Infections caused by human immunodeficiency viruses (HIV) are a global health burden. Despite progress in antiretroviral therapy, HIV still causes significant deaths. Our lab focuses on understanding HIV's genetic machinery and drug resistance mechanisms. We engineer more accurate DNA synthesizing enzymes for biotech tools and study their roles in viral replication. Our research aims to improve therapies and develop new strategies against HIV's resistance and spread, as well as other viruses with related enzymes and replication mechanisms (e.g. hepatitis B virus and herpesviruses).

Our group works in different aspects of the molecular mechanisms mediating animal viruses pathogenesis. The information obtained is being used for the development of new antiviral strategies.

Control of cell division and genome replication: implications of epigenetic modifications

Studying virus factories as scaffolds for viral replication and morphogenesis. Development of new imaging technologies to study viruses in cells and to visualize macromolecular complexes in their natural environment. New antivirals and drug repurposing.

Application of state-of-the-art methodolgies in electron microscopy and three-dimensional reconstruction to study viruses, mainly influenza A virus; and macromolecuar aggregates.

Activation, proliferation and apoptosis are basic mechanisms for regulation of activated/memory T cell expansion, known as homeostasis. Our research is focused on the identification of differences in the control of expansion between autoimmune and normal memory T cells. The unique characteristics of autoimmune memory T cells might be of therapeutic relevance for autoimmunity treatment.

The overall objective of our group is to understand nanomedicines-mediated molecular and cellular mechanisms in distinct biomedical applications oriented to cancer and autoimmunity treatment, and to use this knowledge to improve nanomedicines functional design for antitumour and autoinmune disease therapies.

The complexity of the B lymphocyte immune response involves changes in cell behavior, switching from highly motile states to stable cell-to-cell interactions (immune synapse), adjustments of the cell mechanical properties (flexibility, stiffness) and cell polarity (MTOC and organelle distribution). Gene mutations or functional alterations in proteins related with these events are frequent in B lymphocyte-pathologies (immunodeficiency, lymphomas), stressing their relevance for B cell function.