Zika virus (ZIKV) infection has been associated with severe complications both in the developing and adult nervous system. To investigate the deleterious effects of ZIKV infection, we used human neural progenitor cells (NPC), derived from induced pluripotent stem cells (iPSC).Evidence favoring a causative role for ZIKV in microcephaly has emerged and was the object of several publications. For instance, ZIKV was detected in the amniotic fluids of two fetuses that presented microcephaly, which strongly suggests intrauterine transmission 7 . In addition, detection of the virus together with numerous alterations in the brain of an aborted fetus, while the virus was not detected in any other fetal tissue, also suggested a neurotropism 8 . Epidemiological data showed varied percentage of risk of microcephaly when infection occurs in the first trimester in different geographical locations, suggesting that other factors such as virus strain and co-infections may also contribute to the development of congenital defects 9 . Therefore, the understanding of the mechanisms involved in the neurotoxicity caused by ZIKV is of great relevance.Studies in animal models have also reinforced the link between ZIKV infection and congenital malformations 10-12 . These, however, do not reproduce properly the human infection, since mice are resistant to ZIKV

Uncertainty remains about how long the protective immune responses against severe acute respiratory syndrome coronavirus 2 persists, and suspected reinfection in recovered patients has been reported. We describe a case of reinfection from distinct virus lineages in Brazil harboring the E484K mutation, a variant associated with escape from neutralizing antibodies.

MicroRNAs are small non-coding RNAs that regulate gene expression post-transcriptionally. They are involved in the regulation of physiological processes, such as adaptation to physical exercise, and also in disease settings, such as systemic arterial hypertension (SAH), type 2 diabetes mellitus (T2D), and obesity. In SAH, microRNAs play a significant role in the regulation of key signaling pathways that lead to the hyperactivation of the renin-angiotensin-aldosterone system, endothelial dysfunction, inflammation, proliferation, and phenotypic change in smooth muscle cells, and the hyperactivation of the sympathetic nervous system. MicroRNAs are also involved in the regulation of insulin signaling and blood glucose levels in T2D, and participate in lipid metabolism, adipogenesis, and adipocyte differentiation in obesity, with specific microRNA signatures involved in the pathogenesis of each disease. Many studies report the benefits promoted by exercise training in cardiovascular diseases by reducing blood pressure, glucose levels, and improving insulin signaling and lipid metabolism. The molecular mechanisms involved, however, remain poorly understood, especially regarding the participation of microRNAs in these processes. This review aimed to highlight microRNAs already known to be associated with SAH, T2D, and obesity, as well as their possible regulation by exercise training.