Displaying publications 1 - 20 of 89 in total

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  1. Das T, Jaffar-Bandjee MC, Hoarau JJ, Krejbich Trotot P, Denizot M, Lee-Pat-Yuen G, et al.
    Prog. Neurobiol., 2010 Jun;91(2):121-9.
    PMID: 20026374 DOI: 10.1016/j.pneurobio.2009.12.006
    Chikungunya virus (CHIKV) is transmitted by Aedes mosquitoes and causes an acute symptomatic illness with fever, skin rash, and incapacitating arthralgia, which can evolve into chronic rheumatoid arthritis in elderly patients. This is a tropical disease originally described in central/east Africa in the 1960s, but its 2004 re-emergence in Africa and rapid spread in lands in and around the Indian Ocean (Reunion island, India, Malaysia) as well as Europe (Italy) led to almost 6 million cases worldwide. The risk of importation and spreading diseases with long-term sequelae is even greater today given the global distribution of the vectors (including in the Americas), increased tourism and the apparent capacity of CHIKV to produce high levels of viremia (10(9)-10(12) virus/ml of blood) and new mutants. CHIKV-associated neuropathology was described early in the 1960s, but it is the unprecedented incidence rate in Indian Ocean areas with efficient clinical facilities that allowed a better description of cases with severe encephalitis, meningoencephalitis, peripheral neuropathies and deaths among newborns (mother-to-child infection), infants and elderly patients. Death rates following CHIKV infection were estimated at 1:1000 cases in la Reunion's outbreak. These clinical observations have been corroborated by experimental infection in several mouse models, leading to CNS pathologies. We further describe in this review the capacity of CHIKV to infect neurons and glial cells, delineate the fundamental innate (intrinsic) immune defence mechanisms to protect from infection and argue about the possible mechanisms involved in the encephalopathy.
    Matched MeSH terms: Chikungunya virus/pathogenicity*
  2. Tongco AMP, Rivera WL
    Trop Biomed, 2023 Jun 01;40(2):129-137.
    PMID: 37650398 DOI: 10.47665/tb.40.2.002
    Chikungunya virus (CHIKV) is a neglected tropical pathogen that causes fever and long-lasting severe arthralgia. Despite its high morbidity, there is still no licensed specific therapeutic option for it. This study proposes a multi-epitope subunit vaccine candidate for CHIKV, designed using computational methods. It was based on the E2 spike glycoprotein in CHIKV, from which T- and B-cell epitopes were predicted and then refined. The pan HLA DR-binding epitope (PADRE) was added to this refined construct, then simulated compared with the native protein, where it was predicted to elicit more than twice the number of antibody titers. Thus, this construct is potentially effective against CHIKV, which further experimentation using live models would be able to verify. This study also demonstrates the feasibility of using rational tools in the future to further optimize vaccine design.
    Matched MeSH terms: Chikungunya virus*
  3. Dass S, Ngui R, Gill BS, Chan YF, Wan Sulaiman WY, Lim YAL, et al.
    Trans R Soc Trop Med Hyg, 2021 08 02;115(8):922-931.
    PMID: 33783526 DOI: 10.1093/trstmh/trab053
    BACKGROUND: We studied the spatiotemporal spread of a chikungunya virus (CHIKV) outbreak in Sarawak state, Malaysia, during 2009-2010.

    METHODS: The residential addresses of 3054 notified CHIKV cases in 2009-2010 were georeferenced onto a base map of Sarawak with spatial data of rivers and roads using R software. The spatiotemporal spread was determined and clusters were detected using the space-time scan statistic with SaTScan.

    RESULTS: Overall CHIKV incidence was 127 per 100 000 population (range, 0-1125 within districts). The average speed of spread was 70.1 km/wk, with a peak of 228 cases/wk and the basic reproduction number (R0) was 3.1. The highest age-specific incidence rate was 228 per 100 000 in adults aged 50-54 y. Significantly more cases (79.4%) lived in rural areas compared with the general population (46.2%, p<0.0001). Five CHIKV clusters were detected. Likely spread was mostly by road, but a fifth of rural cases were spread by river travel.

