RESUMO
Throughout the year 2019, Nigeria had sporadic outbreaks of yellow fever (YF), which began in the northern region of the country. Indeed, controlling the bites and population of Aedes mosquitoes and vaccination are the only effective means of preventing YF. Vectorial migration, sylvan-to-urban spillover, immunization failure and, perhaps, genetic modification of YFV could be reasons for the re-emergence of YF at the community, state and national levels. This article offers a critical review of the vector biology, YF vaccine immunodynamics and environmental drivers of YFV infections, with the aim of understanding the interplay of these factors in the re-emergence of YF and risk assessment of living in or travelling to areas where YF is endemic.
RESUMO
Summary: T helper 17 (Th17) are a CD4+ T subpopulation cells which are involved in the host protection against microbes such as extracellular and intracellular bacteria, parasites, fungi, and viruses. Monogenic defects including those mutations in some genes such as the signal transducer and activator of transcription (STAT)1 and 3, dedicator of cytokinesis 8 (DOCK8), autoimmune regulator (AIRE), and interleukin 17 receptor A (IL-17RA) can lead to impairment in Th17 cell development and function along with the concomitant increased risk for chronic mucocutaneous candidiasis (CMC). The immunologic abnormalities in these patients include low frequency of Th17 cells; defective cutaneous or in vitro T cell response to Candida species, and/or autoantibodies against relevant cytokines. This review outlines the biological characteristics and functionality of Th17 cells, as well as the clinical features of individuals with genetic defects associated with Th17 deficiency.