Chikungunya Virus Infection, Brazzaville, Republic of Congo, 2011

Mombouli, Jean-Vivien; Bitsindou, P; Elion, Darrel O.A.; Grolla, Allen; Feldmann, Heinz; Niama, Fabien Roch; Parra, Henri‐Joseph; Munster, Vincent J.

doi:10.3201/eid1909.130451

Cited by 44 publications

(32 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Subsequently, the CHIKV IOL was introduced to India [ 17 , 18 ] and the surrounding islands, Sri Lanka [ 19 ] and the Maldives. In Africa, the CHIKV E1-226V variant was also implicated outbreaks in Cameroon [ 20 ], Gabon [ 21 , 22 ] and Congo [ 23 ]. This variant also caused the first European CHIKV outbreak in Italy in 2007 [ 24 ].…”

Section: Chikungunya Infection and Vector Life History Traitsmentioning

confidence: 99%

Chikungunya Virus–Vector Interactions

Coffey

Failloux

Weaver

2014

Viruses

140

129

View full text Add to dashboard Cite

Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that causes chikungunya fever, a severe, debilitating disease that often produces chronic arthralgia. Since 2004, CHIKV has emerged in Africa, Indian Ocean islands, Asia, Europe, and the Americas, causing millions of human infections. Central to understanding CHIKV emergence is knowledge of the natural ecology of transmission and vector infection dynamics. This review presents current understanding of CHIKV infection dynamics in mosquito vectors and its relationship to human disease emergence. The following topics are reviewed: CHIKV infection and vector life history traits including transmission cycles, genetic origins, distribution, emergence and spread, dispersal, vector competence, vector immunity and microbial interactions, and co-infection by CHIKV and other arboviruses. The genetics of vector susceptibility and host range changes, population heterogeneity and selection for the fittest viral genomes, dual host cycling and its impact on CHIKV adaptation, viral bottlenecks and intrahost diversity, and adaptive constraints on CHIKV evolution are also discussed. The potential for CHIKV re-emergence and expansion into new areas and prospects for prevention via vector control are also briefly reviewed.

show abstract

Section: Chikungunya Infection and Vector Life History Traitsmentioning

confidence: 99%

Chikungunya Virus–Vector Interactions

Coffey

Failloux

Weaver

2014

Viruses

140

129

View full text Add to dashboard Cite

show abstract

“…According to the World Health Organisation (WHO), as of July 26 th , a total of 11,083 suspected cases had been reported, of which 91% (10,066/11,083) originated from the Department of Brazzaville and 9% (1,117/11,083) from the Department of Pool (located in the south of the Republic of Congo). The most affected area in Brazzaville was the district of Makélékélé, which accounted for 65.7% of the total number of reported cases (7,279 cases) [16] , [17] .…”

Section: Introductionmentioning

confidence: 99%

First Reported Chikungunya Fever Outbreak in the Republic of Congo, 2011

et al. 2014

Self Cite

View full text Add to dashboard Cite

BackgroundChikungunya is an Aedes -borne disease characterised by febrile arthralgia and responsible for massive outbreaks. We present a prospective clinical cohort study and a retrospective serological study relating to a CHIK outbreak, in the Republic of Congo in 2011.Methodology and FindingsWe analysed 317 suspected cases, of which 308 (97.2%) lived in the city of Brazzaville (66.6% in the South area). Amongst them, 37 (11.7%) were CHIKV+ve patients (i.e., biologically confirmed by a real-time RT-PCR assay), of whom 36 (97.3%) had fever, 22 (66.7%) myalgia and 32 (86.5%) arthralgia. All tested negative for dengue. The distribution of incident cases within Brazzaville districts was compared with CHIKV seroprevalence before the outbreak (34.4% in 517 blood donors), providing evidence for previous circulation of CHIKV. We applied a CHIK clinical score to 126 patients recruited within the two first day of illness (including 28 CHIKV+ves (22.2%)) with sensitivity (78.6%) and specificity (72.4%) values comparing with those of the referent study in Reunion Island. The negative predictive value was high (92%), but the positive predictive value (45%) indicate poor potential contribution to medical practice to identify CHIKV+ve patients in low prevalence outbreaks. However, the score allowed a slightly more accurate follow-up of the evolution of the outbreak than the criterion "fever+arthralgia". The complete sequencing of a Congolase isolate (Brazza_MRS1) demonstrated belonging to the East/Central/South African lineage and was further used for producing a robust genome-scale CHIKV phylogenetic analysis.Conclusions/SignificanceWe describe the first Chikungunya outbreak declared in the Republic of Congo. The seroprevalence study conducted amongst blood donors before outbreak provided evidence for previous CHIKV circulation. We suggest that a more systematic survey of the entomological situation and of arbovirus circulation is necessary in Central Africa for better understanding the environmental, microbiological and sociological determinants of emergence.