    CONCLUSIONS: CHIKV initially spread quickly in rural areas mainly via roads, with lesser involvement of urban areas. Delayed spread occurred via river networks to more isolated areas in the rural interior. Understanding the patterns and timings of arboviral outbreak spread may allow targeted vector control measures at key transport hubs or in large transport vehicles.

    Matched MeSH terms: Chikungunya virus*
  4. Hapuarachchi HC, Bandara KB, Sumanadasa SD, Hapugoda MD, Lai YL, Lee KS, et al.
    J Gen Virol, 2010 Apr;91(Pt 4):1067-76.
    PMID: 19955565 DOI: 10.1099/vir.0.015743-0
    Chikungunya fever swept across many South and South-east Asian countries, following extensive outbreaks in the Indian Ocean Islands in 2005. However, molecular epidemiological data to explain the recent spread and evolution of Chikungunya virus (CHIKV) in the Asian region are still limited. This study describes the genetic Characteristics and evolutionary relationships of CHIKV strains that emerged in Sri Lanka and Singapore during 2006-2008. The viruses isolated in Singapore also included those imported from the Maldives (n=1), India (n=2) and Malaysia (n=31). All analysed strains belonged to the East, Central and South African (ECSA) lineage and were evolutionarily more related to Indian than to Indian Ocean Islands strains. Unique genetic characteristics revealed five genetically distinct subpopulations of CHIKV in Sri Lanka and Singapore, which were likely to have emerged through multiple, independent introductions. The evolutionary network based on E1 gene sequences indicated the acquisition of an alanine to valine 226 substitution (E1-A226V) by virus strains of the Indian sublineage as a key evolutionary event that contributed to the transmission and spatial distribution of CHIKV in the region. The E1-A226V substitution was found in 95.7 % (133/139) of analysed isolates in 2008, highlighting the widespread establishment of mutated CHIKV strains in Sri Lanka, Singapore and Malaysia. As the E1-A226V substitution is known to enhance the transmissibility of CHIKV by Aedes albopictus mosquitoes, this observation has important implications for the design of vector control strategies to fight the virus in regions at risk of chikungunya fever.
    Matched MeSH terms: Chikungunya virus/classification*; Chikungunya virus/genetics
  5. Soon YY, Junaidi I, Kumarasamy V, Chem YK, Juliana R, Chua KB
    Med J Malaysia, 2007 Aug;62(3):214-7.
    PMID: 18246910 MyJurnal
    Since its isolation in Tanzania in 1953, chikungunya virus has caused periodic outbreaks in both tropical Africa and Asia. In the last decade, the virus has shown not only increased activity but has expanded its geographical locations, thus classical delineation of various genotypes of chikungunya virus to specific geographic locales no longer holds true. Rapid mass movement of people and the constant presence of the right vectors in this region could have contributed to the change in virus ecology. This paper documents the first detection of chikungunya virus of Central/East genotype in Malaysia from a patient who was most likely infected with the virus during her visit to India. Without good Aedes vector measures, only time will tell whether this genotype rather than the existing endemic genotype will subsequently cause the next chikungunya outbreak in Malaysia.
    Matched MeSH terms: Chikungunya virus/genetics*; Chikungunya virus/isolation & purification
  6. Sam IC, Loong SK, Michael JC, Chua CL, Wan Sulaiman WY, Vythilingam I, et al.
    PLoS One, 2012;7(11):e50476.
    PMID: 23209750 DOI: 10.1371/journal.pone.0050476
    Mosquito-borne Chikungunya virus (CHIKV) has recently re-emerged globally. The epidemic East/Central/South African (ECSA) strains have spread for the first time to Asia, which previously only had endemic Asian strains. In Malaysia, the ECSA strain caused an extensive nationwide outbreak in 2008, while the Asian strains only caused limited outbreaks prior to this. To gain insight into these observed epidemiological differences, we compared genotypic and phenotypic characteristics of CHIKV of Asian and ECSA genotypes isolated in Malaysia.
    Matched MeSH terms: Chikungunya virus/classification; Chikungunya virus/genetics*
  7. Rougeron V, Sam IC, Caron M, Nkoghe D, Leroy E, Roques P
    J Clin Virol, 2015 Mar;64:144-52.
