Hundreds of tourists from South and South East Asia have been going home to the US, and Europe with Chikungunya virus. Quiescent for many years this mosquito-borne virus has reemerged in the last 2 years in India, South East Asia and Indian Ocean Islands. In the island of Réunion, the main industry, tourism has been badly hit after the virus infected as many as one in 3 inhabitants, according to reports.
Chikungunya infection is similar to dengue-debilitating but not usually deadly, the sufferer has fever, headache, fatigue, nausea, vomiting, muscle pain, rash, and joint pain. The lasting joint pain is characteristic of the disease and distinguishes it from dengue. The virus was first isolated in Tanzania during an epidemic of dengue-like disease in 1952-53. CAB Abstracts Archive has the abstracts of the reports of this epidemic. As for most viral diseases there isn’t a specific antiviral. A search of Global Health showed vaccine studies were begun but as yet there is no vaccine available (see continuation).
The current outbreak appears to stem from a new African strain which got into the mosquito vectors Aedes aegypti and albopictus that bite humans. US public health officials are concerned because these vectors are found in the southern states and so Chikungunya virus may gain a hold there as dengue has done. In Réunion there is evidence this strain could be more deadly than usual as over 200 deaths have been reported.
An Epidemic of Virus Disease in Southern Province, Tanganyika Territory, in 1952-53. II. General Description and Epidemiology.
LUMSDEN, W. H. R. / Trans. R. Soc. trop. Med. Hyg., 1955, Vol.49, No.1, pp.33-57 , 8 ref. In the first part of this paper, an account is given of the clinical features of a virus disease that occurred in epidemic form in the Southern Province of Tanganyika in 1952-53, and which appeared from these features to be dengue. This disease had not previously been recorded from the area. The following is based on the author’s summary of the second part. An epidemic of a dengue-like fever affected the Newala and Masasi Districts of Southern Province, Tanganyika, during 1952 and 1953. The topography, climate, water supply, vegetation and population of the area affected are described. The disease was most active on the Makonde Plateau in Newala District, but the surrounding lowlands were also affected. The plateau, lying at about 2, 000 ft. above sea level, is of sandstone, highly porous and practically devoid of surface water. The population, nevertheless, is dense and the people habitually store water in their houses, which are consequently infested with Aëdes aegypti (L.) and Culex pipiens fatigans [Culex quinquefasciatus] Wied. The first cases in the epidemic occurred on the south-eastern fringe of the plateau in July 1952. The densely populated south-western part became involved in September and thereafter spread was rapid. In January 1953, 49 of 62 localities were involved simultaneously. A rapid decline then set in. Incidence varied between 13 and 95 per cent. among 13 plateau localities and between 0 and 37 per cent. among eight lowland localities. In plateau localities in contact with woodland, the incidence in adults or adult males was significantly lower than in children. Escape from attack was most common among males over 45 years of age and was not associated with travel to coastal localities. It is assumed that these men were protected by some previous local experience not shared by the women and children. Once infection had been introduced into a house, all the inmates tended to be attacked. The results of catches of insects in houses are reported, and the methods by which laboratory animals were inoculated in attempts to isolate virus are described. Virus was isolated from all the mosquito groupings used (Anopheles spp., Aëdes aegypti and C. p. fatigans) and possibly also from Cimex hemipterus (F.). The occurrence of the various arthropods in the houses and their habits are discussed in relation to the disease incidence. The evidence points to A. aegypti as the vector. Other related entomological work is reported, and a complete list of the biting arthropods seen is given. The rise and spread of the epidemic is discussed. It is considered likely that the disease originated in the Rovuma Valley and was spread about the plateau by natives visiting between hut groups. The behaviour of A. aegypti is discussed in relation to the spread of the virus. Its habit of biting on the verandah of huts by day is considered important.
Phase II safety and immunogenicity study of live chikungunya virus vaccine TSI-GSD-218.
Edelman, R. , Tacket, C. O. , Wasserman, S. S. , Bodison, S. A. , Perry, J. G. , Mangiafico, J. A. / American Journal of Tropical Medicine and Hygiene, 2000, Vol.62, No.6, pp.681-685, 30 ref. We conducted a phase II, randomized, double blind, placebo-controlled, safety and immunogenicity study of a serially passaged plaque purified live chikungunya vaccine in 73 healthy adult volunteers from The University of Maryland, Baltimore, Maryland, USA. Fifty nine volunteers were immunized one time, subcutaneously, with the CHIK vaccine and 14 were immunized with placebo (tissue culture fluid). Vaccines were clinically evaluated intensively for one month and had repeated blood draws for serological assays (50% plaque reduction neutralization test) for one year. Except for transient arthralgia in five CHIK vaccinees, the number and severity of local and systaemic reactions and abnormal laboratory tests after immunization were similar in CHIK vaccinees and placebo recipients. Fifty-seven (98.3%) of 58 evaluable CHIK vaccinees developed CHIK neutralizing antibody by day 28; 85% of vaccinees remained seropositive at one year after immunization. No placebo recipients seroconverted. This promising live vaccine was safe, produced well tolerated side effects and was highly immunogenic. It is, therefore, a promising vaccine for use in alphavirus naive individuals.
Novel chikungunya virus variant in travellers returning from Indian Ocean islands.
