Chikungunya virus assumes epidemic proportions

How the disease became an epidemic

Published: Friday 30 June 2006

a recent study has thrown light on how the chikungunya virus attained epidemic proportions in the Indian Ocean region since September 2005. A team of researchers at the Institut Pasteur in Paris, has spotted several changes in the genetic makeup of the little-known virus that may have helped it proliferate.

Over the past year, outbreaks of the disease have been reported from several islands, with the worst affected being Reunion Island (of France) where almost one-third of the population has been infected. In India, too, a large number of cases have been reported from several states, the maximum -- 155,000 -- being from Karnataka.

The scientists say the magnitude of the epidemic in the Indian Ocean and the description of new clinical forms of the disease highlight "the critical lack of understanding of the physiology of the disease and the biology of the virus". Chikungunya virus spreads to humans through mosquito bites. Symptoms include inflammation of the joints, fever, headache and a skin rash. No specific treatment is available. Most patients get better after a few days, but the pain in the joints can persist.


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For the study, the team led by Sylvain Brisse used viral strains isolated from six patients from Reunion Island and the Seychelles. First, they compared these strains with those collected during two earlier outbreaks in Tanzania (in 1953) and Senegal (in 1983). This helped ascertain major genetic mutations (changes) in the virus. To observe recent genetic changes, they selected three of the strains from early 2005 (before it became an epidemic) and three from 2005 end. This enabled them to compare the genetic makeup of the virus before and after the outbreak.

The study, reported in PLoS Medicine (Vol 3, No 7, July 2006), found that there were changes in several viral proteins. Most of the changes were present from the beginning of the outbreak, but others appeared halfway through it and just before the infection rates rose rapidly.

A recent change that stood out was in a protein called e 1, which helps the virus infect the cells of its mosquito and human hosts. The production of e 1 normally requires cholesterol, which the virus takes from its host. Low availability of cholesterol in mosquitoes prevents the virus from easily infecting their cells. But the change in e 1 appears to have lessened the dependence of the virus on cholesterol, allowing it to proliferate in mosquitoes and affect humans on an epidemic scale, the scientists suggest. A similar change was earlier seen to help a close relative of chikungunya virus to proliferate in mosquitoes.

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