    PMID: 25453326 DOI: 10.1016/j.jcv.2014.08.032
    Chikungunya virus (CHIKV) is an alphavirus of the Togaviridae family that causes chronic and incapacitating arthralgia in human populations. Since its discovery in 1952, CHIKV was responsible for sporadic and infrequent outbreaks. However, since 2005, global Chikungunya outbreaks have occurred, inducing some fatalities and associated with severe and chronic morbidity. Chikungunya is thus considered as an important re-emerging public health problem in both tropical and temperate countries, where the distribution of the Aedes mosquito vectors continues to expand. This review highlights the most recent advances in our knowledge and understanding of the epidemiology, biology, treatment and vaccination strategies of CHIKV.
    Matched MeSH terms: Chikungunya virus/genetics; Chikungunya virus/pathogenicity; Chikungunya virus/physiology*
  8. Sam IC, Sulaiman AB
    Med J Malaysia, 2006 Jun;61(2):264-9.
    PMID: 16898330 MyJurnal
    Chikungunya virus (CHIKV) is a mosquito-borne alphavirus which causes epidemic fever, rash and polyarthralgia in Africa and Asia. Two outbreaks have been reported in Malaysia, in Klang, Selangor (1998) and Bagan Panchor, Perak (2006). It is not known if the outbreaks were caused by the recent introduction of CHIKV, or if the virus was already circulating in Malaysia. Seroprevalence studies from the 1960s suggested previous disease activity in certain parts of the country. In Asia, CHIKV is thought to be transmitted by the same mosquitoes as dengue, Aedes aegypti and Ae. albopictus. Due to similarities in clinical presentation with dengue, limited awareness, and a lack of laboratory diagnostic capability, CHIKV is probably often underdiagnosed or misdiagnosed as dengue. Treatment is supportive. The prognosis is generally good, although some patients experience chronic arthritis. With no vaccine or antiviral available, prevention and control depends on surveillance, early identification of outbreaks, and vector control. CHIKV should be borne in mind in sporadic cases, and in patients epidemiologically linked to ongoing local or international outbreaks or endemic areas.
    Matched MeSH terms: Chikungunya virus/genetics; Chikungunya virus/immunology; Chikungunya virus/isolation & purification*
  9. Ooi MK, Gan HM, Rohani A, Syed Hassan S
    Genome Announc, 2016;4(4).
    PMID: 27563048 DOI: 10.1128/genomeA.00876-16
    Here, we report the complete genome sequence of a chikungunya virus coinfection strain isolated from a dengue virus serotype 2-infected patient in Malaysia. This coinfection strain was determined to be of the Asian genotype and contains a novel insertion in the nsP3 gene.
    Matched MeSH terms: Chikungunya virus
  10. Yap ML, Klose T, Urakami A, Hasan SS, Akahata W, Rossmann MG
    Proc Natl Acad Sci U S A, 2017 12 26;114(52):13703-13707.
    PMID: 29203665 DOI: 10.1073/pnas.1713166114
    Cleavage of the alphavirus precursor glycoprotein p62 into the E2 and E3 glycoproteins before assembly with the nucleocapsid is the key to producing fusion-competent mature spikes on alphaviruses. Here we present a cryo-EM, 6.8-Å resolution structure of an "immature" Chikungunya virus in which the cleavage site has been mutated to inhibit proteolysis. The spikes in the immature virus have a larger radius and are less compact than in the mature virus. Furthermore, domains B on the E2 glycoproteins have less freedom of movement in the immature virus, keeping the fusion loops protected under domain B. In addition, the nucleocapsid of the immature virus is more compact than in the mature virus, protecting a conserved ribosome-binding site in the capsid protein from exposure. These differences suggest that the posttranslational processing of the spikes and nucleocapsid is necessary to produce infectious virus.
    Matched MeSH terms: Chikungunya virus/metabolism; Chikungunya virus/ultrastructure*; Chikungunya virus/chemistry*
  11. Wei Chiam C, Fun Chan Y, Chai Ong K, Thong Wong K, Sam IC
    J Gen Virol, 2015 Nov;96(11):3243-3254.