show abstract

“…CHIKV caused an explosive outbreak of disease beginning in 2004 that expanded to areas beyond the historical range of the virus, including Europe and many islands in the Indian Ocean (1,2,13), and produced more-severe illness than previously observed (14)(15)(16)(17). CHIKV continues to spread to new regions (18)(19)(20)(21)(22), and currently there are no available vaccines or treatments for this disease (23).…”

mentioning

confidence: 99%

A Single-Amino-Acid Polymorphism in Chikungunya Virus E2 Glycoprotein Influences Glycosaminoglycan Utilization

Silva

Khomandiak

Ashbrook

et al. 2014

J Virol

115

140

View full text Add to dashboard Cite

Chikungunya virus (CHIKV) is a reemerging arbovirus responsible for outbreaks of infection throughout Asia and Africa, causing an acute illness characterized by fever, rash, and polyarthralgia. Although CHIKV infects a broad range of host cells, little is known about how CHIKV binds and gains access to the target cell interior. In this study, we tested whether glycosaminoglycan (GAG) binding is required for efficient CHIKV replication using CHIKV vaccine strain 181/25 and clinical isolate SL15649. Preincubation of strain 181/25, but not SL15649, with soluble GAGs resulted in dose-dependent inhibition of infection. While parental Chinese hamster ovary (CHO) cells are permissive for both strains, neither strain efficiently bound to or infected mutant CHO cells devoid of GAG expression. Although GAGs appear to be required for efficient binding of both strains, they exhibit differential requirements for GAGs, as SL15649 readily infected cells that express excess chondroitin sulfate but that are devoid of heparan sulfate, whereas 181/25 did not. We generated a panel of 181/25 and SL15649 variants containing reciprocal amino acid substitutions at positions 82 and 318 in the E2 glycoprotein. Reciprocal exchange at residue 82 resulted in a phenotype switch; Gly 82 results in efficient infection of mutant CHO cells but a decrease in heparin binding, whereas Arg 82 results in reduced infectivity of mutant cells and an increase in heparin binding. These results suggest that E2 residue 82 is a primary determinant of GAG utilization, which likely mediates attenuation of vaccine strain 181/25. IMPORTANCE Chikungunya virus (CHIKV) infection causes a debilitating rheumatic disease that can persist for months to years, and yet there are no licensed vaccines or antiviral therapies. Like other alphaviruses, CHIKV displays broad tissue tropism, which is thought to be influenced by virus-receptor interactions. In this study, we determined that cell-surface glycosaminoglycans are utilized by both a vaccine strain and a clinical isolate of CHIKV to mediate virus binding. We also identified an amino acid polymorphism in the viral E2 attachment protein that influences utilization of glycosaminoglycans. These data enhance an understanding of the viral and host determinants of CHIKV cell entry, which may foster development of new antivirals that act by blocking this key step in viral infection.

show abstract

Chikungunya Virus Infection, Brazzaville, Republic of Congo, 2011

Cited by 44 publications

References 10 publications

Chikungunya Virus–Vector Interactions

Chikungunya Virus–Vector Interactions

First Reported Chikungunya Fever Outbreak in the Republic of Congo, 2011

A Single-Amino-Acid Polymorphism in Chikungunya Virus E2 Glycoprotein Influences Glycosaminoglycan Utilization

Contact Info

Product

Resources

About