Chikungunya virus with E1-A226V mutation causing two outbreaks in 2010, Guangdong, China

Wu, De; Zhang, Yonghui; ZhouHui, Qiong; Jing, Kou; Liang, Wenjia; Zhang, Huan; Monagin, Corina; Zhang, Qiao‐Li; Li, Wenjie; Zhong, Huan; He, Jianfeng; Li, Hui; Cai, Shumin; Ke, Changwen; Lin, Junyu

doi:10.1186/1743-422x-10-174

Cited by 32 publications

(25 citation statements)

References 24 publications

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“…All of these Laotian CHIKV strains were closely related to the CHIIKV strains that caused outbreaks in Cambodia, but not high bootstrap support values below 70 (Fig. 4) [18] and clustered together with other isolates from recent outbreaks in Asian countries (Thailand, Myanmar, China, Cambodia, Malaysia, Sri Lanka, and India) [18, 30, 34]. A high degree of sequence similarity between the Laotian and Cambodian strains and the fact that the Cambodian CHIKV outbreak occurred in 2011 where sharing borders with southern Laos and data from community survey [11], we suggested that CHIKV ECSA genotype is still endemic or is continuously reintroduced to the area and has invaded various regions of Laos.…”

Section: Discussionmentioning

confidence: 99%

Co-circulation of the dengue with chikungunya virus during the 2013 outbreak in the southern part of Lao PDR

et al. 2016

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BackgroundDuring the 2013 outbreak, 4638 infection cases and 32 deaths have been recorded in the southern part of Laos. In recent years, the chikungunya virus (CHIKV) emerged in the part of the country bordering Cambodia. Dengue virus (DENV) and CHIKV are transmitted by common mosquito vectors. Both diseases have similar clinical presentations; therefore, CHIKV infections might go undiagnosed in DENV-endemic areas. Thus, rapid detection and accurate diagnosis are crucial for differentiating between the two viruses (DENV and CHIKV). In this study, we demonstrated that CHIKV and two serotypes of DENV are circulating in Laos. In addition, we encountered patients that had been concurrently infected with multiple DENV serotypes or DENV and CHIKV.MethodsPlasma samples were collected from 40 patients with suspected DENV infections during an outbreak between July and August 2013. The reverse transcription polymerase chain reaction was performed to detect the four DENV serotypes and CHIKV using specific primers. Specifically, the complete envelope gene sequences of the viruses were sequenced and subjected to phylogenetic analysis.ResultsForty acute-phase plasma samples from patients with suspected dengue infections were tested for the presence of DENV viral RNA using molecular methods. Among the 40 samples, 14 samples were positive for DENV, 2 samples were positive for both viruses (DENV-2 and DENV-3), whereas DENV-1 and DENV-4 were not detected during the study period. We also encountered 10 samples that were positive for CHIKV. Of the 10 CHIKV-positive samples, 3 samples were co-infected by DENV-2, and 2 samples were co-infected by DENV-3. Phylogenetic analysis revealed that the 2013 dengue outbreak in Laos involved DENV-2 genotype Asian I and DENV-3 genotype II. Moreover, the Laotian CHIKV strains grouped together with those isolated during outbreaks on the Indian Ocean Islands within the East Central South African genotype.ConclusionsThese findings revealed that two serotypes (DENV-2 and DENV-3) and CHIKV were detected. Furthermore, infection of multiple DENV serotypes and CHIKV was also observed in the 2013 dengue outbreak. This is the first documented evidence of co-infection with CHIKV and one of two DENV serotypes.

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Section: Discussionmentioning

confidence: 99%

Co-circulation of the dengue with chikungunya virus during the 2013 outbreak in the southern part of Lao PDR

et al. 2016

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“…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).…”

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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

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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.

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“…, 26 This mutation was subsequently imported to Italy, and has since appeared in China and Papua New Guinea 2527 - 29 However, this mutation does not appear to dominate in the major chikungunya outbreaks that occurred in India 2006-2010 30…”

Section: Discussionmentioning

confidence: 99%

Assessing the Origin of and Potential for International Spread of Chikungunya Virus from the Caribbean

et al. 2014

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Background: For the first time, an outbreak of chikungunya has been reported in the Americas. Locally acquired infections have been confirmed in fourteen Caribbean countries and dependent territories, Guyana and French Guiana, in which a large number of North American travelers vacation. Should some travelers become infected with chikungunya virus, they could potentially introduce it into the United States, where there are competent Aedes mosquito vectors, with the possibility of local transmission. Methods: We analyzed historical data on airline travelers departing areas of the Caribbean and South America, where locally acquired cases of chikungunya have been confirmed as of May 12th, 2014. The final destinations of travelers departing these areas between May and July 2012 were determined and overlaid on maps of the reported distribution of Aedes aeygpti and albopictus mosquitoes in the United States, to identify potential areas at risk of autochthonous transmission. Results: The United States alone accounted for 52.1% of the final destinations of all international travelers departing chikungunya indigenous areas of the Caribbean between May and July 2012. Cities in the United States with the highest volume of air travelers were New York City, Miami and San Juan (Puerto Rico). Miami and San Juan were high travel-volume cities where Aedes aeygpti or albopictus are reported and where climatic conditions could be suitable for autochthonous transmission. Conclusion: The rapidly evolving outbreak of chikungunya in the Caribbean poses a growing risk to countries and areas linked by air travel, including the United States where competent Aedes mosquitoes exist. The risk of chikungunya importation into the United States may be elevated following key travel periods in the spring, when large numbers of North American travelers typically vacation in the Caribbean.

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Chikungunya virus with E1-A226V mutation causing two outbreaks in 2010, Guangdong, China

Cited by 32 publications

References 24 publications

Co-circulation of the dengue with chikungunya virus during the 2013 outbreak in the southern part of Lao PDR

Co-circulation of the dengue with chikungunya virus during the 2013 outbreak in the southern part of Lao PDR

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

Assessing the Origin of and Potential for International Spread of Chikungunya Virus from the Caribbean

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