    PMID: 26276497 DOI: 10.1099/jgv.0.000263
    Chikungunya virus (CHIKV), an alphavirus of the family Togaviridae, causes fever, polyarthritis and rash. There are three genotypes: West African, Asian and East/Central/South African (ECSA). The latter two genotypes have caused global outbreaks in recent years. Recent ECSA CHIKV outbreaks have been associated with severe neurological disease, but it is not known if different CHIKV genotypes are associated with different neurovirulence. In this study, the neurovirulence of Asian (MY/06/37348) and ECSA (MY/08/065) strains of CHIKV isolated in Malaysia were compared. Intracerebral inoculation of either virus into suckling mice was followed by virus titration, histopathology and gene expression analysis of the harvested brains. Both strains of CHIKV replicated similarly, yet mice infected with MY/06/37348 showed higher mortality. Histopathology findings showed that both CHIKV strains spread within the brain (where CHIKV antigen was localized to astrocytes and neurons) and beyond to skeletal muscle. In MY/06/37348-infected mice, apoptosis, which is associated with neurovirulence in alphaviruses, was observed earlier in brains. Comparison of gene expression showed that a pro-apoptotic gene (eIF2αK2) was upregulated at higher levels in MY/06/37348-infected mice, while genes involved in anti-apoptosis (BIRC3), antiviral responses and central nervous system protection (including CD40, IL-10RA, MyD88 and PYCARD) were upregulated more highly in MY/08/065-infected mice. In conclusion, the higher mortality observed following MY/06/37348 infection in mice is due not to higher viral replication in the brain, but to differentially expressed genes involved in host immune responses. These findings may help to identify therapeutic strategies and biomarkers for neurological CHIKV infections.
    Matched MeSH terms: Chikungunya virus/classification; Chikungunya virus/genetics; Chikungunya virus/isolation & purification*; Chikungunya virus/pathogenicity*
  12. Nayar SK, Noridah O, Paranthaman V, Ranjit K, Norizah I, Chem YK, et al.
    Med J Malaysia, 2007 Oct;62(4):335-6.
    PMID: 18551940 MyJurnal
    During an outbreak of chikungunya in a dengue hyperendemic area within the Kinta district of Perak, two patients with acute febrile illness were laboratory confirmed to have co-infection of both dengue and chikungunya viruses in their blood. The concomitant presence of two types of viruses transmitted by the same vector in a susceptible population contributed to the resultant event. A good understanding of virus vector ecology in association with population dynamics and wider application of improved laboratory techniques by using different cell-lines suited for optimal replication of each type of virus and the correct utilization of powerful molecular techniques will enhance accurate diagnosis of these infectious diseases.
    Matched MeSH terms: Chikungunya virus*
  13. Ahmad NA, Vythilingam I, Lim YAL, Zabari NZAM, Lee HL
    Am J Trop Med Hyg, 2017 Jan 11;96(1):148-156.
    PMID: 27920393 DOI: 10.4269/ajtmh.16-0516
    Wolbachia-based vector control strategies have been proposed as a means to augment the currently existing measures for controlling dengue and chikungunya vectors. Prior to utilizing Wolbachia as a novel vector control strategy, it is crucial to understand the Wolbachia-mosquito interactions. In this study, field surveys were conducted to screen for the infection status of Wolbachia in field-collected Aedes albopictus The effects of Wolbachia in its native host toward the replication and dissemination of chikungunya virus (CHIKV) was also studied. The prevalence of Wolbachia-infected field-collected Ae. albopictus was estimated to be 98.6% (N = 142) for females and 95.1% (N = 102) for males in the population studied. The Ae. albopictus were naturally infected with both wAlbA and wAlbB strains. We also found that the native Wolbachia has no impact on CHIKV infection and minimal effect on CHIKV dissemination to secondary organs.
    Matched MeSH terms: Chikungunya virus/isolation & purification*
  14. Khor CS, Teoh BT, Sam SS, Khoo HY, Azizan NS, CheMatSeri A, et al.
    J Infect Dev Ctries, 2023 Jan 31;17(1):118-124.
