RESUMO
Zika virus (ZIKV) infection is a major public health threat, making the study of its biology a matter of great importance. By analyzing the viral-host protein interactions, new drug targets may be proposed. In this work, we showed that human cytoplasmic dynein-1 (Dyn) interacts with the envelope protein (E) of ZIKV. Biochemical evidence indicates that the E protein and the dimerization domain of the heavy chain of Dyn binds directly without dynactin or any cargo adaptor. Analysis of this interactions in infected Vero cells by proximity ligation assay suggest that the E-Dyn interaction is dynamic and finely tuned along the replication cycle. Altogether, our results suggest new steps in the replication cycle of the ZIKV for virion transport and indicate a suitable molecular target to modulate infection by ZIKV.
Assuntos
Infecção por Zika virus , Zika virus , Chlorocebus aethiops , Humanos , Animais , Dineínas do Citoplasma , Células Vero , Transporte BiológicoRESUMO
Diabetes mellitus (DM) leads to microvascular, macrovascular, and neurological complications. Less is understood about the mechanisms of this disease that give rise to weak bones. The many molecular mechanisms proposed to explain the damage caused by chronic hyperglycemia are organ and tissue dependent. Since all the different treatments for DM involve therapeutic activity combined with side effects and each patient represents a unique condition, there is no generalized therapy. The alterations stemming from hyperglycemia affect metabolism, osmotic pressure, oxidative stress, and inflammation. In part, hemodynamic modifications are linked to the osmotic potential of the excess of carbohydrates implicated in the disease. The change in osmotic balance increases as the disease progresses because hyperglycemia becomes chronic. The aim of the current contribution is to provide an updated overview of the molecular mechanisms that participate in the development and treatment of diabetes.