Persistence of chikungunya ECSA genotype and local outbreak in an upper medium class neighborhood in Northeast Brazil.
Goes de Jesus J., da Luz Wallau G., Lima Maia M., Xavier J., Oliveira Lima MA., Fonseca V., Salgado de Abreu A., Fraga de Oliveira Tosta S., Ramos do Amaral H., Andrade Barbosa Lima I., Viana Silva P., Carlos Dos Santos D., Sousa de Oliveira A., Campos de Souza S., Barreto Falcão M., Cerqueira E., Ceschini Machado L., Sobral MC., Teodoro Rezende TM., Ribeiro Pereira M., Mota Pereira F., Pereira Gusmão Maia Z., Freitas de Oliveira França R., Luiz de Abreu A., Campelo de Albuquerque E Melo CF., Rodrigues Faria N., Venâncio da Cunha R., Giovanetti M., Alcantara LCJ.
The chikungunya East/Central/South/Africa virus lineage (CHIKV-ECSA) was first detected in Brazil in the municipality of Feira de Santana (FS) by mid 2014. Following that, a large number of CHIKV cases have been notified in FS, which is the second-most populous city in Bahia state, northeastern Brazil, and plays an important role on the spread to other Brazilian states due to climate conditions and the abundance of competent vectors. To better understand CHIKV dynamics in Bahia state, we generated 5 complete genome sequences from a local outbreak raised in Serraria Brasil, a neighbourhood in FS, by next-generation sequencing using Illumina approach. Phylogenetic reconstructions revealed that the new FS genomes belongs to the ECSA genotype and falls within a single strongly supported monophyletic clade that includes other older CHIKV sequences from the same location, suggesting the persistence of the virus during distinct epidemic seasons. We also performed minor variants analysis and found a small number of SNPs per sample (b_29L and e_45SR = 16 SNPs, c_29SR = 29 and d_45PL and f_45FL = 21 SNPs). Out of the 93 SNPs found, 71 are synonymous, 21 are non-synonymous and one generated a stop codon. Although those mutations are not related to the increase of virus replication and/or infectivity, some SNPs were found in non-structural proteins which may have an effect on viral evasion from the mammal immunological system. These findings reinforce the needing of further studies on those variants and of continued genomic surveillance strategies to track viral adaptations and to monitor CHIKV epidemics for improved public health control.