Parola, P. , Lamballerie, X. de , Jourdan, J. , Rovery, C. , Vaillant, V. , Minodier, P. , Brouqui, P. , Flahault, A. , Raoult, D. , Charrel, R. N. Emerging Infectious Diseases, 2006, Vol. 12, No. 10, pp. 1493-1499, 37 Chikungunya virus (CHIKV) emerged in Indian Ocean islands in 2005 and is causing an ongoing outbreak that involves >260,000 patients, including travelers returning home from these islands. We investigated cases in 4 patients returning from Mayotte and Reunion Islands with CHIKV infection and a nurse infected in metropolitan France after direct contact with the blood of a traveler. Four patients had tenosynovitis and pain at wrist pressure, and 1 had life-threatening manifestations. Four CHIKV strains were isolated, including 1 from the patient with the autochthonous case. The complete genomic sequence identified a new CHIKV variant emerging from the East/central African evolutionary lineage. Aedes albopictus, the implicated vector of CHIKV in Indian Ocean islands, has dispersed worldwide in recent decades. High viral loads in patients returning from Indian Ocean islands to countries where Ae. albopictus is prevalent may be a source of epidemics.
Chikungunya outbreaks caused by African genotype, India.
Yergolkar, P. N. , Tandale, B. V. , Arankalle, V. A. , Sathe, P. S. , Sudeep, A. B. , Gandhe, S. S. , Gokhle, M. D. , Jacob, G. P. , Hundekar, S. L. , Mishra, A. C. / Emerging Infectious Diseases, 2006, Vol. 12, No. 10, pp. 1580-1583 Chikungunya fever is reported in India after 32 years. Immunoglobulin M antibodies and virus isolation confirmed the cause. Phylogenic analysis based on partial sequences of NS4 and E1 genes showed that all earlier isolates (1963-1973) were Asian genotype, whereas the current and Yawat (2000) isolates were African genotype.
Chikungunya virus strains, Reunion Island outbreak.
Bessaud, M. , Peyrefitte, C. N. , Pastorino, B. A. M. , Tock, F. , Merle, O. , Colpart, J. J. , Dehecq, J. S. , Girod, R. , Jaffar-Bandjee, M. C. , Glass, P. J. , Parker, M. , Tolou, H. J. , Grandadam, M. / Emerging Infectious Diseases, 2006, Vol.12, No.10, pp.1604-1606, 10 ref. An outbreak of Chikungunya fever in Reunion Island beginning during March 2005 is reported; however, the number of cases remained low until December of the same year when numbers shot up to >3500 confirmed and approx equal to 250000 suspected cases. Mortality reached >200 persons. Besides the common encephalitic form of the disease, previously unreported complications were also recorded, including vertical transmission, myocarditis, hepatitis and external dermal lesions. Serum samples from the patients incubated with C6/36 cells yielded the Chikungunya virus; the virus was also isolated from cerebrospinal fluid and cornea specimens, as well as from mosquitoes collected in the island (Aedes albopictus and Culex quinquefasciatus). The results of the sequence analysis of the CHIKV strains isolated indicated that the strains responsible for the outbreak have a common origin with those circulating in East and Central Africa.
Genome microevolution of chikungunya viruses causing the Indian Ocean outbreak.
Schuffenecker, I. , Iteman, I. , Michault, A. , Murri, S. , Frangeul, L. , Vaney, M. C. , Lavenir, R. , Pardigon, N. , Reynes, J. M. , Pettinelli, F. , Biscornet, L. , Diancourt, L. , Michel, S. , Duquerroy, S. , Guigon, G. , Frenkiel, M. P. , Bréhin, A. C. , Cubito, N. , Desprès, P. , Kunst, F. , Rey, F. A. , Zeller, H. , Brisse, S. / PLoS Medicine, 2006, Vol. 3, No. 7, pp. e263, 44 ref. Background: A chikungunya virus outbreak of unprecedented magnitude is currently ongoing in Indian Ocean territories. In Réunion Island, this alphavirus has already infected about one-third of the human population. The main clinical symptom of the disease is a painful and invalidating poly-arthralgia. Besides the arthralgic form, 123 patients with a confirmed chikungunya infection have developed severe clinical signs (neurological signs or fulminant hepatitis). Methods and Findings: This paper reports the nearly complete genome sequence of 6 selected viral isolates (isolated from 5 sera and one cerebrospinal fluid), along with partial sequences of the glycoprotein E1 from 127 patients in Réunion, Seychelles, Mauritius, Madagascar and Mayotte islands. The results indicated that the outbreak was initiated by a strain related to East-African isolates, from which viral variants have evolved following a traceable microevolution history. Unique molecular features of the outbreak isolates were identified. Notably, in the region coding for the non-structural proteins, 10 amino acid changes were found, 4 of which were located in alphavirus-conserved positions of nsP2 (which contains helicase, protease and RNA triphosphatase activities) and of the polymerase nsP4. The sole isolate obtained from the cerebrospinal fluid showed unique changes in nsP1 (T301I), nsP2 (Y642N) and nsP3 (E460 deletion), not obtained from isolates from sera. In the structural proteins region, 2 noteworthy changes (A226V and D284E) were observed in the membrane fusion glycoprotein E1. Homology 3D modelling allowed mapping of these 2 changes to regions important for membrane fusion and virion assembly. The E1-A226V was absent in the initial strains but was observed in >90% of subsequent viral sequences from Réunion, denoting evolutionary success possibly due to adaptation to the mosquito vector. Conclusions: The unique molecular features of the analysed Indian Ocean isolates of chikungunya virus demonstrate their high evolutionary potential and suggest possible clues for understanding the atypical magnitude and virulence of this outbreak.