Abstract
Chikungunya virus (CHIKV) is a re-emerging pathogen of global importance. We attempted to gain an insight into the organisation, distribution and mutational load of the virus strains reported from different parts of the world. We describe transmission dynamics and genetic characterisation of CHIKV across the globe during the last 65 years from 1952 to 2017. The evolutionary pattern of CHIKV was analysed using the E1 protein gene through phylogenetic, Bayesian and Network methods with a dataset of 265 sequences from various countries. The time to most recent common ancestor of the virus was estimated to be 491 years ago with an evolutionary rate of 2.78 × 10-4 substitutions/site/year. Genetic characterisation of CHIKV strains was carried out in terms of variable sites, selection pressure and epitope mapping. The neutral selection pressure on the E1 gene of the virus suggested a stochastic process of evolution. We identified six potential epitope peptides in the E1 protein showing substantial interaction with human MHC-I and MHC-II alleles. The present study augments global epidemiological and population dynamics of CHIKV warranting undertaking of appropriate control measures. The identification of epitopic peptides can be useful in the development of epitope-based vaccine strategies against this re-emerging viral pathogen.
Highlights
Chikungunya fever is caused by Chikungunya virus (CHIKV), an arboviral pathogen that has caused numerous outbreaks across the globe
CHIKV consists of three separate clades namely (i) The ‘West African’, (ii) ‘Asian’ and (iii) ‘East Central South African’ (ECSA) [3]
We evaluated the transmission dynamics of the CHIKV across the globe using phylogenetic, Network and Bayesian analysis focusing on all the three genotypes comprising West African, Asia and ECSA
Summary
Chikungunya fever is caused by Chikungunya virus (CHIKV), an arboviral pathogen that has caused numerous outbreaks across the globe. Increased global travel from CHIKV endemic regions has been the major cause of dispersal of the virus to non-endemic regions of the Americas and Europe. The genomic analyses of CHIKV sequences reported from India during the 2009–2010 outbreak revealed mutations in the structural and non-structural regions that contribute to the adaptations of the virus to locally available vector populations [7, 8]. The virus has caused many epidemics with the co-circulation of ECSA (East Central and South African) and Asian genotypes, affecting millions of people [9, 10]. The re-emergence of this virus is probably due to mutational changes, increased efficiency of vector transmission, immunologically naive populations, enhanced global dissemination, inadequate public health infrastructure, unforeseen environmental and social factors [11]
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