Abstract
An unprecedented epidemic of chikungunya virus (CHIKV) infection recently started in countries of the Indian Ocean area, causing an acute and painful syndrome with strong fever, asthenia, skin rash, polyarthritis, and lethal cases of encephalitis. The basis for chikungunya disease and the tropism of CHIKV remain unknown. Here, we describe the replication characteristics of recent clinical CHIKV strains. Human epithelial and endothelial cells, primary fibroblasts and, to a lesser extent, monocyte-derived macrophages, were susceptible to infection and allowed viral production. In contrast, CHIKV did not replicate in lymphoid and monocytoid cell lines, primary lymphocytes and monocytes, or monocyte-derived dendritic cells. CHIKV replication was cytopathic and associated with an induction of apoptosis in infected cells. Chloroquine, bafilomycin-A1, and short hairpin RNAs against dynamin-2 inhibited viral production, indicating that viral entry occurs through pH-dependent endocytosis. CHIKV was highly sensitive to the antiviral activity of type I and II interferons. These results provide a general insight into the interaction between CHIKV and its mammalian host.
Highlights
Chikungunya virus (CHIKV), an alphavirus belonging to the Togaviridae family, was first isolated from a febrile individual in Tanzania in 1952 [1,2]
The most recent epidemic reemergences were documented in Kinshasa, (50,000 estimated cases in 1999–2000), in Indonesia (2001–2003), the Indian Ocean islands of Mayotte, Mauritius, Reunion, and the Seychelles (270,000 cases in 2005–2006 in La Reunion island), and in India (1.4 to 6.5 million estimated cases in 2006–2007)
We have studied the replication characteristics and the tropism of clinical chikungunya virus (CHIKV) strains from La Reunion
Summary
Chikungunya virus (CHIKV), an alphavirus belonging to the Togaviridae family, was first isolated from a febrile individual in Tanzania in 1952 [1,2]. CHIKV is transmitted to humans by several species of mosquitoes, with Aedes aegypti and A. albopictus being the two main vectors. The symptoms generally start 4–7 d after the bite. Acute infection lasts 1–10 d and is characterized by a painful polyarthralgia, high fever, asthenia, headache, vomiting, rash, and myalgia [2,3,4]. In Swahili, the term ‘‘chikungunya’’ means ‘‘the bent walker’’. In numerous patients, a chronic and incapacitating arthralgia persists for months. During the last 50 years, CHIKV has caused a number of outbreaks in East and South Africa and in Southeast Asia [5]. The most recent epidemic reemergences were documented in Kinshasa (50,000 estimated cases in 1999–2000) [6], Indonesia (2001–2003) [7], the Indian Ocean islands of Mayotte, Mauritius, Reunion, and the Seychelles (270,000 cases in 2005–2006 in La Reunion island) [5]), and India (1.4 to 6.5 million estimated cases in 2006–2007) [8,9,10]
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