Salvan & Mouchet 1994). Interestingly, the sequencing of viral strains from La Réunion demonstrated the emergence of a mutation in the course of the outbreak and the mutation was detected in the majority of the viral population (Schuffenecker et al. 2006). This mutation was shown to be associated with a better transmission rate by Ae. albopictus (Tsetdatkin et al. 2007, Vazeille et al. 2007). Furthermore, viral particles could be detected in the salivary glands at day 2 post-infection and high densities of viral particles were observed in eggs at day 6 post-infection. This last observation raised con--infection. This last observation raised concerns of possible maintenance of the virus on the island through vertical transmission, a mechanism by which arboviruses can be maintained in nature when climate conditions are unfavourable to the activity of adults: infected females die but the virus can survive in their desiccated eggs. The frequency of this phenomenon is extremely variable depending on the mosquito species and the virus. Vertical transmission of CHIKV has not yet been demonstrated in the laboratory (Jupp et al. 1981, Mourya 1987, but has been proven to occur in the field in Ae. albopictus, in La Réunion (Delatte et al. 2008) and in Madagascar (Ratsitorahina et al. 2008). However, the transmission rate was low and only viral RNA was detected, with no virus isolated. Therefore, we attempted to demonstrate vertical transmission under laboratory conditions with Ae. albopictus from La Réunion and the epidemic viral strain in order to assess the potential risk of maintenance of CHIKV on the island. MATERIALS AND METHODS Mosquitoes 633± 1°C with 80% relative humidity and a 16:8 h photoperiod. Adults were given 10% sucrose solution and females fed on a mouse...

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Failure to demonstrate experimental vertical transmission of the epidemic strain of Chikungunya virus in Aedes albopictus from La Réunion Island, Indian Ocean

Vazeille

Mousson

Failloux

2009

Mem. Inst. Oswaldo Cruz

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“…Between 2000 and 2013, outbreaks or sporadic cases were reported in 2000 in the Democratic Republic of Congo [40], in 2006 in Cameroon [41], in Gabon [42] and in Guinea [43], in 2011 in the Republic of Congo [44] and in 2013 in Sierra Leone [45], while a recent study suggests endemic circulation of CHIKV in Tanzania [47]. The outbreaks in Grande Comore Island and Reunion were particularly massive, considering that they involved, respectively, 65 and 35 % of the total population of these islands [48,49]. Moreover in 2005, in reunion, the above mentioned mutation of ECSA occurred [8], and the new strain IOL caused important outbreaks in other continents.…”

Section: Epidemiology Of Chikv By Continentmentioning

confidence: 99%

Emergence and Surveillance of Chikungunya

et al. 2015

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Chikungunya virus (CHIKV), an arbovirus transmitted by Aedes mosquitoes, causes a disease characterised by fever, headache, skin rash, myalgias and severe arthralgias: the latter can persist for years. Following the first report in Africa in 1952, sporadic epidemics have been registered in Africa and in Asia before 2000. Since 2005, huge outbreaks have been reported, caused by globalisation (increasing displacement of humans and mosquitoes) and by an evolutionary success related to the adaptation of CHIKV to the mosquito vector: Therefore, CHIKV spread also in Europe, Oceania and the Americas. In endemic areas, seroprevalence studies could contribute to early detection of epidemics and to have a real picture of the burden of this disease. In temperate areas where Aedes aegypti and/or Aedes albopictus are present, CHIKV control measures require surveillance of imported and autochthonous cases, rapid diagnosis to detect local outbreaks and entomological surveillance.

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“…Alphaviruses are mosquito-borne plus-strandenveloped RNA viruses that cause both encephalomyelitis (Venezuelan, western and eastern equine encephalitis viruses) and arthritis (Sindbis, Ross River, and Chikungunya viruses). The encephalitic alphaviruses are endemic in the Americas, while the rapidly emerging arthritic alphaviruses that can also cause neurologic disease are now found worldwide [2,[4][5][6][7]. Currently, there are no treatments or vaccines licensed for these infections.…”

Section: Introductionmentioning

confidence: 99%

Alphavirus Encephalomyelitis: Mechanisms and Approaches to Prevention of Neuronal Damage

Griffin

2016

Neurotherapeutics

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Mosquito-borne viruses are important causes of death and long-term neurologic disability due to encephalomyelitis. Studies of mice infected with the alphavirus Sindbis virus have shown that outcome is dependent on the age and genetic background of the mouse and virulence of the infecting virus. Agedependent susceptibility reflects the acquisition by neurons of resistance to virus replication and virus-induced cell death with maturation. In mature mice, the populations of neurons most susceptible to infection are in the hippocampus and anterior horn of the spinal cord. Hippocampal infection leads to long-term memory deficits in mice that survive, while motor neuron infection can lead to paralysis and death. Neuronal death is immune-mediated, rather than a direct consequence of virus infection, and associated with entry and differentiation of pathogenic T helper 17 cells in the nervous system. To modulate glutamate excitotoxicity, mice were treated with an N-methyl-D-aspartate receptor antagonist, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor antagonists or a glutamine antagonist. The N-methyl-D-aspartate receptor antagonist MK-801 protected hippocampal neurons but not motor neurons, and mice still became paralyzed and died. α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor antagonists GYKI-52466 and talampanel protected both hippocampal and motor neurons and prevented paralysis and death. Glutamine antagonist 6-diazo-5-l-norleucine protected hippocampal neurons and improved memory generation in mice surviving infection with an avirulent virus. Surprisingly, in all cases protection was associated with inhibition of the antiviral immune response, reduced entry of inflammatory cells into the central nervous system, and delayed virus clearance, emphasizing the importance of treatment approaches that include prevention of immunopathologic damage.

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A Major Epidemic of Chikungunya Virus Infection on Réunion Island, France, 2005–2006

Cited by 443 publications

References 6 publications

Failure to demonstrate experimental vertical transmission of the epidemic strain of Chikungunya virus in Aedes albopictus from La Réunion Island, Indian Ocean

Failure to demonstrate experimental vertical transmission of the epidemic strain of Chikungunya virus in Aedes albopictus from La Réunion Island, Indian Ocean

Emergence and Surveillance of Chikungunya

Alphavirus Encephalomyelitis: Mechanisms and Approaches to Prevention of Neuronal Damage

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