My laboratory studies the interplay between cellular metabolic dysregulation and viral replication and persistence, with particular focus on latent infections by human retroviruses (HIV and HTLV) and, more recently, human coronaviruses. Our research is oriented toward translational applications, aiming to identify novel biomarkers of disease progression and therapeutic targets to selectively eliminate infected cells or inhibit viral replication. All projects integrate multi-omics approaches (mainly single-cell and bulk transcriptomics, proteomics, and metabolomics) with wet lab experiments, primarily on primary blood cells and patient-derived samples in collaboration with clinical centres.

Specific projects include:

• Characterisation of the role of mitochondrial metabolism in latent HIV infection. After integrating its genome into host cells, the human immunodeficiency virus (HIV) can persist in a latent form that is refractory to current antiretroviral therapy. This remains the major barrier to achieving a scalable and safe cure for HIV infection. Metabolic signatures associated with latent HIV infection can be exploited to selectively eliminate latently infected cells, as demonstrated in laboratory tests (e.g., Shytaj et al.,EMBO Mol Med, 2021) and in early-phase clinical trials (Diaz et al.,  J. Antimicrob. Agents, 2019). This project focusses on the role of mitochondria, key regulators of cellular energy. By combining subcellular multi-omics, multicolour flow cytometry, high-resolution imaging, and biochemical assays we study changes in mitochondrial structure and function during active and latent HIV infection.
• Investigation of latent HIV infection in lymphoid tissue using tonsil organoids. By infecting tonsil organoids with an HIV construct that allows distinguishing between active and latent infection at the single-cell level we explore how HIV-induced metabolic dysregulation in infected cells relates to the spatial organisation of surrounding cells and to the organoid/tissue architecture.
• Identification of therapeutic markers to selectively eliminate HTLV-1 infected cells. The human T-lymphotropic virus 1 (HTLV-1) infects an estimated 5–10 million people worldwide and can lead to severe diseases, including neurodegeneration and an aggressive leukaemia/lymphoma characterised by poor prognosis and high resistance to chemotherapy. By combining metabolomic profiling of a cohort of individuals living with HTLV-1, stratified by clinical status, with proteomic and metabolomic analyses from cellular models, we aim to identify highly selective markers of druggable potential that could be targeted to eliminate HTLV-1 infected cells and tumour cells.