    PMID: 36795935 DOI: 10.3855/jidc.16613
    INTRODUCTION: Chikungunya fever is a mosquito-borne viral disease that usually presents with prominent arthralgia. An outbreak of chikungunya fever was reported in Tanjung Sepat, Malaysia in 2019. The outbreak was limited in size with a low number of cases being reported. The present study sought to determine the possible variables that could have affected the transmission of the infection.

    METHODOLOGY: A cross-sectional study involving 149 healthy adult volunteers from Tanjung Sepat was performed soon after the outbreak had subsided. All the participants donated blood samples and completed the questionnaires. Laboratory detection of anti-CHIKV IgM and IgG antibodies was performed using enzyme-linked immunoassays (ELISA). Risk factors associated with chikungunya seropositivity were determined using logistic regression.

    RESULTS: The majority (72.5%, n = 108) of the study participants tested positive for CHIKV antibodies. Only 8.3% (n = 9) of the participants out of all the seropositive volunteers had an asymptomatic infection. Participants who resided with a febrile (p < 0.05, Exp(B) = 2.2, confidence interval [CI] 1.3-3.6) or a CHIKV-diagnosed person (p < 0.05, Exp(B) = 2.1, CI 1.2-3.6) in the same household were found likely to be tested positive for CHIKV antibodies.

    CONCLUSIONS: Findings from the study support that asymptomatic CHIKV infections and indoor transmission occurred during the outbreak. Hence, widespread community testing and indoor use of mosquito repellent are among the possible measures that can be implemented to reduce CHIKV transmission during an outbreak.

    Matched MeSH terms: Chikungunya virus*
  15. Thayan R, Yusof MA, Saat Z, Sekaran SD, Wang SM
    Methods Mol Biol, 2016;1426:11-9.
    PMID: 27233257 DOI: 10.1007/978-1-4939-3618-2_2
    Molecular surveillance of Chikungunya virus (CHIKV) is important as it provides data on the circulating CHIKV genotypes in endemic countries and enabling activation of measures to be taken in the event of a pending outbreak. Molecular surveillance is carried out by first detecting CHIKV in susceptible humans or among field-caught mosquitoes. This is followed by sequencing a selected region of the virus which will provide evidence on the source of the virus and possible association of the virus to increased cases of Chikungunya infections.
    Matched MeSH terms: Chikungunya virus/classification; Chikungunya virus/genetics*; Chikungunya virus/isolation & purification
  16. Wong HV, Chan YF, Sam IC, Sulaiman WY, Vythilingam I
    Methods Mol Biol, 2016;1426:119-28.
    PMID: 27233266 DOI: 10.1007/978-1-4939-3618-2_11
    In vivo infection of mosquitoes is an important method to study and characterize arthropod-borne viruses. Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that is transmitted primarily by Aedes mosquitoes. In this chapter, we describe a protocol for infection of CHIKV in two species of Aedes mosquitoes, Aedes aegypti and Aedes albopictus, together with the isolation of CHIKV in different parts of the infected mosquito such as midgut, legs, wings, salivary gland, head, and saliva. This allows the study of viral infection, replication and dissemination within the mosquito vector.
    Matched MeSH terms: Chikungunya virus/isolation & purification; Chikungunya virus/pathogenicity*; Chikungunya virus/physiology
  17. Tan KK, Sy AK, Tandoc AO, Khoo JJ, Sulaiman S, Chang LY, et al.
    Sci Rep, 2015 Jul 23;5:12279.
    PMID: 26201250 DOI: 10.1038/srep12279
    Outbreaks involving the Asian genotype Chikungunya virus (CHIKV) caused over one million infections in the Americas recently. The outbreak was preceded by a major nationwide outbreak in the Philippines. We examined the phylogenetic and phylogeographic relationships of representative CHIKV isolates obtained from the 2012 Philippines outbreak with other CHIKV isolates collected globally. Asian CHIKV isolated from the Philippines, China, Micronesia and Caribbean regions were found closely related, herein denoted as Cosmopolitan Asian CHIKV (CACV). Three adaptive amino acid substitutions in nsP3 (D483N), E1 (P397L) and E3 (Q19R) were identified among CACV. Acquisition of the nsP3-483N mutation in Compostela Valley followed by E1-397L/E3-19R in Laguna preceded the nationwide spread in the Philippines. The China isolates possessed two of the amino acid substitutions, nsP3-D483N and E1-P397L whereas the Micronesian and Caribbean CHIKV inherited all the three amino acid substitutions. The unique amino acid substitutions observed among the isolates suggest multiple independent virus dissemination events. The possible biological importance of the specific genetic signatures associated with the rapid global of the virus is not known and warrant future in-depth study and epidemiological follow-up. Molecular evidence, however, supports the Philippines outbreak as the possible origin of the CACV.
