Genomic epidemiology of Chikungunya virus in Colombia reveals genetic variability of strains and multiple geographic introductions in outbreak, 2014.

Chikungunya virus (CHIKV) is considered a public health problem due to its rapid spread and high morbidity. This study aimed to determine the genetic diversity and phylogenetic relationships of CHIKVs in Colombia. A descriptive and retrospective study was carried out using sera of patients infected with Chikungunya during the outbreak in Colombia. The whole genomes of CHIKV (n = 16) were sequenced with an Illumina Hi-seq 2500 and were assembled using the Iterative Virus Assembler software. A Bayesian inference phylogenetic analysis was carried out with 157 strains of worldwide origin. The Colombian CHIKV sequences were grouped in the Asian genotype; however, three independent phylogenetic subclades were observed, probably the result of three separate introductions from Panama, Nicaragua, and St. Barts. Each subclade showed several different non-synonymous mutations (nsP2-A153V; nsp2-Y543H; nsp2-G720A; nsP3-L458P; Capside R78Q), that may have functional consequences for CHIKV biology and pathogenesis. These same mutations may affect the efficacy of potential CHIKV vaccines.

Genome Sequence of "Candidatus Rickettsia colombianensi," a Novel Tick-Associated Bacterium Distributed in Colombia.

This is the first report of the genome sequence of "Candidatus Rickettsia colombianensi" strain Adcor 2, deposited in DDBJ/ENA/GenBank under the accession number RAQN00000000 The draft genome showed 36.01% similarity with that of Rickettsia monacensis strain IrR/Munich (NCBI accession number LN794217), 37.81% similarity with that of Rickettsia heilongjiangensis 054 (NCBI accession number CP002912), and 43.88% similarity with that of Rickettsia tamurae AT-1 (NCBI accession number CCMG01000001).

Dengue virus potentially promotes migratory responses on endothelial cells by enhancing pro-migratory soluble factors and miRNAs.

The most life-threatening effect of the Dengue virus (DENV) infection is an acute destabilization of the microvascular endothelial cell (MEC) barrier leading to plasma leakage, hypovolemic shock and haemorrhage. However, the underlying cellular mechanisms responsible for the dysfunction of MECs are not well understood. To identify potential cellular processes altered during DENV infection of MECs, expression profiles of cytokines/growth factors and microRNAs were measured by Luminex assay and next generation sequencing, respectively. Synchronously DENV2-infected MECs increase the secretion of IL-6, IL-8, FGF-2, GM-CSF, G-CSF, TGF-α, GRO, RANTES, MCP-1 and MCP-3. Conditioned media of infected MECs increased the migration of non-infected MECs. Furthermore, six miRNAs deregulated at 24 hpi were predicted to regulate host genes involved in cell migration and vascular developmental processes such as angiogenesis. These in silico analyses provide insights that support that DENV promotes an acute migratory phenotype in MECs that contributes to the vascular destabilization observed in severe dengue cases.