
Maria Nevot Banús
Degree in Pharmacy and PhD from the University of Barcelona. Since 2007, her scientific career has focused on the study of RNA viruses, specifically HIV, HCV and, since 2020, SARS-CoV-2. As a postdoctoral researcher at IrsiCaixa, she has participated in studies of inhibition of HIV replication using interfering RNA, to explore the evolutionary capacity and mechanisms of viral escape (Nevot et al., 2011, DOI: 10.1016 / j.jmb.2011.08.035). She has also been involved in studies with HIV and HCV co-infected patients, specifically in cases of acute hepatitis in HIV-positive patients, of which an increase is being observed in recent years (Nevot et al., 2014, DOI: 10.1111 / JVH. 12254). Until 2020, her work was focused on studying the effect of synonymous mutations on the replicative and evolutionary capacity of HIV-1 (Martrus et al Retrovirology 2013; Martinez et al Trends in Microbiology 2016; Nevot et al J Virol 2018).
Since joining the Translational Research in Immunology and Aging (TRIA) group in 2020, she has focused on studying the post COVID-19 condition with the aim of elucidating the underlying pathophysiological mechanisms causing this new disease. Her work has focused on exploring the different hypotheses in the origin of this condition (immune dysfunction, viral persistence, autoimmunity, endothelial damage, etc.), with special emphasis on the role of NK cells.
Detection of a sexually transmitted hepatitis C virus protease inhibitor-resistance variant in a human immunodeficiency virus-infected homosexual man.
Molecular basis of the association of H208Y and thymidine analogue resistance mutations M41L, L210W and T215Y in the HIV-1 reverse transcriptase of treated patients.
Changes in codon-pair bias of human immunodeficiency virus type 1 have profound effects on virus replication in cell culture.
HIV-1 lethality and loss of Env protein expression induced by single synonymous substitutions in the virus genome intronic splicing silencer.
Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy.