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How did chikungunya reach the Indian Ocean?
Newsdesk
How did chikungunya reach the Indian Ocean? distant islands—Réunion, Seychelles, Mauritius, Madagascar, and Mayotte. Réunion, where the infection has been exhaustively documented, appears to be the worst-affected island, although Pialoux suspects some islands have played down the outbreak for fear of an adverse impact on tourism. “In Africa”, explains Ernest Gould (Centre for Hydrology and Ecology, Oxford, UK), “CHIKV has a forest reservoir in wild primates and their mosquitoes but breaks away sporadically to cause local epidemics”. The virus also appears in tropical Asia, where it is maintained in an urban human-mosquito-human cycle, typically with Ae aegypti mosquito vectors. But Ae aegypti is rare in Réunion, and the vector there is “undoubtedly” Ae albopictus, according to Paul Reiter (Institut Pasteur, Paris, France). So far CHIKV has not been isolated from Ae albopictus, a species of Asian origin now abundant in Réunion. “Ae albopictus has been incriminated, but there’s no proof yet”, Reiter adds. Gould thinks mosquitoes could have multiplied by laying their eggs in the pools of water that form in discarded tyres. “Used car tyres are transported globally in their millions, and it is recognised that Ae albopictus is particularly adept at exploiting this method of dispersal and amplification.” “Modern transportation makes viruses very mobile”, says Reiter, who
Bob Edme/AP/Empics
The epidemic of chikungunya* that has swept through the idyllic islands of the Indian Ocean is now, thankfully, in decline. In Réunion, where a third of the 775 000 population have been infected since the virus appeared there in March 2005, the weekly number of cases fell from a peak of 25 000 in early February 2006 to 130 in the last week of July. Although chikungunya, a tropical arboviral disease transmitted by Aedes mosquitoes, crops up from time to time in Africa—where it was first identified in 1953—it has never before been seen in the islands of the midIndian Ocean. So how did the virus (CHIKV) get there? The answer seems to be a mixture of human activities, a non-immune population, and, possibly, virus adaptation. The main clinical features of chikungunya are fever, headache, rash, and debilitating arthralgia. Until the current epidemic, says Gilles Pialoux (Hôpital Tenon, Paris, France), no deaths had been reported, “but the 237 deaths in Réunion and the appearance of severe forms of the disease, including CNS involvement and fulminant hepatitis, have taken everyone by surprise, as has the unprecedented size of the epidemic.” The epidemic started with outbreaks in Kenya in 2004 and the Comoros Islands early in 2005. CHIKV was not new to these regions. But then it struck virgin territory in the more
A worker sprays a chemical product in a bid to eradicate mosquitoes in Panianyn, Réunion
http://infection.thelancet.com Vol 6 September 2006
is “absolutely certain” that air travellers brought CHIKV to the islands. Infected tourists are now turning up in Europe too. “If they develop viraemia during or after their return home, they could present a potential threat of outbreaks in parts of Europe where Ae albopictus circulates, such as Italy, the southern coast of France, and Spain,” warns Stephen Higgs (University of Texas, Galveston, TX, USA). The Indian Ocean strains were initially closely related to each other and to east African strains. But the virus has evolved since then, and French scientists have identified a mutation that might have improved the virus’ ability to invade mosquito cells and replicate. The mutation (E1-A226V) was absent in the initial strains but was later found in over 90% of viral sequences from Réunion. The team speculate that the mutation may have enhanced the ability of the virus to reproduce in insect cells that are naturally low in cholesterol. Non-mutated virus needs cholesterol to infect the cells of its mosquito and human hosts. Has the virus also acquired a higher neurovirulence? This could explain the unusually severe cases. Higgs is cautious of the “cholesterol” hypothesis: “Until it can be tested we can’t really attribute the scale of the epidemic to this one factor”. It could simply be, he says, that the virus was introduced into a region where the people were highly susceptible, and without effective mosquito control there was nothing to stop it. “Given that resources for vector control and appropriate expertise have declined in many areas of the world, alas we may be seeing such epidemics more often.” Although the epidemic is now declining, Higgs warns that the islands might not have seen the last of CHIKV—a similar pattern of decline was seen last year before a resurgence of cases in February 2006.
*The name chikungunya comes from the Makonde language of Tanzania and Mozambique, not from Swahili, as is often said. For more information see http://www.answers.com For more information about the evolution of CHIKV see PLoS Med 2006; 3: 1058–70.
Dorothy Bonn 543
How did chikungunya reach the Indian Ocean? distant islands—Réunion, Seychelles, Mauritius, Madagascar, and Mayotte. Réunion, where the infection has been exhaustively documented, appears to be the worst-affected island, although Pialoux suspects some islands have played down the outbreak for fear of an adverse impact on tourism. “In Africa”, explains Ernest Gould (Centre for Hydrology and Ecology, Oxford, UK), “CHIKV has a forest reservoir in wild primates and their mosquitoes but breaks away sporadically to cause local epidemics”. The virus also appears in tropical Asia, where it is maintained in an urban human-mosquito-human cycle, typically with Ae aegypti mosquito vectors. But Ae aegypti is rare in Réunion, and the vector there is “undoubtedly” Ae albopictus, according to Paul Reiter (Institut Pasteur, Paris, France). So far CHIKV has not been isolated from Ae albopictus, a species of Asian origin now abundant in Réunion. “Ae albopictus has been incriminated, but there’s no proof yet”, Reiter adds. Gould thinks mosquitoes could have multiplied by laying their eggs in the pools of water that form in discarded tyres. “Used car tyres are transported globally in their millions, and it is recognised that Ae albopictus is particularly adept at exploiting this method of dispersal and amplification.” “Modern transportation makes viruses very mobile”, says Reiter, who
Bob Edme/AP/Empics
The epidemic of chikungunya* that has swept through the idyllic islands of the Indian Ocean is now, thankfully, in decline. In Réunion, where a third of the 775 000 population have been infected since the virus appeared there in March 2005, the weekly number of cases fell from a peak of 25 000 in early February 2006 to 130 in the last week of July. Although chikungunya, a tropical arboviral disease transmitted by Aedes mosquitoes, crops up from time to time in Africa—where it was first identified in 1953—it has never before been seen in the islands of the midIndian Ocean. So how did the virus (CHIKV) get there? The answer seems to be a mixture of human activities, a non-immune population, and, possibly, virus adaptation. The main clinical features of chikungunya are fever, headache, rash, and debilitating arthralgia. Until the current epidemic, says Gilles Pialoux (Hôpital Tenon, Paris, France), no deaths had been reported, “but the 237 deaths in Réunion and the appearance of severe forms of the disease, including CNS involvement and fulminant hepatitis, have taken everyone by surprise, as has the unprecedented size of the epidemic.” The epidemic started with outbreaks in Kenya in 2004 and the Comoros Islands early in 2005. CHIKV was not new to these regions. But then it struck virgin territory in the more
A worker sprays a chemical product in a bid to eradicate mosquitoes in Panianyn, Réunion
http://infection.thelancet.com Vol 6 September 2006
is “absolutely certain” that air travellers brought CHIKV to the islands. Infected tourists are now turning up in Europe too. “If they develop viraemia during or after their return home, they could present a potential threat of outbreaks in parts of Europe where Ae albopictus circulates, such as Italy, the southern coast of France, and Spain,” warns Stephen Higgs (University of Texas, Galveston, TX, USA). The Indian Ocean strains were initially closely related to each other and to east African strains. But the virus has evolved since then, and French scientists have identified a mutation that might have improved the virus’ ability to invade mosquito cells and replicate. The mutation (E1-A226V) was absent in the initial strains but was later found in over 90% of viral sequences from Réunion. The team speculate that the mutation may have enhanced the ability of the virus to reproduce in insect cells that are naturally low in cholesterol. Non-mutated virus needs cholesterol to infect the cells of its mosquito and human hosts. Has the virus also acquired a higher neurovirulence? This could explain the unusually severe cases. Higgs is cautious of the “cholesterol” hypothesis: “Until it can be tested we can’t really attribute the scale of the epidemic to this one factor”. It could simply be, he says, that the virus was introduced into a region where the people were highly susceptible, and without effective mosquito control there was nothing to stop it. “Given that resources for vector control and appropriate expertise have declined in many areas of the world, alas we may be seeing such epidemics more often.” Although the epidemic is now declining, Higgs warns that the islands might not have seen the last of CHIKV—a similar pattern of decline was seen last year before a resurgence of cases in February 2006.
*The name chikungunya comes from the Makonde language of Tanzania and Mozambique, not from Swahili, as is often said. For more information see http://www.answers.com For more information about the evolution of CHIKV see PLoS Med 2006; 3: 1058–70.
Dorothy Bonn 543