AS CONTRIBUIÇÕES DA ISO 26000

A ISO 26000 é a primeira norma internacional de Responsabilidade Social Empresarial. Teve o início doseu desenvolvimento em 2005, mas foi só em novembro de 2010 que foi publicada em Genebra-Suíça. A normafoi elaborada por meio de um processo que envolveu cerca de 450 especialistas de 99 países, liderados por umengenheiro brasileiro, Jorge Cajazeira. Esta norma foi criada para uso de qualquer tipo de organização nos setorespúblico e privado e sem fins lucrativos, independente do seu tamanho e da sua experiência com o tema responsabilidadesocial ou atividade. A norma internacional veio com a proposta de ser um guia para as organizações e nãocomo certificadora, tem sete princípios, e os temas principais do documento são direitos humanos, práticas de trabalho,meio ambiente, governança organizacional, práticas leais de operação, relacionamento com consumidores,envolvimento comunitário e desenvolvimento e possui um capítulo específico de orientação sobre como integrarresponsabilidade social nas organizações. O método de abordagem utilizado neste trabalho foi a prática de pesquisadocumental caracterizada pela pesquisa direto das fontes, realizada a partir de documentos

Viral immunogenicity determines epidemiological fitness in a cohort of DENV-1 infection in Brazil

<div><p>The dynamics of dengue virus (DENV) circulation depends on serotype, genotype and lineage replacement and turnover. In São José do Rio Preto, Brazil, we observed that the L6 lineage of DENV-1 (genotype V) remained the dominant circulating lineage even after the introduction of the L1 lineage. We investigated viral fitness and immunogenicity of the L1 and L6 lineages and which factors interfered with the dynamics of DENV epidemics. The results showed a more efficient replicative fitness of L1 over L6 in mosquitoes and in human and non-human primate cell lines. Infections by the L6 lineage were associated with reduced antigenicity, weak B and T cell stimulation and weak host immune system interactions, which were associated with higher viremia. Our data, therefore, demonstrate that reduced viral immunogenicity and consequent greater viremia determined the increased epidemiological fitness of DENV-1 L6 lineage in São José do Rio Preto.</p></div

Replicative fitness in mosquitoes under selective pressure of DENV-1 lineages.

<p>(A and B) Viral cDNA copy number of L1 or L6 viruses in PPCampos. (A) and Dom Pedro (B). (C and D) Proportion of the infection rate (IR), disseminated infection rate (DIR) and vector competence (VC) of L1 or L6 viruses in PPCampos (C) and Dom Pedro (D). (E) Coinfection of L1 and L6 isolates in Aag-2 cells (MOI = 0.1) (Student’s T test).</p

Evolutionary relationship between DENV-1 isolates and co-circulation of the two lineages from SJRP.

<p>(A) Phylogenetic tree of DENV-1 after Bayesian inference based on envelope nucleotide sequences with aa substitutions, characterizing the L1 and L6 lineages from SJRP, which are shown in blue and red, respectively. (B) Comparison of amino acid substitutions between the representative complete genome sequences of L1 and L6 lineages from SJRP (287/2011 and 484/2012, respectively). (C) Circulation of DENV-1 lineages (L1 and L6) in SJRP from 2008 to 2015 based on sequencing and genotyping data.</p

Replicative fitness in cell culture and cross-reactive immunity of DENV-1 lineages.

<p>(A) Growth curves of L1 or L6 isolates infected at an MOI of 0.1 in mosquito (C6/36 and Aag-2), human (HepG2) and non-human primate (Vero E6 and LLC-MK2) cell lines (<i>P</i> ≤ 0.05, Student’s T test). (B) Proportion of L1 or L6 DENV-1 cases classified as primary (negative IgG) or secondary (positive IgG) DENV infections (Fisher’s exact test).</p

sfRNA and expression of type I interferon antiviral responses by DENV-1 lineages.

<p>(A) Ratio of sfRNA:gRNA in HepG2 cells infected with L1 or L6 viruses at an MOI of 1.0 (Student’s T test). (B) Quantification of IFN-α1/13 production in supernatants of HepG2 cells by an ELISA (Chi-squared test). (C) Viral cDNA copy number of DENV-2, L1 or L6 viruses in HBMECs (before or after treatment with IFN-β) using real-time PCR. (D) IFN-induced luciferase activity in HBMECs that were mock-treated or infected with DENV-2, L1 or L6 DENV-1 in the presence or absence of IFN-β (Student’s T test). (E) Quantification of IFN-α2 production in negative controls and L1 or L6 DENV-1-infected patients using the Luminex assay (Mann-Whitney test).</p

Quantification of cytokines, chemokines, adhesion molecules and growth factors showing significant differences in L1 or L6 DENV-1-infected patients.

<p>(A) IL-1RA. (B) IL-12p40. (C) IL-7. (D) IL-17a. (E) IL-13. (F) EGF. (G) VEGF. (H) CCL11. (Mann-Whitney test). See also <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006525#pntd.0006525.s003" target="_blank">S3 Fig</a>.</p

Viral load quantification of DENV-1-infected patients using real-time PCR.

<p>Viral load quantification of DENV-1-infected patients using real-time PCR.</p

Proposed model for L6 lineage (red) dominant circulation without L1 lineage replacement (blue) in the SJRP population, with the main differences found between the two DENV-1 lineages.

<p>Proposed model for L6 lineage (red) dominant circulation without L1 lineage replacement (blue) in the SJRP population, with the main differences found between the two DENV-1 lineages.</p