Our current research is focused on two major projects. On the one hand and for the last 20 years, our laboratory has centered on the effect of herpesvirus infection on neurodegeneration. Specifically, we have addressed the characterization and assessment of the role of herpes simplex virus type 1 infection –HSV-1- in neurodegeneration or demyelination diseases, such as multiple sclerosis. In this sense, the main fields of study are viral entry into human oligodendrocyte lines, cycle, acquisition of the lipid envelope, viral transport and egress, involvement of microvesicles in the process and, in parallel, characterization of antiherpetic agents capable of penetrating the CNS. For instance, we have demonstrated that HSV-1 can leave cells enclosed within microvesicles that allow the virus to increase its tropism and spread throughout the host, evading the immune response. In addition, our group assessed the role of the MAL protein (which plays an important role in the compaction and stability of myelin) in HSV-1 infection, demonstrating that MAL is crucial in the infection of oligodendrocytes. Besides, we are interested in characterizing the effect of herpesviruses on the development of autophagy mechanisms. Our results suggest that HSV-1 interferes with the maturation of autophagosomes in human oligodendroglioma and primary murine oligodendrocyte precursor cells.