    Matched MeSH terms: Chikungunya virus/classification; Chikungunya virus/genetics*; Chikungunya virus/isolation & purification
  18. Sam IC, Kümmerer BM, Chan YF, Roques P, Drosten C, AbuBakar S
    Vector Borne Zoonotic Dis, 2015 Apr;15(4):223-30.
    PMID: 25897809 DOI: 10.1089/vbz.2014.1680
    Chikungunya virus (CHIKV) is an Aedes-borne alphavirus, historically found in Africa and Asia, where it caused sporadic outbreaks. In 2004, CHIKV reemerged in East Africa and spread globally to cause epidemics, including, for the first time, autochthonous transmission in Europe, the Middle East, and Oceania. The epidemic strains were of the East/Central/South African genotype. Strains of the Asian genotype of CHIKV continued to cause outbreaks in Asia and spread to Oceania and, in 2013, to the Americas. Acute disease, mainly comprising fever, rash, and arthralgia, was previously regarded as self-limiting; however, there is growing evidence of severe but rare manifestations, such as neurological disease. Furthermore, CHIKV appears to cause a significant burden of long-term morbidity due to persistent arthralgia. Diagnostic assays have advanced greatly in recent years, although there remains a need for simple, accurate, and affordable tests for the developing countries where CHIKV is most prevalent. This review focuses on recent important work on the epidemiology, clinical disease and diagnostics of CHIKV.
    Matched MeSH terms: Chikungunya virus/genetics; Chikungunya virus/immunology; Chikungunya virus/isolation & purification*
  19. Wong HV, Vythilingam I, Sulaiman WY, Lulla A, Merits A, Chan YF, et al.
    Am J Trop Med Hyg, 2016 Jan;94(1):182-6.
    PMID: 26598564 DOI: 10.4269/ajtmh.15-0318
    Vertical transmission may contribute to the maintenance of arthropod-borne viruses, but its existence in chikungunya virus (CHIKV) is unclear. Experimental vertical transmission of infectious clones of CHIKV in Aedes aegypti mosquitoes from Malaysia was investigated. Eggs and adult progeny from the second gonotrophic cycles of infected parental mosquitoes were tested. Using polymerase chain reaction (PCR), 56.3% of pooled eggs and 10% of adult progeny had detectable CHIKV RNA, but no samples had detectable infectious virus by plaque assay. Transfected CHIKV RNA from PCR-positive eggs did not yield infectious virus in BHK-21 cells. Thus, vertical transmission of viable CHIKV was not demonstrated. Noninfectious CHIKV RNA persists in eggs and progeny of infected Ae. aegypti, but the mechanism and significance are unknown. There is insufficient evidence to conclude that vertical transmission exists in CHIKV, as positive results reported in previous studies were almost exclusively based only on viral RNA detection.
    Matched MeSH terms: Chikungunya virus/genetics*; Chikungunya virus/isolation & purification*
  20. Apandi Y, Lau SK, Izmawati N, Amal NM, Faudzi Y, Mansor W, et al.
    PMID: 21329313
    Malaysia experienced its first outbreak of chikungunya virus (CHIKV) infection in late 1998 in Klang District in Selangor; six years later the virus re-emerged in the state of Perak. All the CHIKV isolates in 1988 and 2006 shared high sequence similarities and belonged to the Asian genotype. In 2007 and 2008 CHIKV infection again reemerged but the genotype was the Central/East African genotype. This strain was found to be similar to the strains causing outbreaks in the India Ocean. In 2009, the strains circulating in Malaysia, including the state of Kelantan, based on the partial E1 gene, also belong to the Central/East African genotype.
    Matched MeSH terms: Chikungunya virus/classification*; Chikungunya virus/isolation & purification*
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